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<h1 data-aos="fade-down" id="covid-19-sentry">Covid-19 Sentry</h1>
<h1 data-aos="fade-right" data-aos-anchor-placement="top-bottom" id="contents">Contents</h1>
<ul>
<li><a href="#from-preprints">From Preprints</a></li>
<li><a href="#from-clinical-trials">From Clinical Trials</a></li>
<li><a href="#from-pubmed">From PubMed</a></li>
<li><a href="#from-patent-search">From Patent Search</a></li>
</ul>
<h1 data-aos="fade-right" id="from-preprints">From Preprints</h1>
<ul>
<li><strong>Securing your relationship: Quality of intimate relationships during the COVID-19 pandemic can be predicted by attachment style</strong> -
<div>
The COVID-19 pandemic along with the restrictions that were introduced within Europe starting spring 2020 allows for the identification of predictors for relationship quality during unstable and stressful times. The present study began as strict measures were enforced in response to the rising spread of the COVID-19 within Austria, Poland, Spain and Czech Republic. Here, we investigated quality of romantic relationships among 313 participants as movement restrictions were implemented and subsequently phased out cross-nationally. Participants completed self-report questionnaires over a period of seven weeks, where we predicted relationship quality and change in relationship quality using machine learning models that include a variety of potential predictors related to psychological, demographic and environmental variables. On average, our machine learning tools predicted 29% (linear models) and 22% (non-linear models) of the variance with regard to relationship quality. Here, the most important predictors consisted of attachment style (anxious attachment being more influential than avoidance), age, and number of conflicts within the relationship. Interestingly, environmental factors such as the local severity of the pandemic did not exert a measurable influence with respect to predicting relationship quality. As opposed to overall relationship quality, the change in relationship quality during lockdown restrictions could not be predicted accurately by our machine learning models when utilizing our selected features. In conclusion, we demonstrate cross-culturally that attachment security is a major predictor of relationship quality during COVID-19 lockdown restrictions, whereas sexual behavior, fear, pathogenic threat and the severity of governmental regulations did not significantly influence the accuracy of prediction.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://psyarxiv.com/huzc2/" target="_blank">Securing your relationship: Quality of intimate relationships during the COVID-19 pandemic can be predicted by attachment style</a>
</div></li>
<li><strong>Containing the Spread of Infectious Disease on College Campuses</strong> -
<div>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
College campuses are highly vulnerable to infectious disease outbreaks, and there is a pressing need to develop better strategies to mitigate their size and duration, particularly as educational institutions around the world reopen to in-person instruction in the midst of the COVID-19 pandemic. Towards addressing this need, we applied a stochastic compartmental model to quantify the impact of university-level responses to past mumps outbreaks in college campuses and used it to determine which control interventions are most effective. Mumps is a very relevant disease in such settings, given its airborne mode of transmission, high infectivity, and recurrence of outbreaks despite availability of a vaccine. Our model aims to simultaneously overcome three crucial issues: stochastic variation in small populations, missing or unobserved case data, and changes in disease transmission rates post-intervention. We tested the model and assessed various interventions using data from the 2014 and 2016 mumps outbreaks at Ohio State University and Harvard University, respectively. Our results suggest that in order to decrease infectious disease incidence on their campuses, universities should apply diagnostic protocols that address false negatives from molecular tests, stricter quarantine policies, and effective awareness campaigns among their students and staff. Our model can be applied to data from other outbreaks in college campuses and similar small-population settings.
</p>
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.07.31.20166348v4" target="_blank">Containing the Spread of Infectious Disease on College Campuses</a>
</div></li>
<li><strong>Covid-19 Pfizer Vaccine: The Worst-Case Scenario</strong> -
<div>
The BioNTech/Pfizer BNT162b2 vaccine against Covid-19 is composed of an RNA having 4284 nucleotides, divided into 6 sections, which bring the information to create a factory of S Spike proteins, the ones used by Sars-CoV-2 (Covid-19) to infect the subject. After that, these proteins are directed outside the cell, triggering the immune reaction and antibody production. The problem is the heavy alteration of the mRNA: the Uracyl is replaced to fool the immune system, the letters of all codon triplets are replaced by a C or a G, to extremely increase the speed of protein production, replacement of some amino acids with Proline, the addition of a not clear sequence (3'-UTR), combined with alternative splicing, which is the possibility of errors in translation of the sequence and synthesis of proteins; they are not produced equal, but slightly different. All this can be the cause of many hereditary diseases and various types of tumors, from appearance to their growth, up to the metastasis formation. In essence, what will be created is anything but well defined as protein S Spike: just a transcription error, wrong production of amino acids, then proteins, to cause serious long-term damage to human health, despite the DNA is not modified, being instead in the cell nucleus and not in the cytoplasm, where the modified mRNA arrives. However, in this case, the correlation between speed of synthesis and protein expression with synthesis errors, as well as the mechanism that could affect the translation of the sequence remain obscure, as many trials are owned by BioNTech/Pfizer.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://osf.io/epr24/" target="_blank">Covid-19 Pfizer Vaccine: The Worst-Case Scenario</a>
</div></li>
<li><strong>Predictions of COVID-19 dynamics in the UK: short-term forecasting and analysis of potential exit strategies</strong> -
<div>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
Efforts to suppress transmission of SARS-CoV-2 in the UK have seen non-pharmaceutical interventions being invoked. The most severe measures to date include all restaurants, pubs and cafes being ordered to close on 20th March, followed by a stay at home order on the 23rd March and the closure of all non-essential retail outlets for an indefinite period. Government agencies are presently analysing how best to develop an exit strategy from these measures and to determine how the epidemic may progress once measures are lifted. Mathematical models are currently providing short and long term forecasts regarding the future course of the COVID-19 outbreak in the UK to support evidence-based policymaking. We present a deterministic, age-structured transmission model that uses real-time data on confirmed cases requiring hospital care and mortality to provide up-to-date predictions on epidemic spread in ten regions of the UK. The model captures a range of age-dependent heterogeneities, reduced transmission from asymptomatic infections and produces a good fit to the key epidemic features over time. We simulated a suite of scenarios to assess the impact of differing approaches to relaxing social distancing measures from 7th May 2020 on the estimated number of patients requiring inpatient and critical care treatment, and deaths. With regard to future epidemic outcomes, we investigated the impact of reducing compliance, ongoing shielding of elder age groups, reapplying stringent social distancing measures using region based triggers and the role of asymptomatic transmission. We find that significant relaxation of social distancing measures from 7th May onwards can lead to a rapid resurgence of COVID-19 disease and the health system being quickly overwhelmed by a sizeable, second epidemic wave. In all considered age-shielding based strategies, we projected serious demand on critical care resources during the course of the pandemic. The reintroduction and release of strict measures on a regional basis, based on ICU bed occupancy, results in a long epidemic tail, until the second half of 2021, but ensures that the health service is protected by reintroducing social distancing measures for all individuals in a region when required. Our work confirms the effectiveness of stringent non-pharmaceutical measures in March 2020 to suppress the epidemic. It also provides strong evidence to support the need for a cautious, measured approach to relaxation of lockdown measures, to protect the most vulnerable members of society and support the health service through subduing demand on hospital beds, in particular bed occupancy in intensive care units.
</p>
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.05.10.20083683v3" target="_blank">Predictions of COVID-19 dynamics in the UK: short-term forecasting and analysis of potential exit strategies</a>
</div></li>
<li><strong>Characterization of cell-cell communication in COVID-19 patients</strong> -
<div>
COVID-19 patients display a wide range of disease severity, ranging from asymptomatic to critical symptoms with high mortality risk. Our ability to understand the interaction of SARS-CoV-2 infected cells within the lung, and of protective or dysfunctional immune responses to the virus, is critical to effectively treat these patients. Currently, our understanding of cell-cell interactions across different disease states, and how such interactions may drive pathogenic outcomes, is incomplete. Here, we developed a generalizable workflow for identifying cells that are differentially interacting across COVID-19 patients with distinct disease outcomes and use it to examine five public single-cell RNA-seq datasets with a total of 85 individual samples. By characterizing the cell-cell interaction patterns across epithelial and immune cells in lung tissues for patients with varying disease severity, we illustrate diverse communication patterns across individuals, and discover heterogeneous communication patterns among moderate and severe patients. We further illustrate patterns derived from cell-cell interactions are potential signatures for discriminating between moderate and severe patients.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.30.424641v1" target="_blank">Characterization of cell-cell communication in COVID-19 patients</a>
</div></li>
<li><strong>Screening a library of FDA-approved and bioactive compounds for antiviral activity against SARS-CoV-2</strong> -
<div>
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has emerged as a major global health threat. The COVID-19 pandemic has resulted in over 80 million cases and 1.7 million deaths to date while the number of cases continues to rise. With limited therapeutic options, the identification of safe and effective therapeutics is urgently needed. The repurposing of known clinical compounds holds the potential for rapid identification of drugs effective against SARS-CoV-2. Here we utilized a library of FDA-approved and well-studied preclinical and clinical compounds to screen for antivirals against SARS-CoV-2 in human pulmonary epithelial cells. We identified 13 compounds that exhibit potent antiviral activity across multiple orthogonal assays. Hits include known antivirals, compounds with anti-inflammatory activity, and compounds targeting host pathways such as kinases and proteases critical for SARS-CoV-2 replication. We identified seven compounds not previously reported to have activity against SARS-CoV-2, including B02, a human RAD51 inhibitor. We further demonstrated that B02 exhibits synergy with remdesivir, the only antiviral approved by the FDA to treat COVID-19, highlighting the potential for combination therapy. Taken together, our comparative compound screening strategy highlights the potential of drug repurposing screens to identify novel starting points for development of effective antiviral mono- or combination therapies to treat COVID-19.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.30.424862v1" target="_blank">Screening a library of FDA-approved and bioactive compounds for antiviral activity against SARS-CoV-2</a>
</div></li>
<li><strong>Direct measurement of B lymphocyte gene expression biomarkers in peripheral blood enables early prediction of seroconversion after vaccination</strong> -
<div>
Vaccination is a common and efficient means to reduce the mortality and morbidity of emerging infectious diseases. Among responders, injected antigen induces acquired immunity pathways and leads to the final production of antigen-specific antibodies. The whole process may take weeks to months, depending on the antigen. Typically, seroconversion to influenza vaccine is expected after one month with a responder rate of ~50%. An early biomarker to predict response is desirable. Peripheral blood gene expression (or transcript abundance, TA) datasets in the public domain were analyzed for early biomarkers among responders. As peripheral blood samples (such as peripheral blood mononuclear cells, PBMC) are cell mixture samples containing various blood cell-types (leukocyte subpopulations, LS). We first develop a model that enables the determination of TA in B lymphocytes of certain genes directly in PBMC samples without the need of prior cell isolation. These genes are called B cell informative genes. Then a ratio of two B cell informative genes (a target gene and a stably expressed reference gene) measured in PBMC was used as a new biomarker to gauge the target gene expression in B lymphocytes. This method having an obvious advantage over conventional methods by eliminating the tedious procedure of cell sorting and enables directly determining TA of a leukocyte subpopulation in cell mixture samples is called Direct LS-TA method. By using a B lymphocyte-specific gene such as TNFRSF17 or TXNDC5 as target genes with either TNFRSF13C or FCRLA as reference genes, the B cell biomarkers were determined directly in PBMC which was highly correlated with TA of target genes in purified B lymphocytes. These Direct LS-TA biomarkers in PBMC increased significantly early after vaccination in both the discovery dataset and a meta-analysis of 7 datasets. Responders had almost a 2-fold higher Direct LS-TA biomarker level of TNFRSF17 (SMD=0.84, 95% CI=0.47-1.21 after log2). And Direct LS-TA biomarkers of TNFRSF17 and TXNDC5 measured at day 7 predict responder with sensitivity values of higher than 0.7. The Area-under curves (AUC) in receiver operation curve (ROC) analysis were over 0.8. Here, we report a straightforward approach to directly analyses B lymphocyte gene expression in PBMC, which could be used in a routine clinical setting as it avoids the labor-intensive procedures of B lymphocyte isolation. And the method allows the practice of precision medicine in the prediction of vaccination response. Furthermore, response to vaccination could be predicted as early as on day 7. As vaccination response is based on the similar acquired immunology pathway in the upcoming worldwide vaccination campaign against COVID-19, these biomarkers could also be useful to predict seroconversion for individuals.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.29.424767v1" target="_blank">Direct measurement of B lymphocyte gene expression biomarkers in peripheral blood enables early prediction of seroconversion after vaccination</a>
</div></li>
<li><strong>Engineering, production and characterization of Spike and Nucleocapsid structural proteins of SARS-CoV-2 in Nicotiana benthamiana as vaccine candidates against COVID-19</strong> -
<div>
The COVID-19 pandemic, which is caused by SARS-CoV-2 has rapidly spread to more than 216 countries and has put global public health at high risk. The world urgently needs a cost-effective and safe SARS-CoV-2 coronavirus vaccine, antiviral and therapeutic drugs to control the COVID-19 pandemic. In this study, we engineered the Nucleocapsid (N) and Spike protein (S) variants (Receptor binding domain, RBD and S1 domain) of SARS-CoV-2 genes and produced in Nicotiana benthamiana plant. The purification yields were at least 20 mg of pure protein/kg of plant biomass for each target protein. The S protein variants of SARS-CoV-2 showed specific binding to angiotensin converting enzyme 2 (ACE2), the SARS-CoV-2 receptor. The purified plant produced N and S variants were recognized by N and S protein specific monoclonal and polyclonal antibodies demonstrating specific reactivity of mAb to plant produced N and S protein variants. In addition, IgG responses of plant produced N and S antigens elicited significantly high titers of antibody in mice. This is the first report demonstrating production of functional active S1 domain and Nucleocapsid protein of SARC-CoV-2 in plants. In addition, in this study, for the first time, we report the co-expression of RBD with N protein to produce a cocktail antigen of SARS-CoV-2, which elicited high-titer antibodies compared to RBD or N proteins. Thus, obtained data support that plant produced N and S antigens, developed in this study, are promising vaccine candidates against COVID-19.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.29.424779v1" target="_blank">Engineering, production and characterization of Spike and Nucleocapsid structural proteins of SARS-CoV-2 in Nicotiana benthamiana as vaccine candidates against COVID-19</a>
</div></li>
<li><strong>Corruption in the Times of Pandemia</strong> -
<div>
The public health and economic crisis caused by the COVID-19 pandemic has pushed governments to substantially and swiftly increase spending. Consequently, public procurement rules have been relaxed in many places to expedite transactions. However, this may also create opportunities for inefficiency and corruption. Using contract-level information on public spending from Colombia’s e-procurement platform, and a difference-in-differences identification strategy, we find that municipalities classified by a machine learning algorithm as more prone to corruption react to the spending surge by using a larger proportion of discretionary non-competitive contracts and increasing their average value, especially to procure crisis-related items. Additionally, in places that rank higher on our corruption scale, contracts signed during the emergency are more likely to have cost overruns, be awarded to campaign donors, and exhibit implementation inefficiencies. Our evidence suggests that these negative shocks may increase waste and corruption, and thus governments should bolster instances of monitoring and oversight.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://osf.io/preprints/socarxiv/js8by/" target="_blank">Corruption in the Times of Pandemia</a>
</div></li>
<li><strong>Pharmacophore-based peptide biologics neutralize SARS-CoV-2 S1 and deter S1-ACE2 interaction in vitro</strong> -
<div>
Effective therapeutics and stable vaccine are the urgent need of the day to combat COVID-19 pandemic. SARS-CoV-2 spike protein has a pivotal role in cell-entry and host immune response, thus regarded as potential drug- and vaccine-target. As the virus utilizes the S1 domain of spike to initiate cell-attachment and S2 domain for membrane fusion, several attempts have been made to design viral-receptor and viral-fusion blockers. Here, by deploying interactive structure-based design and pharmacophore-based approaches, we designed short and stable peptide-biologics i.e. CoV-spike-neutralizing peptides (CSNPs) including CSNP1, CSNP2, CSNP3, CSNP4. We could demonstrate in cell culture experiments that CSNP2 binds to S1 at submicromolar concentration and abrogates the S1-hACE2 interaction. CSNP3, a modified and downsized form of CSNP2, could neither interfere with the S1-hACE2 interaction nor bind to S1. CSNP4 exhibited dose-dependent binding to both S1 and hACE2 and abolished the S1-hACE2 interaction in vitro. CSNP4 possibly enhance the mAb-based S1 neutralization by limiting the spontaneous movement of spike receptor-binding domain (RBD), whereas CSNP2 allowed RBD-mAb binding without any steric hindrance. Taken together, we suggest that CSNP2 and CSNP4 are potent and stable candidate peptides that can neutralize the SARS-CoV-2 spike and possibly pose the virus to host immune surveillance.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.30.424801v1" target="_blank">Pharmacophore-based peptide biologics neutralize SARS-CoV-2 S1 and deter S1-ACE2 interaction in vitro</a>
</div></li>
<li><strong>In vitro Targeting of Transcription Factors to Control the Cytokine Release Syndrome in COVID-19</strong> -
<div>
Treatment of the cytokine release syndrome (CRS) has become an important part of rescuing hospitalized COVID-19 patients. Here, we systematically explored the transcriptional regulators of inflammatory cytokines involved in the COVID-19 CRS to identify candidate transcription factors (TFs) for therapeutic targeting using approved drugs. We integrated a resource of TF-cytokine gene interactions with single-cell RNA-seq expression data from bronchoalveolar lavage fluid cells of COVID-19 patients. We found 581 significantly correlated interactions, between 95 TFs and 16 cytokines upregulated in the COVID-19 patients, that may contribute to pathogenesis of the disease. Among these, we identified 19 TFs that are targets of FDA approved drugs. We investigated the potential therapeutic effect of 10 drugs and 25 drug combinations on inflammatory cytokine production in peripheral blood mononuclear cells, which revealed two drugs that inhibited cytokine production and numerous combinations that show synergistic efficacy in downregulating cytokine production. Further studies of these candidate repurposable drugs could lead to a therapeutic regimen to treat the CRS in COVID-19 patients.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.29.424728v1" target="_blank">In vitro Targeting of Transcription Factors to Control the Cytokine Release Syndrome in COVID-19</a>
</div></li>
<li><strong>Meta-analysis of virus-induced host gene expression reveals unique signatures of immune dysregulation induced by SARS-CoV-2</strong> -
<div>
The clinical outcome of COVID-19 has an extreme age, genetic and comorbidity bias that is thought to be driven by an impaired immune response to SARS-CoV-2, the causative agent of the disease. The unprecedented impact of COVID-19 on global health has resulted in multiple studies generating a variety of large gene expression datasets in a relatively short period of time. In order to better understand the immune dysregulation induced by SARS-CoV-2, we carried out a meta-analysis of these transcriptomics data available in the published literature. Datasets included both those available from SARS-CoV-2 infected cell lines in vitro and those from patient samples. We focused our analysis on the identification of viral perturbed host functions as captured by co-expressed gene module analysis. Transcriptomics data from lung biopsies and nasopharyngeal samples, as opposed to those available from other clinical samples and infected cell lines, provided key signatures on the role of the host's immune response on COVID-19 pathogenesis. For example, severity of infection and patients' age are linked to the absence of stimulation of the RIG-I-like receptor signaling pathway, a known critical immediate line of defense against RNA viral infections that triggers type-I interferon responses. In addition, co-expression analysis of age-stratified transcriptional data provided evidence that signatures of key immune response pathways are perturbed in older COVID-19 patients. In particular, dysregulation of antigen-presenting components, down-regulation of cell cycle mechanisms and signatures of hyper-enriched monocytes were strongly correlated with the age of older individuals infected with SARS-CoV-2. Collectively, our meta-analysis highlights the ability of transcriptomics and gene-module analysis of aggregated datasets to aid our improved understanding of the host-specific disease mechanisms underpinning COVID-19.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.29.424739v1" target="_blank">Meta-analysis of virus-induced host gene expression reveals unique signatures of immune dysregulation induced by SARS-CoV-2</a>
</div></li>
<li><strong>H3N2 outbreak from New York (2014-2015) shows sequence fragments matching to Escherichia phage Lambda have integrated into influenza genomes</strong> -
<div>
Letter Influenza (commonly known as ”the flu”) has 4 types - out of which 3 (A/B/C) infect humans [1]. Influenza A and B genomes each have 8 negative-sense, single-stranded viral RNA segments (C has a 7-segment genome) [2]. Two of these segments - glycoproteins hemagglutinin (HA) and neuraminidase on the surface of the virus - are used to subtype the virus [3]. The ability of these segments to mix and match (HxNx, currently there are 129 subtypes) creates a constantly mutating virus - making it difficult to devise an effective virus [4, 5]. Also, the hemagglutinin gene causes aberrant coagulation leading to a hyper-inflammatory response [6]. Lab-edited influenza viruses in circulation This is compounded by the escape of viruses being modified in laboratories that are trying to enhance the speed of development of therapeutics. For example, Covid19 patients from Wuhan and Hong Kong were infected with Influenza A appended with DNA-expression vector sequences facilitating protein transcrip- tion (18s) [7]. In another example, canine 28s was found to be integrated with Influenza A genomes in patients from Hong Kong [8]. Madin Darby canine kidney cell-lines are used to make Influenza vaccines, suggesting that some of these viruses might have escaped into circulation. ”Flucelvax Quadrivalent is the only cell-based inactivated flu vaccine that has been licensed by the FDA for use in the United States.” (https://www.cdc.gov/flu/prevent/cell-based.htm) H3N2 genomic reads have sequence fragments that match to Escherichia phage Lambda (among others) Here, Influenza samples isolated from human respiratory tract 2014-2015 from New York (Accid:PRJNA431639 [9], n=122) shows the integration of some sequence fragments matching to the Escherichia phage Lambda ev017 (Accid:NC 049948.1) in all of the eight fragments. In order to exclude the possibility of sequencing artifacts, only the occurrence of exact reads in different samples were recorded (Table 1). SPADES assembler generates full length segments along with the Escherichia phage Lambda The SPADES assembler [10] makes full length segments from these sequences (SI:spades.contigs.fa) showing the same integration. Fig 1 shows these exogenous sequences flanking a full length polymerase PA (segment 3) - note how the ends have complimentary runs of TTT (UUU) and AAA, which helps the RNA fold onto itself, probably helping better packing.
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://osf.io/8htn9/" target="_blank">H3N2 outbreak from New York (2014-2015) shows sequence fragments matching to Escherichia phage Lambda have integrated into influenza genomes</a>
</div></li>
<li><strong>Resuming professional football during the Covid-19 pandemic in a country with high infection rates A prospective cohort study</strong> -
<div>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
Objectives: The risk of viral transmission associated with contact sports such as Football during the COVID-19 pandemic is unknown. The aim of this study was to describe the development of infective and immune status of professional football players, team staff and league officials over a truncated football season resumed at the height of the Covid-19 pandemic in a country with high infection rates and to investigate the clinical symptoms related to Covid-19 infection in professional football players. Methods: Prospective cohort study of 1337 football players, staff and officials during a truncated football season (9 weeks) with a tailored infection control program based on preventive measures and regular SarS-CoV-2 PCR swab testing (every 3-5 days) combined with serology testing for immunity (every 4 weeks). Clinical symptoms in positive participants were recorded using a 26-item, Likert-scale-based scoring system. Results: During the study period, 85 subjects returned positive (cycle threshold (cT)&lt;30) or reactive (30&lt;cT&lt;40) PCR tests, of which 36 were players. The infection rate was in line with that of the general population at the time. More than half of the infected were asymptomatic, the remaining had only mild symptoms, no one required hospitalization. Symptom severity was associated to lower cT values. Social contacts and family were the most common sources of infection, no infection could be traced to training or matches. Conclusion: Sports played outdoors involving close contact between athletes represent a limited risk for SARS-CoV-2 infection and severe illness when preventive measures are in place.
</p>
</div>
<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.11.17.20233023v2" target="_blank">Resuming professional football during the Covid-19 pandemic in a country with high infection rates A prospective cohort study</a>
</div></li>
<li><strong>SARS-CoV-2 infections in people with PCD: neither frequent, nor particularly severe</strong> -
<div>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
People with pre-existing chronic health conditions are reportedly at high risk of getting the coronavirus disease (COVID-19) and of having a severe disease course but little data exist on rare diseases such as Primary Ciliary Dyskinesia (PCD). We studied risk and severity of SARS-CoV-2 infections among people with PCD using data from the COVID-PCD, a participatory study that collects data in real-time directly from people with PCD. Data was collected using online questionnaires. A baseline questionnaire collected information on demographic data, information about the PCD diagnosis and severity. A short weekly questionnaire collected information about current symptoms and incident SARS-CoV-2 infections. 578 people participated in the COVID-PCD by December 7, 2020, with a median number of follow-up weeks of 9 (interquartile range: 4-19 weeks). 256 (45%) of the participants had been tested for SARS-CoV-2 and 12 tested positive prior to study entry or during study follow up (2.1% of the total included population, 95% confidence interval (CI) 1.1-3.6%). 4 people tested positive during the study follow-up, corresponding to an incidence rate of 2.5 per 100 person-years (95% CI: 0.9-6.5). Overall, reported severity was mild with two reporting no symptoms, eight reporting mild symptoms, one reporting severe symptom without hospitalisation, and one reporting hospitalisation for 9 days. The study suggests that with careful personal protection, people with PCD do not seem to have an increased risk of infection with SARS-COV-2, nor an especially severe disease course.
</p>
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<div class="article-link article-html-link">
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.20.20248420v2" target="_blank">SARS-CoV-2 infections in people with PCD: neither frequent, nor particularly severe</a>
</div></li>
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<h1 data-aos="fade-right" id="from-clinical-trials">From Clinical Trials</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Evaluation of the Efficacy of High Doses of Methylprednisolone in SARS-CoV2 ( COVID-19) Pneumonia Patients</strong> - <b>Condition</b>:   Covid19<br/><b>Intervention</b>:   Drug: Methylprednisolone, Placebo<br/><b>Sponsor</b>:   Azienda Unità Sanitaria Locale Reggio Emilia<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Dendritic Cell Vaccine to Prevent COVID-19</strong> - <b>Condition</b>:   COVID-19<br/><b>Intervention</b>:   Biological: AV-COVID-19<br/><b>Sponsors</b>:   Indonesia-MoH;   Aivita Biomedical, Inc.;   PT AIVITA Biomedika Indonesia;   National Institute of Health Research and Development, Ministry of Health Republic of Indonesia;   RSUP Dr. Kariadi Semarang, indonesia;   Faculty of Medicine University of Diponegoro, Indonesia<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Effect of Dalcetrapib in Patients With Confirmed Mild to Moderate COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Drug: Dalcetrapib;   Other: Placebo<br/><b>Sponsors</b>:   DalCor Pharmaceuticals;   The Montreal Health Innovations Coordinating Center (MHICC);   Covance<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>suPAR-Guided Anakinra Treatment for Management of Severe Respiratory Failure by COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Drug: Anakinra;   Drug: Placebo<br/><b>Sponsor</b>:   Hellenic Institute for the Study of Sepsis<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Evaluating the Impact of EnteraGam In People With COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Dietary Supplement: Bovine Plasma-Derived Immunoglobulin Concentrate;   Other: Standard of care<br/><b>Sponsors</b>:   Entera Health, Inc;   Lemus Buhils, SL;   Clinical Research Unit, IMIM (Hospital del Mar Medical Research Institute)<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Efficacy and Safety of Remdesivir and Tociluzumab for the Management of Severe COVID-19: A Randomized Controlled Trial</strong> - <b>Conditions</b>:   Covid19;   Covid-19 ARDS<br/><b>Interventions</b>:   Drug: Remdesivir;   Drug: Tocilizumab<br/><b>Sponsors</b>:   M Abdur Rahim Medical College and Hospital;   First affiliated Hospital of Xi'an Jiaoting University<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Inhaled Ivermectin and COVID-19</strong> - <b>Condition</b>:   COVID-19<br/><b>Intervention</b>:   Drug: Ivermectin Powder<br/><b>Sponsor</b>:   Mansoura University<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Effect of Tenofovir/Emtricitabine in Patients Recently Infected With SARS-COV2 (Covid-19) Discharged Home</strong> - <b>Condition</b>:   Covid19<br/><b>Intervention</b>:   Drug: tenofovir disoproxil and emtricitabine<br/><b>Sponsor</b>:   University Hospital, Caen<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Safety and Immunogenicity of Two Different Strengths of the Inactivated COVID 19 Vaccine ERUCOV-VAC</strong> - <b>Condition</b>:   COVID-19 Vaccine<br/><b>Interventions</b>:   Biological: ERUCOV-VAC;   Other: Placebo Vaccine<br/><b>Sponsors</b>:   Health Institutes of Turkey;   TC Erciyes University<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>AZD1222 Vaccine in Combination With rAd26-S, Recombinant Adenovirus Type 26 Component of Gam-COVID-Vac Vaccine, for the Prevention of COVID-19</strong> - <b>Condition</b>:   COVID-19<br/><b>Interventions</b>:   Biological: AZD1222;   Biological: rAd26-S<br/><b>Sponsors</b>:   AstraZeneca;   R-Pharm<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Anti-COVID19 AKS-452 - ACT Study</strong> - <b>Condition</b>:   Covid19<br/><b>Intervention</b>:   Biological: AKS-452<br/><b>Sponsors</b>:   University Medical Center Groningen;   Akston Biosciences Corporation<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Study in Adults to Determine the Safety and Immunogenicity of AZD1222, a Non-replicating ChAdOx1 Vector Vaccine, Given in Combination With rAd26-S, Recombinant Adenovirus Type 26 Component of Gam-COVID-Vac Vaccine, for the Prevention of COVID-19.</strong> - <b>Condition</b>:   COVID-19<br/><b>Interventions</b>:   Biological: AZD1222;   Biological: rAd26-S<br/><b>Sponsors</b>:   R-Pharm;   AstraZeneca<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Surgical Face Mask Effects in Patients With COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Intervention</b>:   Other: Sit-To-Stand test<br/><b>Sponsor</b>:   Cliniques universitaires Saint-Luc- Université Catholique de Louvain<br/><b>Not yet recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Evaluation of Prognostic Modification in COVID-19 Patients in Early Intervention Treatment</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Drug: Azithromycin / Ivermectin / Ribaroxaban / Paracetamol;   Drug: Azithromycin / Ribaroxaban / Paracetamol<br/><b>Sponsors</b>:   Gilberto Cruz Arteaga;   Coordinación de Investigación en Salud, Mexico<br/><b>Recruiting</b></p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Dendritic Cell Vaccine, AV-COVID-19, to Prevent COVID-19 Infection</strong> - <b>Condition</b>:   COVID-19<br/><b>Interventions</b>:   Biological: AV-COVID-19;   Other: GM-CSF<br/><b>Sponsors</b>:   Aivita Biomedical, Inc.;   PT AIVITA Biomedika Indonesia;   Indonesia Ministry of Health;   National Institute of Health Research and Development, Ministry of Health Republic of Indonesia<br/><b>Recruiting</b></p></li>
</ul>
<h1 data-aos="fade-right" id="from-pubmed">From PubMed</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Therapeutic approaches against coronaviruses acute respiratory syndrome</strong> - Coronaviruses represent global health threat. In this century, they have already caused two epidemics and one serious pandemic. Although, at present, there are no approved drugs and therapies for the treatment and prevention of human coronaviruses, several agents, FDA-approved, and preclinical, have shown in vitro and/or in vivo antiviral activity. An in-depth analysis of the current situation leads to the identification of several potential drugs that could have an impact on the fight against...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The British variant of the new coronavirus-19 (Sars-Cov-2) should not create a vaccine problem</strong> - Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a highly contagious virus that infects humans and a number of animal species causing coronavirus disease-19 (COVID-19), a respiratory distress syndrome which has provoked a global pandemic and a serious health crisis in most countries across our planet. COVID-19 inflammation is mediated by IL-1, a disease that can cause symptoms such as fever, cough, lung inflammation, thrombosis, stroke, renal failure and headache, to name a few....</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Hydroxychloroquine Inhibits the Trained Innate Immune Response to Interferons</strong> - Hydroxychloroquine is being investigated for a potential prophylactic effect in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but its mechanism of action is poorly understood. Circulating leukocytes from the blood of coronavirus disease 2019 (COVID-19) patients show increased responses to Toll-like receptor ligands, suggestive of trained immunity. By analyzing interferon responses of peripheral blood mononuclear cells from healthy donors conditioned with heat-killed...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Lycorine, a non-nucleoside RNA dependent RNA polymerase inhibitor, as potential treatment for emerging coronavirus infections</strong> - CONCLUSIONS: Lycorine is a potent non-nucleoside direct-acting antiviral against emerging coronavirus infections and acts by inhibiting viral RdRp activity; therefore, lycorine may be a candidate against the current COVID-19 pandemic.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The PIKfyve Inhibitor Apilimod: A Double-Edged Sword against COVID-19</strong> - The PIKfyve inhibitor apilimod is currently undergoing clinical trials for treatment of COVID-19. However, although apilimod might prevent viral invasion by inhibiting host cell proteases, the same proteases are critical for antigen presentation leading to T cell activation and there is good evidence from both in vitro studies and the clinic that apilimod blocks antiviral immune responses. We therefore warn that the immunosuppression observed in many COVID-19 patients might be aggravated by...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Blocking Effect of Demethylzeylasteral on the Interaction between Human ACE2 Protein and SARS-CoV-2 RBD Protein Discovered Using SPR Technology</strong> - The novel coronavirus disease (2019-nCoV) has been affecting global health since the end of 2019, and there is no sign that the epidemic is abating. Targeting the interaction between the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein and the human angiotensin-converting enzyme 2 (ACE2) receptor is a promising therapeutic strategy. In this study, surface plasmon resonance (SPR) was used as the primary method to screen a library of 960 compounds. A compound 02B05...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Fucoidan and Lung Function: Value in Viral Infection</strong> - Compromised lung function is a feature of both infection driven and non-infective pathologies. Viral infections-including the current pandemic strain SARS-CoV-2-that affect lung function can cause both acute and long-term chronic damage. SARS-CoV-2 infection suppresses innate immunity and promotes an inflammatory response. Targeting these aspects of SARS-CoV-2 is important as the pandemic affects greater proportions of the population. In clinical and animal studies, fucoidans have been shown to...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Conus venom fractions inhibit the adhesion of Plasmodium falciparum erythrocyte membrane protein 1 domains to the host vascular receptors</strong> - Using high-throughput BioPlex assays, we determined that six fractions from the venom of Conus nux inhibit the adhesion of various recombinant PfEMP-1 protein domains (PF08_0106 CIDR1α3.1, PF11_0521 DBL2β3, and PFL0030c DBL3X and DBL5e) to their corresponding receptors (CD36, ICAM-1, and CSA, respectively). The protein domain-receptor interactions permit P. falciparum-infected erythrocytes (IE) to evade elimination in the spleen by adhering to the microvasculature in various organs including the...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Uncovering Flexible Active Site Conformations of SARS-CoV-2 3CL Proteases through Protease Pharmacophore Clusters and COVID-19 Drug Repurposing</strong> - The infectious SARS-CoV-2 causes COVID-19, which is now a global pandemic. Aiming for effective treatments, we focused on the key drug target, the viral 3C-like (3CL) protease. We modeled a big dataset with 42 SARS-CoV-2 3CL protease-ligand complex structures from ∼98.7% similar SARS-CoV 3CL protease with abundant complex structures. The diverse flexible active site conformations identified in the dataset were clustered into six protease pharmacophore clusters (PPCs). For the PPCs with distinct...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>In silico analysis of phytochemicals as potential inhibitors of proteases involved in SARS-CoV-2 infection</strong> - In silico analysis of six phytochemicals, flabelliferin, marmelosin, piperine, ocimin, curcumin and leucoanthocyanin, along with three drug compounds, nelfinavir, remdesivir and hydroxychloroquine, as positive control against drug targets of one SARS-CoV-2 viral protease, COVID-19 main protease (SARS CoV-2 3CL<sup>(pro)/M</sup>(pro)), two coronavirus proteases, SARS-CoV main peptidase (SARS CoV M^(pro)), SARS-CoV main proteinase (SARS CoV 3CL^(pro)), and one human cellular transmembrane serine proteinase...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling</strong> - Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has quickly spread worldwide and has affected more than 10 million individuals. A typical feature of COVID-19 is the suppression of type I and III interferon (IFN)-mediated antiviral immunity. However, the molecular mechanism by which SARS-CoV-2 evades antiviral immunity remains elusive. Here, we reported that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The potential mechanism of N-acetylcysteine in treating COVID-19</strong> - N-Acetylcysteine (NAC) has been proposed and used to treat coronavirus disease 2019 (COVID-19). By reviewing the existing pathological studies of COVID-19, it was found that abundant mucus secretion, formation of a hyaline membrane (supportive of acute respiratory distress syndrome), and interstitial fibrous exudation may be important characteristics of COVID-19 and may be pathological targets of drug therapy. In addition, multiple extrapulmonary organ injuries in COVID-19 may be associated with...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The fight against human viruses: how NMR can help</strong> - CONCLUSION: Considering the NMR-based work conducted on different viruses, we believe that in the close future much more NMR efforts will be devoted to discover novel anti SARS-CoV-2 agents.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>A Review of Treatment of Coronavirus Disease 2019 (COVID-19): Therapeutic Repurposing and Unmet Clinical Needs</strong> - For the initial phase of pandemic of coronavirus disease 2019 (COVID-19), repurposing drugs that in vitro inhibit severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) have been attempted with overlooked or overestimated efficacy owing to limited clinical evidence. Most early clinical trials have the defects of study design, small sample size, non-randomized design, or different timings of treatment initiation. However, well-designed studies on asymptomatic or mild, or pediatric cases of...</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Remdesivir potently inhibits carboxylesterase-2 through covalent modifications: signifying strong drug-drug interactions</strong> - Remdesivir was recently approved to treat COVID-19. While this antiviral agent delivers clinical benefits, several safety concerns in many cases have been raised. This study reports that remdesivir at nanomolar concentrations inhibits carboxylesterase-2 (CES2) through covalent modifications. CES2 is a major drug-metabolizing enzyme. The combination of high potency with irreversible inhibition concludes that cautions must be exercised when remdesivir is used along with drugs hydrolyzed by CES2.</p></li>
</ul>
<h1 data-aos="fade-right" id="from-patent-search">From Patent Search</h1>
<ul>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Covid 19 - Chewing Gum</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU313269181">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>A traditional Chinese medicine composition for COVID-19 and/or influenza and preparation method thereof</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU313300659">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>STOCHASTIC MODEL METHOD TO DETERMINE THE PROBABILITY OF TRANSMISSION OF NOVEL COVID-19</strong> - The present invention is directed to a stochastic model method to assess the risk of spreading the disease and determine the probability of transmission of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2). - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=IN313339294">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The use of human serum albumin (HSA) and Cannabigerol (CBG) as active ingredients in a composition for use in the treatment of Coronavirus (Covid-19) and its symptoms</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU313251184">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The use of human serum albumin (HSA) and Cannabigerol (CBG) as active ingredients in a composition for use in the treatment of Coronavirus (Covid-19) and its symptoms</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU313251182">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>"AYURVEDIC PROPRIETARY MEDICINE FOR TREATMENT OF SEVERWE ACUTE RESPIRATORY SYNDROME CORONAVIRUS 2 (SARS-COV-2."</strong> - AbstractAyurvedic Proprietary Medicine for treatment of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)In one of the aspect of the present invention it is provided that Polyherbal combinations called Coufex (syrup) is prepared as Ayurvedic Proprietary Medicine , Aqueous Extracts Mixing with Sugar Syrup form the following herbal aqueous extract coriandrum sativum was used for the formulation of protek.Further another Polyherbal combination protek as syrup is prepared by the combining an aqueous extract of the medicinal herbs including Emblica officinalis, Terminalia chebula, Terminalia belerica, Aegle marmelos, Zingiber officinale, Ocimum sanctum, Adatoda zeylanica, Piper lingum, Andrographis panivulata, Coriandrum sativum, Tinospora cordiofolia, cuminum cyminum,piper nigrum was used for the formulation of Coufex. - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=IN312324209">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>제2형 중증급성호흡기증후군 코로나바이러스 감염 질환의 예방 또는 치료용 조성물</strong> - 본 발명은 화학식 1로 표시되는 화합물, 또는 이의 약학적으로 허용가능한 염; 및 글루카곤 수용체 작용제(glucagon receptor agonist), 위 억제 펩타이드(gastric inhibitory peptide, GIP), 글루카곤-유사 펩타이드 1(glucagon-like peptide 1, GLP-1) 및 글루카곤 수용체/위 억제 펩타이드/글루카곤-유사 펩타이드 1(Glucagon/GIP/GLP-1) 삼중 완전 작용제(glucagon receptors, gastric inhibitory peptide and glucagon-like peptide 1 (Glucagon/GIP/GLP-1) triple full agonist)로 이루어진 군으로부터 선택된 1종 이상;을 포함하는 제2형 중증급성호흡기증후군 코로나바이러스 감염 질환 예방 또는 치료용 약학적 조성물을 제공한다. - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=KR313434044">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Haptens, hapten conjugates, compositions thereof and method for their preparation and use</strong> - A method for performing a multiplexed diagnostic assay, such as for two or more different targets in a sample, is described. One embodiment comprised contacting the sample with two or more specific binding moieties that bind specifically to two or more different targets. The two or more specific binding moieties are conjugated to different haptens, and at least one of the haptens is an oxazole, a pyrazole, a thiazole, a nitroaryl compound other than dinitrophenyl, a benzofurazan, a triterpene, a urea, a thiourea, a rotenoid, a coumarin, a cyclolignan, a heterobiaryl, an azo aryl, or a benzodiazepine. The sample is contacted with two or more different anti-hapten antibodies that can be detected separately. The two or more different anti-hapten antibodies may be conjugated to different detectable labels. - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU311608060">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>SARS-CoV-2 RBD共轭纳米颗粒疫苗</strong> - 本发明涉及免疫医学领域，具体而言，涉及一种SARS‑CoV‑2 RBD共轭纳米颗粒疫苗。该疫苗包含免疫原性复合物，所述免疫原性复合物包含：a）与SpyCatcher融合表达的载体蛋白自组装得到的纳米颗粒载体；b）与SpyTag融合表达的SARS‑CoV‑2病毒的RBD抗原；所述载体蛋白选自Ferritin、mi3和I53‑50；所述载体蛋白与所述抗原之间通过SpyCatcher‑SpyTag共价连接。 - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=CN313355625">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Устройство электронного контроля и дистанционного управления аппарата искусственной вентиляции легких</strong> - Полезная модель относится к медицинской технике, а именно к устройствам для воздействия на дыхательную систему пациента смесью различных газов, в частности, к устройствам для проведения искусственной вентиляции легких (ИВЛ). Технический результат предлагаемой полезной модели заключается в решении технической проблемы, состоящей в необходимости расширения арсенала технических средств, предназначенных для электронного контроля и управления ИВЛ, путем реализации возможности дистанционного управления аппаратами ИВЛ в медицинских учреждениях, не оборудованных кабельными вычислительными сетями. Указанный технический результат достигается благодаря тому, что в известное устройство электронного контроля и дистанционного управления аппарата ИВЛ, содержащее центральный микроконтроллер, а также программно-аппаратные средства управления функциями доставки воздушной смеси пациенту и многоуровневой тревожной сигнализации об отклонениях от нормативных условий и технических неполадках в аппарате ИВЛ, введены связанные друг с другом микроконтроллер связи и дистанционного управления и радиомодем, выполненный с возможностью связи с точками доступа радиканальной сети, при этом центральный микроконтроллер устройства выполнен с дополнительными входом/выходом, которые связаны с управляющими выходом/входом микроконтроллера связи и дистанционного управления, а, в зависимости от типа применяемой в медицинском учреждении радиоканальной сети связи и передачи данных, радиомодем может быть выполнен в виде интерфейсного аудиомодуля Bluetooth 4.0 BLE, приемопередающего модуля Wi-Fi либо устройства "малого радиуса действия", работающего по технологии LoRa на нелицензируемых частотах мегагерцового диапазона, например, в диапазоне 868 МГц. 3 з.п. ф-лы, 1 ил. - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=RU313244211">link</a></p></li>
</ul>
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<h1 data-aos="fade-down" id="daily-dose">Daily-Dose</h1>
<h1 data-aos="fade-right" data-aos-anchor-placement="top-bottom" id="contents">Contents</h1>
<ul>
<li><a href="#from-new-yorker">From New Yorker</a></li>
<li><a href="#from-vox">From Vox</a></li>
<li><a href="#from-the-hindu-sports">From The Hindu: Sports</a></li>
<li><a href="#from-the-hindu-national-news">From The Hindu: National News</a></li>
<li><a href="#from-bbc-europe">From BBC: Europe</a></li>
<li><a href="#from-ars-technica">From Ars Technica</a></li>
<li><a href="#from-jokes-subreddit">From Jokes Subreddit</a></li>
</ul>
<h1 data-aos="fade-right" id="from-new-yorker">From New Yorker</h1>
<ul>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The Plague Year</strong> - The mistakes and the struggles behind America’s coronavirus tragedy. - <a href="https://www.newyorker.com/magazine/2021/01/04/the-plague-year">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The Trümperdämmerung Is a Fitting End to 2020</strong> - The President is careening through his final days in office with reckless disdain—for everything. - <a href="https://www.newyorker.com/news/letter-from-trumps-washington/the-trumperdammerung-is-a-fitting-end-to-2020">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The Next Big Challenge: Trump-Proofing the Presidency</strong> - Trump’s departure will prompt cries of relief in many parts of the country, but there is now vital work to be done. - <a href="https://www.newyorker.com/news/our-columnists/the-next-big-challenge-trump-proofing-the-presidency">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The Deep Origins of Latino Support for Trump</strong> - The leaders of the Hispanic Republican movement today haven’t felt such momentum for twenty years. - <a href="https://www.newyorker.com/news/the-political-scene/the-deep-origins-of-latino-support-for-trump">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Can Wall Street’s Heaviest Hitter Step Up to the Plate on Climate Change?</strong> - More significant than BlackRock executives’s pledges is the firm’s continued inclusion of fossil-fuel companies in its index funds. - <a href="https://www.newyorker.com/news/annals-of-a-warming-planet/can-wall-streets-heaviest-hitter-step-up-to-the-plate-on-climate-change">link</a></p></li>
</ul>
<h1 data-aos="fade-right" id="from-vox">From Vox</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The UK coronavirus mutation has been found in the US</strong> -
<figure>
<img alt="" src="https://cdn.vox-cdn.com/thumbor/z4hiXUP3U9Km0646GDsqupBy98M=/260x0:1820x1170/1310x983/cdn.vox-cdn.com/uploads/chorus_image/image/68569350/Covid_UK.0.jpg"/>
<figcaption>
Illustration by Zac Freeland/Vox
</figcaption>
</figure></li>
</ul>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
What scientists have learned about the Covid-19 variants in the UK, South Africa, and now, the US.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="7E5mgC">
A new, seemingly more contagious variety of SARS-CoV-2 — the virus that causes <a href="https://www.vox.com/coronavirus-covid19">Covid-19</a> — that has been spreading rapidly in the United Kingdom has now been found in the United States in at least two locations.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="zduS7x">
California <a href="https://sacramento.cbslocal.com/2020/12/30/covid-19-mutant-variant-strain-b117-california/">Gov. Gavin Newsom</a> announced December 30 that the new strain, known as B.1.1.7 (we’ll call it the UK variant, for simplicity’s sake), was detected in the southern part of the state. It’s the second report of the UK variant in the US in as many days, following news that the variant was found in a male Colorado National Guard member in his 20s with no history of travel, a sign that the virus is spreading locally.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="dCIJyi">
“There is a lot we don’t know about this COVID-19 variant, but scientists in the United Kingdom are warning the world that it is significantly more contagious,” said Colorado Gov. Jared Polis, in a <a href="https://twitter.com/GovofCO/status/1344031800230780933">statement</a>.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="BMyEkP">
The evidence that this new strain spreads more easily between people is not rock solid, but it’s concerning enough to have forced dramatic action, like shutting down travel <a href="https://www.npr.org/sections/coronavirus-live-updates/2020/12/21/948751745/travel-from-the-u-k-shut-down-as-nations-assess-threat-of-new-coronavirus-strain">from the United Kingdom</a> earlier this month. But it wasn’t enough: The variant has now been detected in <a href="https://www.cbc.ca/news/canada/toronto/ontario-confirms-first-cases-covid19-uk-variant-1.5855361">Canada</a>, <a href="https://www.theguardian.com/world/2020/dec/26/spain-and-sweden-report-cases-of-uk-covid-variant">Spain, Sweden</a>,<a href="https://www.aljazeera.com/news/2020/12/26/which-countries-have-reported-new-variants-of-covid-19"> France, and Italy</a>, among others.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="2QC8m1">
At the moment, it doesn’t appear as though the new UK variant of SARS-CoV-2 is more dangerous in individuals. It doesn’t seem to make people sicker, nor is it more likely to kill them. “I think the key point is that there is no evidence now … that this virus is more pathogenic — creates more problems, more morbidity and mortality — than the previous virus,” <a href="https://www.hhs.gov/about/news/2020/05/15/trump-administration-announces-framework-and-leadership-for-operation-warp-speed.html">Moncef Slaoui</a>, the scientific lead for Operation Warp Speed, said during a December 21 <a href="https://www.youtube.com/watch?v=5G8uPGyDjic">press conference</a>.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="UQZE1g">
What it does appear to do, at least based on preliminary evidence, is spread more quickly among people. That alone is a problem: The coronavirus spreads fast enough as it is. Compounding concerns is that the UK variant echoes a similar story in <a href="https://apnews.com/article/new-coronavirus-strain-south-africa-31a0d5840a17fa5c82f2ecd14ba9921b">South Africa</a>, where a strain called 501.V2 has become the dominant version among new cases of the virus. Scientists are wondering whether that strain is more transmissible, too.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="xH22Yl">
The virus has been continually changing its genetics through the course of the pandemic. That’s what RNA-based viruses like SARS-CoV-2 do — they mutate. Most of the time, the mutations mean nothing. But this time, something is different.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="FV0paB">
“I’ve spent a lot of time this year reminding people that mutations are normal,” molecular epidemiologist <a href="http://emmahodcroft.com/">Emma Hodcroft</a>, who works on a project called <a href="https://nextstrain.org/">Nextstrain</a>, said. For the entire pandemic, scientists the world over have been feeding Nextstrain sequences of the virus, and Hodcroft and her colleagues have been tracking its genetic changes closely.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="uimlqr">
In the past, mutations haven’t warranted big newspaper headlines. “I’m now finding myself singing a slightly different tune,” Hodcroft said. This time, there does seem to be evidence that the new strain is something worth being vigilant about. “We probably should consider taking some precautionary measures while we’re trying to find out more,” she added.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="EF6z4U">
At the same time, Covid-19 is surging around the world, even without these new mutations. Scientists are still trying to figure out what these new variants of the coronavirus actually mean for the pandemic. It’s also unclear where else the UK variant may have already spread, aside from the countries where it has been detected. While it was reported in the US only this week, it could have been in the country for much longer. “The variant could already be in the United States without having been detected,” the US Centers for Disease Control and Prevention <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/scientific-brief-emerging-variant.html">reported</a> December 22.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="3WdEPP">
The good news is that we already know how to respond to these new variants: in the same way we’ve been responding to the pandemic overall. The virus still transmits primarily through viral-laden breaths in the air. Mask-wearing, social distancing, and good indoor ventilation are as critical as ever.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="eAp9uo">
There’s a lot about this story that’s potentially very alarming or confusing. And the story is not yet complete, as scientists need more evidence to understand whether these new variants pose a new threat.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="BGroeT">
To add some clarity, here’s what researchers have learned so far. Let’s start with the basics.
</p>
<h3 id="JqQobE">
Viral mutations, explained
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="A4GeiD">
Viral mutations. New strains. Increased transmission. It all sounds like scary science fiction. But to demystify things, and to understand why scientists are a little concerned about this new variant — and why most variants don’t faze them — it’s worth understanding how viruses mutate in the first place.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="OM33h7">
“Oftentimes, I think the word mutation in general conjures up a lot of things in people’s minds, like, you know, Ninja Turtles or X-Men or cancer, like zombie apocalypse-type stuff,” <a href="https://ghss.georgetown.edu/people/angela-rasmussen/">Angela Rasmussen</a>, a virologist with Georgetown’s Center for Global Health Science and Security, said. “A mutation is just a lot more mundane than that.”
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="YBXhRm">
Viruses mutate because they’re constantly making copies of themselves in enormous numbers. To accomplish this, they have to hijack the hardware of a host cell that they infect. However, this process can be a bit sloppy.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="1wBIEt">
Within a human body, a virus can replicate itself millions or billions of times, Hodcroft explains. If you were writing a draft of something millions of times on a computer, extremely quickly, you’d probably make some typos. That’s what’s happening with the viruses. “They make a typo” in their genetic code, she says. One letter of their ribonucleic acid (RNA) chain is replaced with another.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="0z91lN">
Viruses that use RNA as their genetic material, like SARS-CoV-2, are particularly vulnerable to mutations since the RNA molecule itself is more unstable than DNA. The process of copying RNA is also more prone to error.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="MH9nOj">
These typos can be very useful for scientists because they happen at a regular rate, and are passed down through generations of the virus as it spreads through a community. Often, scientists can use these subtle changes to trace certain strains’ lineage and their spread through a population.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="l0NhR9">
The majority of these typos are inconsequential when it comes to human health. “One typo, or even a few typos, doesn’t usually change how the virus works,” Hodcroft says. Some even harm the virus. “You’re much more likely to break it than to make it better” when it comes to mutations, she says.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="HGkWRP">
But in rare instances, some mutations can give a virus an advantage, like allowing it to infect cells more readily or spread among people faster. Those mutant strains can then become dominant within a population.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="hav0re">
That might be what we’re looking at here with the UK variant; this new strain may have accumulated typos that could make it more easily transmitted between people.
</p>
<h3 id="2dmw3O">
Four lines of evidence converging on this new mutation being more transmissible
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="5Y51zQ">
So why do scientists think this variant is more transmissible?
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Jct7w8">
They don’t have this nailed down yet for sure, but four converging streams of evidence are all pointing in the same direction. “That’s making people feel like maybe there is something here to be worried about,” Hodcroft says. “Each one of these things on their own, I would say is not necessarily convincing.” But all together, they paint a concerning picture.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="HpnQaU">
One is that in the areas of the UK where this new variant is spreading, it is accounting for a larger proportion of new cases. “What this implies is that this new variant is spreading better than other variants that are circulating in the same region,” she says.
</p>
<div id="uHkWsG">
<blockquote class="twitter-tweet">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
National testing data shows increased prevalence of the variant in positive cases over time. This is detected incidentally by the commonly used 3-gene PCR test because 69-70del leads to a negative signal. But this does not effect the results of the test. 7/<br/>h/t <a href="https://twitter.com/The_Soup_Dragon?ref_src=twsrc%5Etfw"><span class="citation">@The_Soup_Dragon</span></a> <a href="https://t.co/aPpAjjb35W">pic.twitter.com/aPpAjjb35W</a>
</p>
— Muge Cevik (<span class="citation">@mugecevik</span>) <a href="https://twitter.com/mugecevik/status/1341094871822680067?ref_src=twsrc%5Etfw">December 21, 2020</a>
</blockquote>
</div>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="aY09i5">
A second is that the increase didn’t co-occur with any overly obvious change in human behavior. “We don’t really have strong evidence that everyone in the southeast [UK where this variant is spreading] has just ripped their masks off and is, you know, totally violating restrictions,” she says. That said, it could be a coincidence. It could be just that people who happen to have contracted this variant have it are spreading it more often via their behavior.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="PqgUXB">
After all, “this new variant has emerged at a time of the year when there has traditionally been increased family and social mixing,” according to the <a href="https://www.ecdc.europa.eu/en/publications-data/threat-assessment-brief-rapid-increase-sars-cov-2-variant-united-kingdom">European Center for Disease Prevention and Control</a>, which estimated that the transmissibility of the new variant has increased by 70 percent compared to prior versions of the virus. Both Rasmussen and Hodcroft say the 70 percent more transmissible figure is most likely an overestimate. A recent, not yet peer-reviewed study from the London School of Hygiene &amp; Tropical Medicine used a mathematical <a href="https://www.nytimes.com/2020/12/23/health/coronavirus-uk-variant.html">model to estimate that the new strain </a>may be 56 percent more infectious.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="1zJydD">
Third, there’s some early data about how this variant acts in Covid-19 patients. “There may be slightly higher viral loads in patients with the variants,” Hodcroft says, suggesting the virus has an easier time replicating in the body. (Viral load refers to the amount of virus in the patient. Rasmussen also cautions that viral load data is really sensitive to timing and when the patient was sampled in the course of the illness, so there needs to be more data to confirm this.)
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="noaKCM">
Finally, the genetic changes in the UK variant mirror changes in the South African variant, which has also been associated with rising case numbers. That makes a plausible link: that this particular genetic change may be behind the increased transmissibility in both variants.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="JtWl8E">
However, this is still short of definitive confirmation that the new variant is more transmissible.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="jEAEmP">
According to Slaoui, figuring this out for certain would require laboratory animal testing to see how easily the virus can spread from one organism to another. But this testing can take several weeks.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="OEUlSn">
In the face of that uncertainty, many urge caution.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="VVoYm6">
Again, there’s still no evidence this new variant causes more severe disease. The evidence points only to increased transmissibility. But a more transmissible virus is still a concern. “In general, the more people get infected, the number of hospitalizations and deaths rise accordingly as a proportion of that number,” Hodcroft says. “So more cases is also bad news.”
</p>
<h3 id="TG5rcr">
What does the mutation ... do?
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="5q1EBv">
The UK variant of SARS-CoV-2 actually contains 23 mutations in the genome of the virus. “We don’t really know what they do,” Rasmussen says. Individually, many of these mutations have already been seen in other strains of the virus around the world. But the combination of these changes in a single virus could be making the new variant more likely to spread.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="gdDdxa">
However, scientists do think that some mutations may be more important than others, and there are several mechanisms by which mutations could make the virus more infectious. Those include:
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ZtKOm3">
</p><ol style="list-style-type: decimal">
<li>The virus could end up with changes to its spike protein that allow it to enter cells more easily.
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"></p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="g29Sx5">
</p><ol start="2" style="list-style-type: decimal">
<li>The virus could develop a mechanism to replicate more quickly inside a body, which would lead “to people becoming infectious faster, or contagious faster than they would with another variant,” Rasmussen explains.
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"></p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="hXzAKl">
</p><ol start="3" style="list-style-type: decimal">
<li>The virus could theoretically have evolved an ability to counteract the cell’s innate immune defenses, making it easier to infect that cell.
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"></p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="NCa9u7">
One of the pathways scientists suspect may be at work stems from the N501Y mutation, where the amino acid asparagine is replaced by the amino acid tyrosine in the 501st position of the viral protein sequence. It’s one of several mutations in the virus’s spike protein in the UK variant, but N501Y is in the part of the spike that actually comes into direct contact with human cells. The same mutation has been found in the South African variant of SARS-CoV-2 that’s also quickly spreading.
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Since the virus attaching to a host cell is critical to the virus’s reproduction, the virus’s spike protein is especially important — and delicate.
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“If you were just making random changes in the lab, almost any change you make in that area would result in just a dead virus that can no longer get into the cell,” said <a href="https://tamut.edu/academics/Colleges-and-Departments/CASE/Undergraduate-Programs/Biology/bneumanCV.pdf">Benjamin Neuman,</a> a virologist at Texas A&amp;M University Texarkana. “That fact that this thing is able to spread at all tells you that it’s at least as good as the original version. The fact that it’s spreading faster may indicate that it’s a little bit better at grabbing on to host cells, which is the first step of the entry process.”
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But this particular N501Y mutation has already been detected in strains that have risen and fallen in other parts of the world over the course of the pandemic. So it may be that the other mutations coupled with N501Y are having some sort of compounding effect. And scientists still need to do more work to determine if this is actually what’s causing the rise of the new SARS-CoV-2 variant in the UK. Finding out the answer could help researchers come up with ways to counter this variety of the coronavirus.
</p>
<h3 id="PfqUji">
How did these coronavirus mutations happen?
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="cptkXt">
Scientists don’t know exactly how the UK variant came to be. But there may be a clue. Hodcroft is struck by the sheer number of mutations in the UK variant — 23 in all — which makes her suspect it’s possible this variant arose in an immunocompromised person. “It’s an above-average number of mutations,” she says.
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In most people, she explains, the immune system mounts a full-on assault on the virus, eliminating it in a matter of a couple of weeks. “In people that have compromised immune systems, though, there’s a very different dynamic,” she says. “So, for one thing, the virus could be in them for months instead of weeks.” That gives the virus more time to evolve, to accumulate mutations that might make it easier to thwart the immune system.
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“It’s one scenario,” she says. “We may never know exactly what happened here.”
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<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="WEpDLh">
The basic truth: The more this virus spreads, the more chances there are for dangerous new variants to emerge. In any person — or <a href="https://www.vox.com/science-and-health/2020/12/16/21826130/coronavirus-covid-19-in-animals-mink-dog-cats-gorillas-tigers">animal, for that matter</a> — the chance for a dangerous new variant to arise is rare. But rare things can happen when there are so many cases: more than <a href="https://coronavirus.jhu.edu/map.html">80 million confirmed cases worldwide</a>.
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Since viruses like SARS-CoV-2 are mutating and since Covid-19 has spread in so many people, it’s theoretically only a matter of time before a certain set of mutations align in a way to give the virus a boost.
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<h3 id="l7vml9">
What can we do about Covid-19 mutants?
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To stop mutations, quite simply, we need to stop the spread of SARS-CoV-2 in general. For one, that helps us deal with the pandemic overall. But “that’s also conveniently how we get fewer emerging variants,” Rasmussen says. “If the virus isn’t replicating, it can’t mutate. And if it can’t mutate, the new variants can’t emerge.”
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We fight the new variant as we would any variant of SARS-CoV-2: with masks, with social distancing, with good hand hygiene. “I don’t think people should be panicking,” Hodcroft says. “Lower case numbers, no matter what the variant, are better.”
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It’s already been said but if we actually follow protocol and have policies that support those protocols a new variant that is more transmissible would be combatted just as an older variant. So like worry less about mutants and more about masking and distancing and vaccination.
</p>
— K. Taylor, Ph.D., M.S. (<span class="citation">@KYT_ThatsME</span>) <a href="https://twitter.com/KYT_ThatsME/status/1340823722136104961?ref_src=twsrc%5Etfw">December 21, 2020</a>
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Scientists have one more tool, though: genetic tracking. At Nextstrain, Hodcroft and her colleagues receive viral genetic sequences from all over the world to try to paint a real-time picture of transmission chains and keep tabs on how the virus is changing. But not every place in the world is providing the same amount of data.
</p>
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The UK does a lot of viral sequencing, for instance. It was able to pick up on the new viral strain quickly because of that. In other locations around the globe, that might not have happened so fast.
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“In the US, it’s a really spotty picture,” Hodcroft says when it comes to sequencing. “Some states have really invested in sequencing; some states haven’t. So for some states, we probably have a fair idea of what’s going on. In other states, we really don’t have many sequences.”
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Overall, the CDC <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/scientific-brief-emerging-variant.html">reports</a> that the US has sequenced only 51,000 of the more than 17 million cases reported in the country. That’s 0.07 percent. In comparison, the UK aims to sequence <a href="https://www.cogconsortium.uk/news_item/how-do-we-collect-and-sequence-sars-cov-2-samples/">10,000 virus samples <em>per week</em></a>, and plans to increase that capacity further. (In addition: The UK sequences the genomes faster than the US,<a href="https://twitter.com/trvrb/status/1341806651225980929"> according to</a> infectious disease researcher Trevor Bedford.) That lack of viral genetic testing creates a big blind spot in the US. The UK variant could have already arrived here undetected “given the small fraction of US infections that have been sequenced,” the CDC <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/scientific-brief-emerging-variant.html">states</a>.
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More sequencing, overall, would lead to the faster detection of new strains and faster means to contain them if they were deemed problematic.
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<h3 id="ql7mht">
Do mutations mean a Covid-19 vaccine won’t work anymore?
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="WWvya2">
With new mutations, there is a concern that a new strain of SARS-CoV-2 could arise that would be different enough from previous versions such that prior exposures — whether through a vaccine or an infection — won’t offer protection. So, yes, it’s possible that the coronavirus could someday mutate in a way that would elude a vaccine or previous immunity.
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Right now, though, scientists think this UK variant would still fall under the same umbrella of protection as earlier strains. If someone received a Covid-19 vaccine for an older generation of the virus, they would likely have protection against this one.
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To explain why, it helps to understand how the immune system deals with viruses. When the human body detects a hostile foreign entity like a virus, it starts to produce antibodies (proteins that attach to the virus or to infected cells). Antibodies can then interfere with how the virus works. They can also flag the virus or virus-infected cells for destruction by other immune cells.
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The specific places where the antibodies attach to the virus are called <a href="https://www.britannica.com/science/epitope">epitopes</a>, and most Covid-19 vaccines target epitopes on the virus’s spike protein (which is what the virus uses to attach to human cells and enter them).
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“The good thing with the vaccine is that it induces an immune response against several epitopes that have been mapped around the spike protein,” Slaoui said. “The chances that one set of mutations would alter all those epitopes, I think, are extremely very low. The expectation, scientifically, is that these kinds of variations are unlikely to escape fully the protective response by the vaccine.”
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More good news: Scientists at the University of Texas Medical Branch have announced (<a href="https://twitter.com/TheMenacheryLab/status/1341460341293723650">via a tweet</a>) preliminary evidence that antibodies that neutralize the more common strain of the virus also neutralize a strain with the N501Y mutation (the one that impacts the part of the virus that comes into direct contact with human cells, as mentioned above). That suggests that an immune system primed — by a natural infection, at least — to fight the old variant can also fight one with this specific mutation.
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<div id="MO9JSj">
<blockquote class="twitter-tweet">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
Some good news (and incredibly fast work) on one of the mutations scientists are worried about: N501Y.<br/>In these lab experiments serum from recovered <a href="https://twitter.com/hashtag/covid19?src=hash&amp;ref_src=twsrc%5Etfw">#covid19</a> patients was just as good at neutralizing virus with the mutation as without it. <a href="https://t.co/SIxfo2x3qp">https://t.co/SIxfo2x3qp</a>
</p>
— Kai Kupferschmidt (<span class="citation">@kakape</span>) <a href="https://twitter.com/kakape/status/1341496927318388739?ref_src=twsrc%5Etfw">December 22, 2020</a>
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Texas A&amp;M’s Neuman noted that there’s also evidence right now showing how well vaccines can protect against mutated forms of the virus in clinical trials. Many of the vaccines being administered were engineered to counter the earliest generations of SARS-CoV-2 but are still showing themselves to be highly effective against Covid-19 caused by more recent versions of the virus.
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“All the tests are being done, all the papers being published, are being done with current strains, which have several mutations relative to [the first iterations of the virus], and it does still seem to be working,” Neuman said.
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Covid-19 vaccine developers say they are keeping a close eye on these changes and testing to make sure their vaccines are still effective. “In terms of the new variant, <a href="https://www.vox.com/22167841/fda-vaccine-approval-pfizer-biontech-covid-19-eua-coronavirus">Pfizer and BioNTech</a> are monitoring SARS-CoV-2 sequence changes and the companies are working to generate data on how well serum from people immunized with [the Pfizer/BioNTech vaccine] may be able to neutralize the new strain,” said a Pfizer spokesperson via email.
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And the new Covid-19 vaccines are well equipped to adapt. The two that have received emergency use authorizations from the Food and Drug Administration — the Pfizer/BioNTech vaccine and the <a href="https://www.vox.com/2020/12/18/22188715/moderna-vaccine-covid-19-fda-emergency-use-authorization-coronavirus">Moderna vaccine</a> — both use <a href="https://www.vox.com/2020/8/13/21359025/coronavirus-vaccine-covid-19-moderna-oxford-mrna-adenovirus">mRNA as their platform</a>. These vaccines deliver the instructions for making the spike protein of SARS-CoV-2 to human cells. Those human cells then manufacture the component themselves, allowing the immune system to use it to prepare for an infection. One huge advantage of this approach is that the mRNA sequence can be altered quickly; the first such vaccines for Covid-19 were <a href="https://nymag.com/intelligencer/2020/12/moderna-covid-19-vaccine-design.html">developed within days</a> after the genetic sequence of the virus was posted online.
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Could manufacturers like Moderna or Pfizer/BioNTech then retool their vaccines to target the new variants without going through the whole tedious clinical trial process again?
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Possibly, according to <a href="https://globalhealth.georgetown.edu/people/jesse-goodman">Jesse Goodman</a>, a former chief scientist at the FDA and a professor of medicine at Georgetown University. He told Vox that vaccines for new variants of the influenza virus are approved every year without large-scale trials. New versions of a Covid-19 vaccine to accommodate mutations similarly might not need another round of study in tens of thousands of people, but may require some testing to figure out dosing and immune response. With such a new virus and brand new vaccines, the regulations for these situations have not yet been laid out.
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Should we expect more mutations in the future?
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Short answer: yes.
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The UK and South African variants are unlikely to be the last to make headlines. Coronavirus is constantly evolving. We should expect it to keep changing slightly.
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“There will be new variants that emerge,” Rasmussen says. The thing is, with each new significant strain, scientists will have to do careful work to determine whether it’s more dangerous.
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And there are some mutations we can perhaps even expect — if not in the coming weeks, over the next several years.
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Recently, virology researchers at the Fred Hutch Cancer Research Center published a <a href="https://www.biorxiv.org/content/10.1101/2020.12.17.423313v1">preprint</a> (i.e., not yet peer-reviewed) study, looking at how a coronavirus that causes the common cold evolved from the 1980s onward. To accomplish that, they got old blood samples, which included antibodies that cling to this particular virus. They also reconstructed pieces of the cold virus from other eras. Basically, they wanted to see if older blood could still neutralize newer virus. If it couldn’t, that would indicate the virus has evolved over time to evade the immune system.
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Here’s what the researchers found: “This other human coronavirus does indeed evolve over the course of multiple years to gradually escape human immunity,” <a href="https://www.fredhutch.org/en/faculty-lab-directory/bloom-jesse.html">Jesse Bloom</a>, a virologist who co-authored the study, says. “So we think this suggests that there’s the potential for SARS-CoV-2 to do the same thing.” But Bloom stresses that this process takes years. It’s enough time to prepare, to monitor, and to potentially tweak vaccine formulations to keep up with the virus’s evolution.
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It’s not like the virus can evolve into an entirely different beast. “It can mutate to maybe escape antibodies,” <a href="https://twitter.com/eguia_rachel">Rachel Eguia</a>, the study’s lead author, says. But it can’t change so much that it alters its ability to enter cells.
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Scientists are also keeping their eyes out for a rapid, major mutation event known as <a href="https://www.ncbi.nlm.nih.gov/books/NBK8439/#:~:text=Viral%20recombination%20occurs%20when%20viruses,some%20genes%20from%20both%20parents.">recombination</a>. That’s where an individual is infected with two different strains of the virus at the same time, allowing the virus strains to swap parts. These new viruses could then evade the antibodies that targeted their predecessors. Some researchers think that recombination might be how <a href="https://advances.sciencemag.org/content/6/27/eabb9153">SARS-CoV-2 originated</a> in the first place.
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“This is all hypothetical in this particular virus, but it happens in other viruses all the time,” Neuman said.
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Faced with these looming challenges, reducing the transmission of the coronavirus in general is still the best way to protect the fragile progress made in the Covid-19 pandemic so far. Reducing transmissions is also one of the best ways to make sure powerful tools like vaccines remain potent for as long as possible. The fact that multiple Covid-19 vaccines are coming out is not a cause for complacency, and these new variants of SARS-CoV-2 highlight how important it is to remain vigilant.
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<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The US is getting an official women’s history museum</strong> -
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<img alt="People walking on the National Mall with the US Capitol in the background." src="https://cdn.vox-cdn.com/thumbor/bW84JbjwN3ERpJUeazO1qHHQoFs=/263x0:4524x3196/1310x983/cdn.vox-cdn.com/uploads/chorus_image/image/68600105/1207278533.0.jpg"/>
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Visitors walk the National Mall in Washington, DC, on March 13, 2020. | Jonathan Newton/The Washington Post via Getty Images
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The Smithsonian Women’s History Act will establish a women’s history museum on the National Mall. Supporters say it’s long overdue.
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It has gotten less attention than expanded unemployment insurance or <a href="https://www.vox.com/2020/12/29/22204468/bernie-sanders-2000-stimulus-checks">the battle over stimulus checks</a>, but tucked into the year-end legislation passed by Congress last week was a provision that could change the way the United States commemorates its history.
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The legislation included the Smithsonian Women’s History Act, the culmination of a years-long effort to establish a women’s history museum in Washington, DC. Backed by Democrats like Rep. Carolyn Maloney of New York and Republicans like Sen. Susan Collins of Maine, the act authorizes the creation of the museum on the National Mall, funded by a combination of federal and private money.
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“For too long, women’s stories have been left out of the telling of our nation’s history, but with this vote, we begin to rectify that,” Maloney said in a statement last week.
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The omnibus legislation also included <a href="https://www.congress.gov/bill/116th-congress/house-bill/2420/text">a provision</a> to establish a National Museum of the American Latino, which will focus on “Latino contributions to life, art, history, and culture in the United States.” Both will be located <a href="https://www.washingtonpost.com/entertainment/museums/smithsonian-museums-latino-womens-history/2020/12/22/4f9211ac-43c6-11eb-b0e4-0f182923a025_story.html">on or around the National Mall</a>, with an exact location to be specified within two years, <a href="https://www.cnn.com/2020/12/22/politics/smithsonian-museums-american-latinos-women-trnd/index.html">according to CNN</a>.
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The bills establishing the museums were blocked earlier this month by Utah Republican Sen. Mike Lee, who argued that they were divisive. “At this moment in the history of our diverse nation, we need our federal government and the Smithsonian Institution itself to pull us closer together and not further apart,” <a href="https://www.cnbc.com/2020/12/22/congress-agrees-to-fund-national-latino-and-womens-history-museums.html">he said</a>.
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But many say that, on the contrary, the museums are long overdue. “Having a museum that features women’s experiences in US history should not be a controversial undertaking by any stretch of the imagination,” Kali Nicole Gross, a professor at Emory University and Rutgers University and co-author of <em>A Black Women’s History of the United States</em>, told Vox. “The fact that it is shows that we have a long way to go still.”
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<h3 id="p9erJ1">
The legislation is the culmination of a years-long process
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The idea of a national women’s history museum first came before Congress in 2003, when Collins and others introduced a bill to establish one, <a href="https://www.cnbc.com/2020/12/22/congress-agrees-to-fund-national-latino-and-womens-history-museums.html">according to CNBC</a>. It didn’t pass, but in 2014, a congressional commission recommended the building of a museum.
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Then, in February 2020, <a href="https://www.cnn.com/2020/12/22/politics/smithsonian-museums-american-latinos-women-trnd/index.html">the House passed the Smithsonian Women’s History Act</a> to establish the museum. But passage of both this bill and legislation to establish the Museum of the American Latino was blocked in the Senate by Lee, who said the US does not need “separate but equal museums,” <a href="https://www.cnn.com/2020/12/22/politics/smithsonian-museums-american-latinos-women-trnd/index.html">according to CNN</a>.
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The Smithsonian “should not have an exclusive museum of American Latino history or a museum of women’s history or museum of American men’s history or Mormon history or Asian American history or Catholic history. American history is an inclusive story that should unite us,” he added.
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But many disagreed, and both proposals ended up included in the omnibus legislation passed last week that included $600 stimulus checks and other Covid-19 relief.
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Lawmakers have applauded the plans for both museums, expressing hope that they will tell the stories of Americans too often left out of history classes and textbooks.
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“With this vote, Latinos and Latinas across our nation will finally have their stories, struggles, and impact on our country validated by the United States Congress,” Sen. Bob Menendez (D-NJ) said in a statement after the legislation’s passage.
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And Maloney <a href="https://maloney.house.gov/media-center/press-releases/maloney-celebrates-women-s-museum-legislation-in-omnibus">said in a statement</a> that it was “fitting” that the bill establishing the women’s history museum was passed “as we mark the centennial of the 19th Amendment and in the year in which we elected our first woman vice president.”
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There’s a lot of work left to be done
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The museums will likely take years to build. The National Museum of African American History, the most recent addition to the Smithsonian, was authorized by Congress in 2003 and opened in 2016, <a href="https://www.cnn.com/2020/12/22/politics/smithsonian-museums-american-latinos-women-trnd/index.html">CNN notes</a>.
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And in the planning process, the key will be an “expansive view” of women’s history, Gross said, including women of different abilities, trans and queer communities, and the experiences of women from all walks of life: “women who were performers, women who were writers, women who were seamstresses, women who were farmers, women who were domestics,” she explained. “I want it all.”
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Such an expansive view could also extend to more experiential ways of teaching history, Gross said, including the history of street harassment in the US. “From the first women starting to work and having to navigate public streets, there were all kinds of perils,” she explained, especially for Black women. “They carried hatpins; they learned how to use their purses and bags defensively to protect themselves.”
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It will be interesting to see if the museum could find a way to recreate or use “that embodied experience” to teach about the misogyny that has been a major part of American history, Gross said.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="rcQODX">
Neither the women’s history museum nor the Museum of the American Latino will start from zero. <a href="https://www.washingtonpost.com/entertainment/museums/smithsonian-museums-latino-womens-history/2020/12/22/4f9211ac-43c6-11eb-b0e4-0f182923a025_story.html">According to the Washington Post</a>, they will build on the work of the American Women’s History Initiative, established in 2018, and the Smithsonian Latino Center, founded in 1997. The Women’s History Initiative has launched several exhibitions and has continued to produce virtual events during the pandemic, including <a href="https://womenshistory.si.edu/events">forthcoming programs</a> on female spies during World War II and sexism in science.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="MeYtl6">
Officials at the Smithsonian say their work on such programs will help make the new museums a success. “The Smithsonian has unparalleled experience building national museums, and is already doing significant work to tell the stories of American Women and Latinos,” the institution <a href="https://www.cnn.com/2020/12/22/politics/smithsonian-museums-american-latinos-women-trnd/index.html">said in a statement to CNN</a>. “We look forward to building two world-class museums to further amplify these stories and help our country learn more about the impact that women and Latinos have had on the fabric of our nation.”
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="kZV6X2">
And however they approach the task ahead, the goal should be to make sure “that any woman can walk into that museum and learn about something that they can relate to,” Gross said.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="6KTAr4">
</p>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The UK approved the Oxford/AstraZeneca Covid-19 vaccine. The US might not get it until April.</strong> -
<figure>
<img alt="" src="https://cdn.vox-cdn.com/thumbor/fTycZQquwhrTteUHBQvuzmLtlTU=/237x0:4021x2838/1310x983/cdn.vox-cdn.com/uploads/chorus_image/image/68599797/1230359489.7.jpg"/>
<figcaption>
People line up to receive vaccinations on December 30 in London. | Hollie Adams/Getty Images
</figcaption>
</figure></li>
</ul>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
The AstraZeneca vaccine is cheaper and easier to distribute than other vaccines being deployed.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="DQYzVR">
The <a href="https://www.gov.uk/government/news/oxford-universityastrazeneca-covid-19-vaccine-approved">United Kingdom</a> on Wednesday authorized its second <a href="https://www.vox.com/covid-19-coronavirus-treatment-prevention-cure-vaccines">Covid-19 vaccine</a> for distribution. Developed by the University of Oxford and AstraZeneca, the newly approved vaccine costs less and is easier to store than the <a href="https://www.vox.com/2020/12/2/21983642/uk-first-approves-pfizer-vaccine-biontech-covid-19">Pfizer/BioNTech</a> vaccine that received similar approval in the UK on December 2.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="NhvZGd">
Officials said the advantages of the Oxford/AstraZeneca vaccine could accelerate the vaccination effort as the UK contends with a new, <a href="https://www.vox.com/science-and-health/22192061/mutant-coronavirus-covid-19-uk-mutation-vaccine">more transmissible variant</a> of SARS-CoV-2, the virus that causes Covid-19.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="GRNvFU">
“This approval means more people can be protected against this virus and will help save lives,” June Raine, chief executive of the UK’s health regulator, the Medicines and Healthcare products Regulatory Agency, said in a <a href="https://www.gov.uk/government/news/oxford-universityastrazeneca-covid-19-vaccine-approved">statement</a>.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="H3PyEa">
The UK aims to vaccinate 1 million people per week and is shifting to a more aggressive vaccination schedule, according to the <a href="https://www.nytimes.com/2020/12/30/world/europe/uk-covid-19-vaccine-oxford-astrazeneca.html">New York Times</a>. The country will administer the first vaccine dose to “as many people as possible,” rather than try to keep supplies in reserve to ensure everyone receives a second dose, as other countries, including the United States, have done so far.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Kep7Fp">
The Oxford/AstraZeneca vaccine’s high stability and low cost could also be a boon to less wealthy nations. If its efficacy is high — and if the vaccine is distributed quickly — it could save countless lives. However, some lingering questions about the results of clinical trials for this vaccine are holding it back from approval in the US, which is conducting its own trials of the vaccine’s effectiveness.
</p>
<h3 id="eo9Dv5">
Why the Oxford/AstraZeneca Covid-19 vaccine is different from those developed by Pfizer/BioNTech and Moderna
</h3>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="YY5UbR">
In the UK, the Oxford/AstraZeneca vaccine is approved for people over the age of 18 and will normally be administered as two doses spaced four to 12 weeks apart. It<strong> </strong>costs $3 to $4 a dose and can be stored in regular refrigerators. By comparison, the <a href="https://www.vox.com/2020/12/17/22180356/moderna-covid-19-vaccine-approved-fda-emergency-use-pfizer">Moderna</a> and Pfizer/BioNTech vaccines that have received emergency use authorizations in the US cost between $15 and $25 per dose and require freezers. The Pfizer/BioNTech vaccine in particular needs <a href="https://www.vox.com/21552934/moderna-pfizer-covid-19-vaccine-biontech-coronavirus-cold-chain">cold storage</a> at minus 70 degrees Celsius (minus 94 degrees Fahrenheit) or lower.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="isbaDh">
The Oxford/AstraZeneca vaccine also uses a <a href="https://www.vox.com/2020/8/13/21359025/coronavirus-vaccine-covid-19-moderna-oxford-mrna-adenovirus">different technology</a> from the Covid-19 immunizations approved so far. The Pfizer/BioNTech and Moderna vaccines harness a molecule called mRNA as their platform to deliver the instructions for making a part of the SARS-CoV-2 virus. Oxford and AstraZeneca used a different innovative method, reprogramming another virus to transmit DNA instructions for making parts of the SARS-CoV-2 virus. Using another virus to package and deliver genetic material helps the Oxford/AstraZeneca vaccine remain stable even at higher temperatures.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Cmhk28">
However, Oxford and AstraZeneca <a href="https://www.vox.com/21590994/oxford-vaccine-results-covid-19-astrazeneca-trial-pfizer-moderna">encountered some problems in their clinical trials</a>, including a dosage mistake that led to one group receiving less than a full dose for their initial shot. So far, its efficacy seems to be less than that of the Moderna and Pfizer/BioNTech vaccines, though well above the 50 percent threshold the Food and Drug Administration and the European Medicines Agency set for vaccine approval.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ahBvS8">
But the <a href="https://www.vox.com/21590994/oxford-vaccine-results-covid-19-astrazeneca-trial-pfizer-moderna">actual efficacy value</a> remains unclear, ranging between 70 percent and 90 percent efficacy in preventing Covid-19. And Oxford and AstraZeneca have been cagey about certain details surrounding their research.
</p>
<aside id="IYTImU">
<div>
</div>
</aside>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="d47yx9">
One reason the Oxford/AstraZeneca vaccine has been approved in the UK but not in the US is that UK regulators evaluate clinical trial data on a rolling basis. The FDA prefers to have more complete trial data. In the US, <a href="https://clinicaltrials.gov/ct2/show/NCT04516746">phase 3 clinical trials</a> of the Oxford/AstraZeneca vaccine are still being conducted.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="KJJBNI">
During a <a href="https://www.politico.com/news/2020/12/30/astrazeneca-vaccine-april-452371">press call on December 30</a>, Moncef Slaoui, the scientific lead for the US government’s Operation Warp Speed, said it might be months before the US gives this vaccine the green light. “We project, if everything goes well, that the readout and emergency use authorization may be granted somewhere early in the month of April,” Slaoui said.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="AZ8gmN">
But as in the UK, having another vaccine available in the US, particularly one that’s cheaper and easier to store, would help control the spread of Covid-19. The US government has already invested <a href="https://www.hhs.gov/coronavirus/explaining-operation-warp-speed/index.html">$1.2 billion</a> in the Oxford/AstraZeneca vaccine and has committed to purchasing <a href="https://www.hhs.gov/about/news/2020/05/21/trump-administration-accelerates-astrazeneca-covid-19-vaccine-to-be-available-beginning-in-october.html">300 million doses</a>.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="C7HkBL">
</p>
<h1 data-aos="fade-right" id="from-the-hindu-sports">From The Hindu: Sports</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Copper Queen, Eagle Prince, Beauteous Maximus and Towns End please</strong> - Copper Queen, Eagle Prince, Beauteous Maximus and Towns End pleased when the horses were exercised here on Thursday (Dec. 31). Inner sand: 600m: Star</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Aus vs Ind third Test | Rohit gears up for Sydney Test with first practice session at MCG</strong> - While Rohit Sharma trained, the rest of the squad took a brief two-day break after India''s fine win in the second Test at MCG.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Goa’s 14-year-old Leon Mendonca becomes India’s 67th Grandmaster</strong> - Mendonca, who achieved the feat at 14 years, 9 months and 17 days, is the second GM from the coastal State.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>ICC Test Ranking: Rahane climbs to 6th, Ashwin to 7th, Kohli remains at No. 2</strong> - New Zealand skipper Williamson described it as “humbling” to overtake Smith, who held the top spot for 313 days this year.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Australia vs India | Shardul likely to play in Sydney Test, Umesh out of series</strong> - Umesh Yadav had hobbled off the field after suffering the injury during the third day of the Boxing Day Test.</p></li>
</ul>
<h1 data-aos="fade-right" id="from-the-hindu-national-news">From The Hindu: National News</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>CBSE Class X, XII exams from May 4 to June 10</strong> - Union Education Minister Ramesh Pokhriyal Nishank on Thursday said Central Board of Secondary Education (CBSE) Class X and Class XII board examination</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Ladakh standoff | China, India in talks to hold 9th round of Commander-level meet: Defence Ministry</strong> - At the latest round of foreign ministry-level talks on December 18, the two sides said that they have agreed to continue work towards ensuring complete disengagement of troops</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>CVC calls for probe into pending corruption cases to be completed by May 2021</strong> - The vigilance body issues order to secretaries of all central government departments, chief executives of public sector banks, insurance companies and undertakings.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Data firm puts Narendra Modi’s net approval at 55%</strong> - Morning Consult, which carries out surveys and research globally, said in its latest survey that over 75% people approve of Modi while 20% disapprove</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Council of Architecture, architects urge IIM-A not to demolish dorms</strong> - Letters term decision ‘cultural vandalism’, call for restoration of iconic buildings</p></li>
</ul>
<h1 data-aos="fade-right" id="from-bbc-europe">From BBC: Europe</h1>
<ul>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Covid: France mobilises 100,000 police to stop New Year's Eve gatherings</strong> - Like other European countries, France will see muted celebrations to mark the last night of the year.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Norway landslide: Houses buried in Gjerdrum village near Oslo</strong> - Ten people are injured and a further 10 are still unaccounted for in Gjerdrum, authorities say.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Bosnia: Hundreds of migrants stuck at fire-gutted camp</strong> - About 900 migrants are stranded in the freezing cold after plans to relocate them are blocked.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Giulio Regeni: Italy condemns Egypt for ruling out charges against police</strong> - Italian prosecutors had accused four Egyptian officers of the murder of a Cambridge student in 2016.</p></li>
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Brexit: New EU trade arrangements to begin after Parliament vote</strong> - The UK's hard-fought agreement with the EU is set to come into force at 23:00 GMT on Thursday.</p></li>
</ul>
<h1 data-aos="fade-right" id="from-ars-technica">From Ars Technica</h1>
<ul>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Basking shark families go on road trips in search of fine dining</strong> - Genetic tagging offers insight into the secret lives of basking sharks. - <a href="https://arstechnica.com/?p=1732410">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Ars Technica’s 2021 Deathwatch—2020 was just the beginning</strong> - These companies might have survived COVID and a recession, but will they survive 2021? - <a href="https://arstechnica.com/?p=1728271">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>That time physicist John Wheeler left classified H-bomb documents on a train</strong> - The whereabouts of the documents remains a mystery to this day. - <a href="https://arstechnica.com/?p=1732329">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Corellium notches partial victory in Apple iOS copyright case</strong> - Security firm's actions both may and may not qualify under fair use, judge held. - <a href="https://arstechnica.com/?p=1732395">link</a></p></li>
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>With the right catalyst, we might make jet fuel from CO₂</strong> - As carbon capture gets cheaper, new applications could look attractive. - <a href="https://arstechnica.com/?p=1732362">link</a></p></li>
</ul>
<h1 data-aos="fade-right" id="from-jokes-subreddit">From Jokes Subreddit</h1>
<ul>
<li><strong>My girlfriend surprised me tonight: she dressed up sexy like a police woman, handcuffed me to the bed and arrested me on suspicion of being good in bed.</strong> - <!-- SC_OFF -->
<div class="md">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
2 minutes later I was released due to lack of evidence.
</p>
</div>
<!-- SC_ON -->
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"> submitted by <a href="https://www.reddit.com/user/Po1sonator"> /u/Po1sonator </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/knjyuo/my_girlfriend_surprised_me_tonight_she_dressed_up/">[link]</a></span> <span><a href="https://www.reddit.com/r/Jokes/comments/knjyuo/my_girlfriend_surprised_me_tonight_she_dressed_up/">[comments]</a></span></p></li>
<li><strong>In 2017, i didn’t jog. In 2018 i didn’t jog. In 2019 i didn’t jog. In 2020 i didn’t jog.</strong> - <!-- SC_OFF -->
<div class="md">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
This is a running joke
</p>
</div>
<!-- SC_ON -->
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"> submitted by <a href="https://www.reddit.com/user/theblackviper69"> /u/theblackviper69 </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/knjt2p/in_2017_i_didnt_jog_in_2018_i_didnt_jog_in_2019_i/">[link]</a></span> <span><a href="https://www.reddit.com/r/Jokes/comments/knjt2p/in_2017_i_didnt_jog_in_2018_i_didnt_jog_in_2019_i/">[comments]</a></span></p></li>
<li><strong>Reddit should rename 'share' to 'spreddit', 'delete' to 'shreddit' and 'karma' to 'creddit'.</strong> - <!-- SC_OFF -->
<div class="md">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
Yet they haven't. I don't geddit.
</p>
</div>
<!-- SC_ON -->
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"> submitted by <a href="https://www.reddit.com/user/RockManDan"> /u/RockManDan </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kneldj/reddit_should_rename_share_to_spreddit_delete_to/">[link]</a></span> <span><a href="https://www.reddit.com/r/Jokes/comments/kneldj/reddit_should_rename_share_to_spreddit_delete_to/">[comments]</a></span></p></li>
<li><strong>A blonde, a brunette, and a redhead walk into a restaurant.</strong> - <!-- SC_OFF -->
<div class="md">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
They are having a fun time and give their waitress a huge tip. Super excited about the tip, the waitress decides to tell them a secret: In the women's bathroom, there is a magical mirror. If you tell it something truthful, you will be greatly rewarded. However, if you lie to the mirror, you will disappear in a poof."
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
Excited to try this mirror out, the women rush to the restroom. The brunette decides to show off and claim she is the most beautiful girl there. "I think I'm the most beautiful person at this restaurant." A million dollars appears in her hands.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
The redhead is feeling a little offended. She decides to show off how smart she is: "I think I'm the smartest person in this restaurant." The keys to a lamborghini magically show up in her purse.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
The blonde, super excited to get something really cool, starts to tell the mirror something: "I think--" poof. she is never seen again
</p>
</div>
<!-- SC_ON -->
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"> submitted by <a href="https://www.reddit.com/user/ZealousidealRise7"> /u/ZealousidealRise7 </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kngxkr/a_blonde_a_brunette_and_a_redhead_walk_into_a/">[link]</a></span> <span><a href="https://www.reddit.com/r/Jokes/comments/kngxkr/a_blonde_a_brunette_and_a_redhead_walk_into_a/">[comments]</a></span></p></li>
<li><strong>A man tells his friend he just opened a brothel.</strong> - <!-- SC_OFF -->
<div class="md">
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
“$100 for anal and $50 for a blow job”, says the man.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
His friend asks “How much for the pussy?”.
</p>
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
“Nah” says the man, “I don’t have any employees yet”.
</p>
</div>
<!-- SC_ON -->
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"> submitted by <a href="https://www.reddit.com/user/RhinoVanHorn"> /u/RhinoVanHorn </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kn4v5r/a_man_tells_his_friend_he_just_opened_a_brothel/">[link]</a></span> <span><a href="https://www.reddit.com/r/Jokes/comments/kn4v5r/a_man_tells_his_friend_he_just_opened_a_brothel/">[comments]</a></span></p></li>
</ul>
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2020.html">19 December, 2020</a></li><li><a href="./archive-daily-dose/18 December, 2020.html">18 December, 2020</a></li><li><a href="./archive-daily-dose/17 December, 2020.html">17 December, 2020</a></li><li><a href="./archive-daily-dose/16 December, 2020.html">16 December, 2020</a></li><li><a href="./archive-daily-dose/15 December, 2020.html">15 December, 2020</a></li><li><a href="./archive-daily-dose/14 December, 2020.html">14 December, 2020</a></li><li><a href="./archive-daily-dose/13 December, 2020.html">13 December, 2020</a></li><li><a href="./archive-daily-dose/12 December, 2020.html">12 December, 2020</a></li><li><a href="./archive-daily-dose/11 December, 2020.html">11 December, 2020</a></li><li><a href="./archive-daily-dose/10 December, 2020.html">10 December, 2020</a></li><li><a href="./archive-daily-dose/09 December, 2020.html">09 December, 2020</a></li><li><a href="./archive-daily-dose/08 December, 2020.html">08 December, 2020</a></li><li><a href="./archive-daily-dose/07 December, 2020.html">07 December, 2020</a></li><li><a href="./archive-daily-dose/06 December, 2020.html">06 December, 2020</a></li><li><a href="./archive-daily-dose/05 December, 2020.html">05 December, 2020</a></li><li><a href="./archive-daily-dose/04 December, 2020.html">04 December, 2020</a></li><li><a href="./archive-daily-dose/03 December, 2020.html">03 December, 2020</a></li><li><a href="./archive-daily-dose/02 December, 2020.html">02 December, 2020</a></li><li><a href="./archive-daily-dose/01 December, 2020.html">01 December, 2020</a></li><li><a href="./archive-daily-dose/30 November, 2020.html">30 November, 2020</a></li><li><a href="./archive-daily-dose/29 November, 2020.html">29 November, 2020</a></li><li><a href="./archive-daily-dose/28 November, 2020.html">28 November, 2020</a></li><li><a href="./archive-daily-dose/27 November, 2020.html">27 November, 2020</a></li><li><a href="./archive-daily-dose/26 November, 2020.html">26 November, 2020</a></li><li><a href="./archive-daily-dose/25 November, 2020.html">25 November, 2020</a></li><li><a href="./archive-daily-dose/24 November, 2020.html">24 November, 2020</a></li><li><a href="./archive-daily-dose/23 November, 2020.html">23 November, 2020</a></li><li><a href="./archive-daily-dose/22 November, 2020.html">22 November, 2020</a></li><li><a href="./archive-daily-dose/21 November, 2020.html">21 November, 2020</a></li><li><a href="./archive-daily-dose/20 November, 2020.html">20 November, 2020</a></li><li><a href="./archive-daily-dose/19 November, 2020.html">19 November, 2020</a></li><li><a href="./archive-daily-dose/18 November, 2020.html">18 November, 2020</a></li><li><a href="./archive-daily-dose/17 November, 2020.html">17 November, 2020</a></li><li><a href="./archive-daily-dose/16 November, 2020.html">16 November, 2020</a></li><li><a href="./archive-daily-dose/15 November, 2020.html">15 November, 2020</a></li><li><a href="./archive-daily-dose/14 November, 2020.html">14 November, 2020</a></li><li><a href="./archive-daily-dose/13 November, 2020.html">13 November, 2020</a></li><li><a href="./archive-daily-dose/12 November, 2020.html">12 November, 2020</a></li><li><a href="./archive-daily-dose/11 November, 2020.html">11 November, 2020</a></li> <ul id="daily-dose-list"><li><a href="./archive-daily-dose/31 December, 2020.html">31 December, 2020</a></li><li><a href="./archive-daily-dose/30 December, 2020.html">30 December, 2020</a></li><li><a href="./archive-daily-dose/29 December, 2020.html">29 December, 2020</a></li><li><a href="./archive-daily-dose/28 December, 2020.html">28 December, 2020</a></li><li><a href="./archive-daily-dose/27 December, 2020.html">27 December, 2020</a></li><li><a href="./archive-daily-dose/26 December, 2020.html">26 December, 2020</a></li><li><a href="./archive-daily-dose/25 December, 2020.html">25 December, 2020</a></li><li><a href="./archive-daily-dose/24 December, 2020.html">24 December, 2020</a></li><li><a href="./archive-daily-dose/23 December, 2020.html">23 December, 2020</a></li><li><a href="./archive-daily-dose/22 December, 2020.html">22 December, 2020</a></li><li><a href="./archive-daily-dose/21 December, 2020.html">21 December, 2020</a></li><li><a href="./archive-daily-dose/20 December, 2020.html">20 December, 2020</a></li><li><a href="./archive-daily-dose/19 December, 2020.html">19 December, 2020</a></li><li><a href="./archive-daily-dose/18 December, 2020.html">18 December, 2020</a></li><li><a href="./archive-daily-dose/17 December, 2020.html">17 December, 2020</a></li><li><a href="./archive-daily-dose/16 December, 2020.html">16 December, 2020</a></li><li><a href="./archive-daily-dose/15 December, 2020.html">15 December, 2020</a></li><li><a href="./archive-daily-dose/14 December, 2020.html">14 December, 2020</a></li><li><a href="./archive-daily-dose/13 December, 2020.html">13 December, 2020</a></li><li><a href="./archive-daily-dose/12 December, 2020.html">12 December, 2020</a></li><li><a href="./archive-daily-dose/11 December, 2020.html">11 December, 2020</a></li><li><a href="./archive-daily-dose/10 December, 2020.html">10 December, 2020</a></li><li><a href="./archive-daily-dose/09 December, 2020.html">09 December, 2020</a></li><li><a href="./archive-daily-dose/08 December, 2020.html">08 December, 2020</a></li><li><a href="./archive-daily-dose/07 December, 2020.html">07 December, 2020</a></li><li><a href="./archive-daily-dose/06 December, 2020.html">06 December, 2020</a></li><li><a href="./archive-daily-dose/05 December, 2020.html">05 December, 2020</a></li><li><a href="./archive-daily-dose/04 December, 2020.html">04 December, 2020</a></li><li><a href="./archive-daily-dose/03 December, 2020.html">03 December, 2020</a></li><li><a href="./archive-daily-dose/02 December, 2020.html">02 December, 2020</a></li><li><a href="./archive-daily-dose/01 December, 2020.html">01 December, 2020</a></li><li><a href="./archive-daily-dose/30 November, 2020.html">30 November, 2020</a></li><li><a href="./archive-daily-dose/29 November, 2020.html">29 November, 2020</a></li><li><a href="./archive-daily-dose/28 November, 2020.html">28 November, 2020</a></li><li><a href="./archive-daily-dose/27 November, 2020.html">27 November, 2020</a></li><li><a href="./archive-daily-dose/26 November, 2020.html">26 November, 2020</a></li><li><a href="./archive-daily-dose/25 November, 2020.html">25 November, 2020</a></li><li><a href="./archive-daily-dose/24 November, 2020.html">24 November, 2020</a></li><li><a href="./archive-daily-dose/23 November, 2020.html">23 November, 2020</a></li><li><a href="./archive-daily-dose/22 November, 2020.html">22 November, 2020</a></li><li><a href="./archive-daily-dose/21 November, 2020.html">21 November, 2020</a></li><li><a href="./archive-daily-dose/20 November, 2020.html">20 November, 2020</a></li><li><a href="./archive-daily-dose/19 November, 2020.html">19 November, 2020</a></li><li><a href="./archive-daily-dose/18 November, 2020.html">18 November, 2020</a></li><li><a href="./archive-daily-dose/17 November, 2020.html">17 November, 2020</a></li><li><a href="./archive-daily-dose/16 November, 2020.html">16 November, 2020</a></li><li><a href="./archive-daily-dose/15 November, 2020.html">15 November, 2020</a></li><li><a href="./archive-daily-dose/14 November, 2020.html">14 November, 2020</a></li><li><a href="./archive-daily-dose/13 November, 2020.html">13 November, 2020</a></li><li><a href="./archive-daily-dose/12 November, 2020.html">12 November, 2020</a></li><li><a href="./archive-daily-dose/11 November, 2020.html">11 November, 2020</a></li>
</ul> </ul>
<h2 id="covid-19">Covid-19</h2> <h2 id="covid-19">Covid-19</h2>
<ul id="covid-19-list"><li><a href="./archive-covid-19/30 December, 2020.html">30 December, 2020</a></li><li><a href="./archive-covid-19/29 December, 2020.html">29 December, 2020</a></li><li><a href="./archive-covid-19/28 December, 2020.html">28 December, 2020</a></li><li><a href="./archive-covid-19/27 December, 2020.html">27 December, 2020</a></li><li><a href="./archive-covid-19/26 December, 2020.html">26 December, 2020</a></li><li><a href="./archive-covid-19/25 December, 2020.html">25 December, 2020</a></li><li><a href="./archive-covid-19/24 December, 2020.html">24 December, 2020</a></li><li><a href="./archive-covid-19/23 December, 2020.html">23 December, 2020</a></li><li><a href="./archive-covid-19/22 December, 2020.html">22 December, 2020</a></li><li><a href="./archive-covid-19/21 December, 2020.html">21 December, 2020</a></li><li><a href="./archive-covid-19/20 December, 2020.html">20 December, 2020</a></li><li><a href="./archive-covid-19/19 December, 2020.html">19 December, 2020</a></li><li><a href="./archive-covid-19/18 December, 2020.html">18 December, 2020</a></li><li><a href="./archive-covid-19/17 December, 2020.html">17 December, 2020</a></li><li><a href="./archive-covid-19/16 December, 2020.html">16 December, 2020</a></li><li><a href="./archive-covid-19/15 December, 2020.html">15 December, 2020</a></li><li><a href="./archive-covid-19/14 December, 2020.html">14 December, 2020</a></li><li><a href="./archive-covid-19/13 December, 2020.html">13 December, 2020</a></li><li><a href="./archive-covid-19/12 December, 2020.html">12 December, 2020</a></li><li><a href="./archive-covid-19/11 December, 2020.html">11 December, 2020</a></li><li><a href="./archive-covid-19/10 December, 2020.html">10 December, 2020</a></li><li><a href="./archive-covid-19/09 December, 2020.html">09 December, 2020</a></li><li><a href="./archive-covid-19/08 December, 2020.html">08 December, 2020</a></li><li><a href="./archive-covid-19/07 December, 2020.html">07 December, 2020</a></li><li><a href="./archive-covid-19/06 December, 2020.html">06 December, 2020</a></li><li><a href="./archive-covid-19/05 December, 2020.html">05 December, 2020</a></li><li><a href="./archive-covid-19/04 December, 2020.html">04 December, 2020</a></li><li><a href="./archive-covid-19/03 December, 2020.html">03 December, 2020</a></li><li><a href="./archive-covid-19/02 December, 2020.html">02 December, 2020</a></li><li><a href="./archive-covid-19/01 December, 2020.html">01 December, 2020</a></li><li><a href="./archive-covid-19/30 November, 2020.html">30 November, 2020</a></li><li><a href="./archive-covid-19/29 November, 2020.html">29 November, 2020</a></li><li><a href="./archive-covid-19/28 November, 2020.html">28 November, 2020</a></li><li><a href="./archive-covid-19/27 November, 2020.html">27 November, 2020</a></li><li><a href="./archive-covid-19/26 November, 2020.html">26 November, 2020</a></li><li><a href="./archive-covid-19/25 November, 2020.html">25 November, 2020</a></li><li><a href="./archive-covid-19/24 November, 2020.html">24 November, 2020</a></li><li><a href="./archive-covid-19/23 November, 2020.html">23 November, 2020</a></li><li><a href="./archive-covid-19/22 November, 2020.html">22 November, 2020</a></li><li><a href="./archive-covid-19/21 November, 2020.html">21 November, 2020</a></li><li><a href="./archive-covid-19/20 November, 2020.html">20 November, 2020</a></li><li><a href="./archive-covid-19/19 November, 2020.html">19 November, 2020</a></li><li><a href="./archive-covid-19/18 November, 2020.html">18 November, 2020</a></li><li><a href="./archive-covid-19/17 November, 2020.html">17 November, 2020</a></li><li><a href="./archive-covid-19/16 November, 2020.html">16 November, 2020</a></li><li><a href="./archive-covid-19/15 November, 2020.html">15 November, 2020</a></li><li><a href="./archive-covid-19/14 November, 2020.html">14 November, 2020</a></li><li><a href="./archive-covid-19/13 November, 2020.html">13 November, 2020</a></li><li><a href="./archive-covid-19/12 November, 2020.html">12 November, 2020</a></li><li><a href="./archive-covid-19/11 November, 2020.html">11 November, 2020</a></li> <ul id="covid-19-list"><li><a href="./archive-covid-19/31 December, 2020.html">31 December, 2020</a></li><li><a href="./archive-covid-19/30 December, 2020.html">30 December, 2020</a></li><li><a href="./archive-covid-19/29 December, 2020.html">29 December, 2020</a></li><li><a href="./archive-covid-19/28 December, 2020.html">28 December, 2020</a></li><li><a href="./archive-covid-19/27 December, 2020.html">27 December, 2020</a></li><li><a href="./archive-covid-19/26 December, 2020.html">26 December, 2020</a></li><li><a href="./archive-covid-19/25 December, 2020.html">25 December, 2020</a></li><li><a href="./archive-covid-19/24 December, 2020.html">24 December, 2020</a></li><li><a href="./archive-covid-19/23 December, 2020.html">23 December, 2020</a></li><li><a href="./archive-covid-19/22 December, 2020.html">22 December, 2020</a></li><li><a href="./archive-covid-19/21 December, 2020.html">21 December, 2020</a></li><li><a href="./archive-covid-19/20 December, 2020.html">20 December, 2020</a></li><li><a href="./archive-covid-19/19 December, 2020.html">19 December, 2020</a></li><li><a href="./archive-covid-19/18 December, 2020.html">18 December, 2020</a></li><li><a href="./archive-covid-19/17 December, 2020.html">17 December, 2020</a></li><li><a href="./archive-covid-19/16 December, 2020.html">16 December, 2020</a></li><li><a href="./archive-covid-19/15 December, 2020.html">15 December, 2020</a></li><li><a href="./archive-covid-19/14 December, 2020.html">14 December, 2020</a></li><li><a href="./archive-covid-19/13 December, 2020.html">13 December, 2020</a></li><li><a href="./archive-covid-19/12 December, 2020.html">12 December, 2020</a></li><li><a href="./archive-covid-19/11 December, 2020.html">11 December, 2020</a></li><li><a href="./archive-covid-19/10 December, 2020.html">10 December, 2020</a></li><li><a href="./archive-covid-19/09 December, 2020.html">09 December, 2020</a></li><li><a href="./archive-covid-19/08 December, 2020.html">08 December, 2020</a></li><li><a href="./archive-covid-19/07 December, 2020.html">07 December, 2020</a></li><li><a href="./archive-covid-19/06 December, 2020.html">06 December, 2020</a></li><li><a href="./archive-covid-19/05 December, 2020.html">05 December, 2020</a></li><li><a href="./archive-covid-19/04 December, 2020.html">04 December, 2020</a></li><li><a href="./archive-covid-19/03 December, 2020.html">03 December, 2020</a></li><li><a href="./archive-covid-19/02 December, 2020.html">02 December, 2020</a></li><li><a href="./archive-covid-19/01 December, 2020.html">01 December, 2020</a></li><li><a href="./archive-covid-19/30 November, 2020.html">30 November, 2020</a></li><li><a href="./archive-covid-19/29 November, 2020.html">29 November, 2020</a></li><li><a href="./archive-covid-19/28 November, 2020.html">28 November, 2020</a></li><li><a href="./archive-covid-19/27 November, 2020.html">27 November, 2020</a></li><li><a href="./archive-covid-19/26 November, 2020.html">26 November, 2020</a></li><li><a href="./archive-covid-19/25 November, 2020.html">25 November, 2020</a></li><li><a href="./archive-covid-19/24 November, 2020.html">24 November, 2020</a></li><li><a href="./archive-covid-19/23 November, 2020.html">23 November, 2020</a></li><li><a href="./archive-covid-19/22 November, 2020.html">22 November, 2020</a></li><li><a href="./archive-covid-19/21 November, 2020.html">21 November, 2020</a></li><li><a href="./archive-covid-19/20 November, 2020.html">20 November, 2020</a></li><li><a href="./archive-covid-19/19 November, 2020.html">19 November, 2020</a></li><li><a href="./archive-covid-19/18 November, 2020.html">18 November, 2020</a></li><li><a href="./archive-covid-19/17 November, 2020.html">17 November, 2020</a></li><li><a href="./archive-covid-19/16 November, 2020.html">16 November, 2020</a></li><li><a href="./archive-covid-19/15 November, 2020.html">15 November, 2020</a></li><li><a href="./archive-covid-19/14 November, 2020.html">14 November, 2020</a></li><li><a href="./archive-covid-19/13 November, 2020.html">13 November, 2020</a></li><li><a href="./archive-covid-19/12 November, 2020.html">12 November, 2020</a></li><li><a href="./archive-covid-19/11 November, 2020.html">11 November, 2020</a></li>
</ul> </ul>
</body></html> </body></html>