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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>Change in mental and physical health, and social relationships, during highly restrictive lockdown in the COVID-19 pandemic: Evidence from Australia</strong> -
 <div>
 We surveyed a sample of people from the Australian public about their concerns and mental health (n = 1599) during COVID-19 lock-down. When estimating their mental health for the previous year 13% of participants reported more negative than positive emotion, whereas this increased to 41% when participants reflected on their prior month during COVID-19 lock-down. A substantial proportion (39-54%) of participants reported deterioration in mental health, physical health, financial situation, and work productivity. Less impact was apparent for social relationships as participants compensated for decreased face-to-face interaction via increased technology-mediated interaction. We found evidence to suggest a general increase in compassion for others, as participants reported that due to the pandemic they were feeling more concerned about the welfare of people close to them (87%), and people in general (84%). However, the extent of increased concern for others was also found to be negatively associated with mental health. Most participants reported a generally favourable attitude regarding the government pandemic response. This study reveals that even when the public are largely supportive of the government response to a pandemic there can still be large public health implications due to the overall level of disruption to people's lives.
 </div>
 <div class="article-link article-html-link">
 🖺 Full Text HTML: <a href="https://psyarxiv.com/zutav/" target="_blank">Change in mental and physical health, and social relationships, during highly restrictive lockdown in the COVID-19 pandemic: Evidence from Australia</a>
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 <li><strong>Analyzing the vast coronavirus literature with CoronaCentral</strong> -
 <div>
 The global SARS-CoV-2 pandemic has caused a surge in research exploring all aspects of the virus and its effects on human health. The overwhelming rate of publications means that human researchers are unable to keep abreast of the research. To ameliorate this, we present the CoronaCentral resource which uses machine learning to process the research literature on SARS-CoV-2 along with articles on SARS-CoV and MERS-CoV. We break the literature down into useful categories and enable analysis of the contents, pace, and emphasis of research during the crisis. These categories cover therapeutics, forecasting as well as growing areas such as "Long Covid" and studies of inequality and misinformation. Using this data, we compare topics that appear in original research articles compared to commentaries and other article types. Finally, using Altmetric data, we identify the topics that have gained the most media attention. This resource, available at https://coronacentral.ai, is updated multiple times per day and provides an easy-to-navigate system to find papers in different categories, focussing on different aspects of the virus along with currently trending articles.
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 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.21.423860v1" target="_blank">Analyzing the vast coronavirus literature with CoronaCentral</a>
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 <li><strong>T cell activation, highly armed cytotoxic cells and a sharp shift in monocytes CD300 receptors expression is characteristic of patients with severe COVID-19</strong> -
 <div>
 COVID-19 manifests with a wide diversity of clinical phenotypes characterized by dysfunctional and exaggerated host immune responses. Many results have been described on the status of the immune system of patients infected with SARS-CoV-2, but there are still aspects that have not been fully characterized. In this study, we have analyzed a cohort of patients with mild, moderate and severe disease. We performed flow cytometric studies and correlated the data with the clinical features and clinical laboratory values of patients. Both conventional and unsupervised data analyses concluded that patients with severe disease are characterized, among others, by a higher state of activation in all T cell subsets, higher expression of perforin and granzyme B in cytotoxic cells, expansion of adaptive NK cells and the accumulation of activated and immature dysfunctional monocytes which are identified by a low expression of HLA-DR and an intriguing abrupt change in the expression pattern of CD300 receptors. More importantly, correlation analysis showed a strong association between the alterations in the immune cells and the clinical signs of severity. These results indicate that patients with severe COVID-19 have a broad perturbation of their immune system, and they will help to understand the immunopathogenesis of severe COVID-19 as well as could be of special value for physicians to decide which specific therapeutic options are most effective for their patients.
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 <div class="article-link article-html-link">
 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.22.423917v1" target="_blank">T cell activation, highly armed cytotoxic cells and a sharp shift in monocytes CD300 receptors expression is characteristic of patients with severe COVID-19</a>
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 <li><strong>SARS-CoV-2 Genomic Surveillance in Costa Rica: Evidence of a Divergent Population and an Increased Detection of a Spike T1117I Mutation</strong> -
 <div>
 Genome sequencing is a key strategy in the surveillance of SARS-CoV-2, the virus responsible for the COVID-19 outbreak. Latin America is the hardest hit region of the world, accumulating almost 25% of COVID-19 cases worldwide. Costa Rica was first exemplary for the region in its pandemic control, declaring a swift state of emergency on March 16th that led to a low quantity of cases, until measures were lifted in early May. From the first detected case in March 6th to November 30th almost 140 000 cases have been reported in Costa Rica, 99.5% of them from May onwards. We analyzed the genomic variability during the SARS-CoV-2 pandemic in Costa Rica using 138 sequences, 52 from the first months of the pandemic, and 86 from the current wave. Three GISAID clades (G, GH, and GR) and three PANGOLIN lineages (B.1, B.1.1, and B.1.291) are predominant, with phylogenetic relationships that are in line with the results of other Latin American countries suggesting introduction and multiple re-introductions from other regions of the world. The sequences from the first months of the pandemic grouped in lineage B.1 and B.1.5 mainly, suggesting low undetected circulation and re-introductions of new lineages not detected in the country during early stages of the pandemic due to the extreme lockdown measures. The whole-genome variant calling analysis identified a total of 177 distinct variants. These correspond mostly to synonymous mutations (41.2%, 73) but 54.8% correspond to non-synonymous mutations (97). The 177 variants showed an expected distribution of a power-law distribution: 106 single nucleotide mutations were identified in single sequences, only 16 single nucleotide mutations were found in &gt;5% sequences, and only three single nucleotide mutations in &gt;25% genomes. These mutations were distributed all over the genome. However, 61.5% were present in ORF1ab, and 15.0% in Spike gene and 9.6% in the Nucleocapsid. Additionally, the prevalence of worldwide-found variant D614G in the Spike (98.6%), ORF8 L84S (1.5%) is similar to what is been found elsewhere. Interestingly, the prevalence of mutation T1117I in the Spike has increased during the current pandemic wave beginning in May 2020 in Costa Rica, reaching 14.5% detection in the full genome analyses in August 2020. This variant has been observed in less than 1% of the GISAID reported sequences in other countries. Structural modeling of the Spike protein with the T1117I mutation suggest a possible effect on the viral oligomerization. Nevertheless, in-vitro experiments are required to prove this in-silico analyses. In conclusion, genome analyses of the SARS-CoV-2 sequences over the course of COVID-19 pandemic in Costa Rica suggests re-introduction of lineages from other countries as travel bans and measures were lifted, similar to results found in other studies, but the Spike-T1117I variant needs to be monitored and studied in further analyses as part of the surveillance program during the pandemic.
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 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.21.423850v1" target="_blank">SARS-CoV-2 Genomic Surveillance in Costa Rica: Evidence of a Divergent Population and an Increased Detection of a Spike T1117I Mutation</a>
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 <li><strong>SARS-CoV-2 testing of 11,884 healthcare workers at an acute NHS hospital trust in England: a retrospective analysis</strong> -
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 Healthcare workers (HCWs) are known to be at increased risk of infection with SARS-CoV-2, although whether these risks are equal across all roles is uncertain. Here we report a retrospective analysis of a large real-world dataset obtained from 10 March to 6 July 2020 in an NHS Foundation Trust in England with 17,126 employees. 3,338 HCWs underwent symptomatic PCR testing (14.4% positive, 2.8% of all staff) and 11,103 HCWs underwent serological testing for SARS-CoV-2 IgG (8.4% positive, 5.5% of all staff). Seropositivity was lower than other hospital settings in England but higher than community estimates. Increased test positivity rates were observed in HCWs from BAME backgrounds and residents in areas of higher social deprivation. A logistic regression model adjusting for these factors showed significant increases in the odds of testing positive in certain occupational groups, most notably domestic services staff, nurses and health-care assistants. PCR testing of symptomatic HCWs appeared to underestimate overall infection levels, probably due to asymptomatic seroconversion. Clinical outcomes were reassuring, with only a small minority of HCWs with COVID-19 requiring hospitalisation (2.3%) or ICU management (0.7%) and with no deaths. Despite a relatively low level of HCW infection compared to other UK cohorts, there were nevertheless important differences in test positivity rates between occupational groups, robust to adjustment for demographic factors such as ethnic background and social deprivation. Quantitative and qualitative studies are needed to better understand the factors contributing to this risk. Robust informatics solutions for HCW exposure data are essential to inform occupational monitoring.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.22.20242362v1" target="_blank">SARS-CoV-2 testing of 11,884 healthcare workers at an acute NHS hospital trust in England: a retrospective analysis</a>
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 <li><strong>Transcriptional and epi-transcriptional dynamics of SARS-CoV-2 during cellular infection</strong> -
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 SARS-CoV-2 uses subgenomic (sg)RNA to produce viral proteins for replication and immune evasion. We applied long-read RNA and cDNA sequencing to in vitro human and primate infection models to study transcriptional dynamics. Transcription-regulating sequence (TRS)-dependent sgRNA was upregulated earlier in infection than TRS-independent sgRNA. An abundant class of TRS-independent sgRNA consisting of a portion of ORF1ab containing nsp1 joined to ORF10 and 3prime UTR was upregulated at 48 hours post infection in human cell lines. We identified double-junction sgRNA containing both TRS-dependent and independent junctions. We found multiple sites at which the SARS-CoV-2 genome is consistently more modified than sgRNA, and that sgRNA modifications are stable across transcript clusters, host cells and time since infection. Our work highlights the dynamic nature of the SARS-CoV-2 transcriptome during its replication cycle. Our results are available via an interactive web-app at http://coinlab.mdhs.unimelb.edu.au/.
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 <div class="article-link article-html-link">
 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.22.423893v1" target="_blank">Transcriptional and epi-transcriptional dynamics of SARS-CoV-2 during cellular infection</a>
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 <li><strong>In Vitro Safety Clinical Trial of the Cardiac Liability of Hydroxychloroquine and Azithromycin as COVID19 Polytherapy</strong> -
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 Despite global efforts, there are no effective FDA-approved medicines for the treatment of SARS-CoV-2 infection. Potential therapeutics focus on repurposed drugs, some with cardiac liabilities. Here we report on a preclinical drug screening platform, a cardiac microphysiological system (MPS), to assess cardiotoxicity associated with hydroxychloroquine (HCQ) and azithromycin (AZM) polytherapy in a mock clinical trial. The MPS contained human heart muscle derived from patient-specific induced pluripotent stem cells. The effect of drug response was measured using outputs that correlate with clinical measurements such as QT interval (action potential duration) and drug-biomarker pairing. Chronic exposure to HCQ alone elicited early afterdepolarizations (EADs) and increased QT interval from day 6 onwards. AZM alone elicited an increase in QT interval from day 7 onwards and arrhythmias were observed at days 8 and 10. Monotherapy results closely mimicked clinical trial outcomes. Upon chronic exposure to HCQ and AZM polytherapy, we observed an increase in QT interval on days 4-8. Interestingly, a decrease in arrhythmias and instabilities was observed in polytherapy relative to monotherapy, in concordance with published clinical trials. Furthermore, biomarkers, most of them measurable in patients serum, were identified for negative effects of single drug or polytherapy on tissue contractile function, morphology, and antioxidant protection. The cardiac MPS can predict clinical arrhythmias associated with QT prolongation and rhythm instabilities. This high content system can help clinicians design their trials, rapidly project cardiac outcomes, and define new monitoring biomarkers to accelerate access of patients to safe COVID-19 therapeutics.
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 <div class="article-link article-html-link">
 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.21.423869v1" target="_blank">In Vitro Safety Clinical Trial of the Cardiac Liability of Hydroxychloroquine and Azithromycin as COVID19 Polytherapy</a>
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 <li><strong>The Ensembl COVID-19 resource: Ongoing integration of public SARS-CoV-2 data</strong> -
 <div>
 The Ensembl COVID-19 browser (covid-19.ensembl.org) was launched in May 2020 in response to the ongoing pandemic. It is Ensembl's contribution to the global efforts to develop treatments, diagnostics and vaccines for COVID-19, and it supports research into the genomic epidemiology and evolution of the SARS-CoV-2 virus. This freely available resource incorporates a new Ensembl gene set, multiple sets of variants, and alignments of annotation from several resources against the reference assembly for SARS-CoV-2. It represents the first virus to be encompassed within the Ensembl platform. Additional data are being continually integrated via our new rapid release protocols alongside tools such as the Ensembl Variant Effect Predictor. Here we describe the data and infrastructure behind the resource and discuss future work.
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 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.18.422865v1" target="_blank">The Ensembl COVID-19 resource: Ongoing integration of public SARS-CoV-2 data</a>
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 <li><strong>Occupational exposures associated with being a COVID-19 case; evidence from three case-control studies</strong> -
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 Background The evidence on risk factors for transmission of SARS-CoV-2 in community settings is sparse, yet this information is key to inform public health action. We investigated factors associated with being a COVID-19 case using data collected through contact tracing. Methods We conducted three retrospective, frequency-matched case-control studies between August 2020 and October 2020 using case data from the NHS Test and Trace programme. Controls were obtained through Market Research Panels. Multivariable analyses provided adjusted odds ratios (aORs) for multiple community exposure settings. We analysed the results in meta-analyses using random effects models to obtain pooled odds ratios (pORs). Results Across all study periods, there was strong statistical evidence that working in healthcare (pOR 2.87, aOR range 2.72-3.08), social care (pOR 4.15, aOR range 2.46-5.41) or hospitality (pOR 2.36, aOR range 2.01-2.63) were associated with increased odds of being a COVID-19 case. There was also evidence that working in warehouse setting was associated with increased odds (pOR 3.86, aOR range 1.06-14.19), with a substantial increase in odds observed over the study periods. A similar pattern was also observed in education and construction. Conclusions The studies indicate that some workplace settings are associated with increased odds of being a case. However, it is not possible to determine how much of the transmission of SARS-CoV-2 took place within the workplace, and how much was associated with social, household or transport exposures.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.21.20248161v1" target="_blank">Occupational exposures associated with being a COVID-19 case; evidence from three case-control studies</a>
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 <li><strong>Analysis of 46,046 SARS-CoV-2 whole-genomes leveraging principal component analysis (PCA)</strong> -
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 Since the beginning of the global SARS-CoV-2 pandemic, there have been a number of efforts to understand the mutations and clusters of genetic lines of the SARS-CoV-2 virus. Until now, phylogenetic analysis methods have been used for this purpose. Here we show that Principal Component Analysis (PCA), which is widely used in population genetics, can not only help us to understand existing findings about the mutation processes of the virus, but can also provide even deeper insights into these processes while being less sensitive to sequencing gaps. Here we describe a comprehensive analysis of a 46,046 SARS-CoV-2 genome sequence dataset downloaded from the GISAID database in June of this year.
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 🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.20.423682v1" target="_blank">Analysis of 46,046 SARS-CoV-2 whole-genomes leveraging principal component analysis (PCA)</a>
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 <li><strong>Detailed disease progression of 213 patients hospitalized with Covid-19 in the Czech Republic: An exploratory analysis</strong> -
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 We collected a multi-centric retrospective dataset of patients (N = 213) who were admitted to ten hospitals in Czech Republic and tested positive for SARS-CoV-2. The dataset contains baseline patient characteristics, breathing support required, pharmacological treatment received and multiple markers on daily resolution. Patients in the dataset were treated with hydroxychloroquine (N = 108), azithromycin (N = 72), favipiravir (N = 9), convalescent plasma (N = 7), dexamethasone (N = 4) and remdesivir (N = 3), often in combination. Most patients were admitted during the first wave of the epidemic. To explore association between treatments and patient outcomes we performed multiverse analysis, observing how the conclusions change between defensible choices of statistical model, predictors included in the model and other analytical degrees of freedom. Weak evidence to constrain the potential efficacy of azithromycin and favipiravir can be extracted from the data. Additionally, we performed external validation of several proposed prognostic models for Covid-19 severity showing that they mostly perform unsatisfactorily on our dataset.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.03.20239863v2" target="_blank">Detailed disease progression of 213 patients hospitalized with Covid-19 in the Czech Republic: An exploratory analysis</a>
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 <li><strong>CovidRiskCalc: An online app to calculate the risk of COVID infection in a gathering</strong> -
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 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 CovidRiskCalc is an evidence based online app which calculates the risk of COVID-19 infection for a person coming into contact during a specific event/gathering with a group of individuals, some of whom may be infected (available at CovidRiskCalc.eu). The user is helped in providing a rough estimate of the COVID-19 prevalence rate in the group. She also inputs the size of the group, the number (and duration) of her contacts and the level of precautions (masks, social distancing, etc.). The app calculates the user9s risk of transmission in a single infected contact; her probability of infection during the entire event and the number of new infections within the group. Two numerical examples are given. The tool, designed for both professionals and the general public, thus quantifies the risks of infection in special populations (social gatherings, prisons, etc.), but also in general ones (stores, stadiums, etc.).
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.01.20241646v2" target="_blank">CovidRiskCalc: An online app to calculate the risk of COVID infection in a gathering</a>
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 <li><strong>Immunogenicity and crossreactivity of antibodies to SARS-CoV-2 nucleocapsid protein</strong> -
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 COVID-19 patients elicit strong responses to the nucleocapsid (N) protein of SARS-CoV-2 but binding antibodies are also detected in prepandemic individuals, indicating potential crossreactivity with common cold human coronaviruses (HCoV) and questioning its utility in seroprevalence studies. We investigated the immunogenicity of the full-length and shorter fragments of the SARS-CoV-2 N protein, and the crossreactivity of antibodies with HCoV. We indentified a C-terminus region in SARS-CoV2 N of minimal sequence homology with HCoV that was more specific and highly immunogenic. IgGs to the full-length SARS-CoV-2 N also recognised N229E N, and IgGs to HKU1 N recognised SARS-CoV-2 N. Crossreactivity with SARS-CoV-2 was stronger for alpha- rather than beta-HCoV despite having less sequence identity, revealing the importance of conformational recognition. Higher preexisting IgG to OC43 N correlated with lower IgG to SARS-CoV-2 in rRT-PCR negative individuals, reflecting less exposure and indicating a potential protective association. Antibodies to SARS-CoV-2 N were higher in patients with more severe and longer symptoms and in females. IgGs remained stable for at least 3 months, while IgAs and IgMs declined faster. In conclusion, N is a primary target of SARS-CoV-2-specific and HCoV crossreactive antibodies, both of which may affect the acquisition of immunity to COVID-19.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.19.20248551v1" target="_blank">Immunogenicity and crossreactivity of antibodies to SARS-CoV-2 nucleocapsid protein</a>
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 <li><strong>Development and Evaluation of Two Rapid Indigenous IgG-ELISA immobilized with ACE-2 Binding Peptides for Detection Neutralizing Antibodies Against SARS-CoV-2</strong> -
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 COVID-19 pandemic situation demands effective serological tests with a view to adopting and developing policy for disease management, determining protective immunity as well as for sero-epidemiological study. Our study aims to develop and evaluate two rapid in-house ELISA assays targeting neutralizing antibodies (IgG) against S1 subunit of spike in SARS-CoV-2 and Receptor Binding Domain (RBD), as well as comparative analysis with nucleocapsid (NCP) ELISA. The assays were conducted with 184 samples in three panels collected from 134 patients. Panel 1 and 2 consist of RT-PCR positive samples collected within two weeks and after two weeks of symptom onset, respectively. Negative samples are included in panel 3 from healthy donors and pre-pandemic dengue patients. The total assay time has been set 30 minutes for both of the ELISA assays. Results show that S1 and RBD ELISA demonstrates 73.68% and 84.21% sensitivities, respectively for samples collected within two weeks, whereas 100% sensitivities were achieved by both for samples that were collected after two weeks of the onset of symptoms. S1-ELISA shows 0% positivity to panel 3 while for RBD-ELISA the figure is 1%. A strong correlation (rs=0.804, p&lt;0.0001)) has been observed between these two assays. When compared with NCP-ELISA, S1 slightly better correlation (rs=0.800, p&lt;0.0001) than RBD (rs=0.740, p&lt;0.0001). Our study suggests S1-ELISA as more sensitive one than the RBD or nucleocapsid ELISA during the later phase of infection, while for overall sero-monitoring RBD specific IgG ELISA is recommended. Moreover, non-reactivity to dengue emphasize the use of these assays for serosurveillance of COVID-19 in the dengue endemic regions.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.12.19.20248535v1" target="_blank">Development and Evaluation of Two Rapid Indigenous IgG-ELISA immobilized with ACE-2 Binding Peptides for Detection Neutralizing Antibodies Against SARS-CoV-2</a>
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 <li><strong>Risk Factors Associated with Increased Antibiotic Use in COVID-19 Hospitalized Patients</strong> -
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 Literature suggests that antibiotic prescribing in COVID-19 patients is high, despite low rates of confirmed bacterial infection. There are little data on what drives prescribing habits. This retrospective, multi-center, observational study sought to determine antibiotic prescribing rates and risk factors for antibiotic prescribing in hospitalized patients. Patients admitted from March 1, 2020 to May 31, 2020 and treated for PCR-confirmed COVID-19 were included. The primary endpoint was the rate of antibiotic use during hospitalization. Secondary endpoints included risk factors associated with antibiotic use, risk factors associated with receiving more than one antibiotic course, and rate of microbiologically confirmed infections. A total of 208 encounters (198 patients) were included in the final analysis. Eighty-three percent of patients received at least one course of antibiotics, despite low rates of microbiologically confirmed infection (12%). Almost one-third of patients (30%) received more than one course of antibiotics. There was a low rate of respiratory cultures obtained (32%). Risk factors identified in a univariate analysis for both antibiotic prescribing and receiving more than one course of antibiotics were more serious illness, increased hospital length of stay, ICU admission, mechanical ventilation, and ARDS. This study highlights the need for increased antibiotic stewardship practices in COVID-19 patients. Further studies should be conducted to determine the utility of different stewardship initiatives in COVID-19 patients.
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 🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.10.21.20217117v2" target="_blank">Risk Factors Associated with Increased Antibiotic Use in COVID-19 Hospitalized Patients</a>
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 <h1 data-aos="fade-right" id="from-clinical-trials">From Clinical Trials</h1>
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 <li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Evaluating Safety, Pharmacokinetics and Clinical Benefit of Silmitasertib (CX-4945) in Subjects With Moderate COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Drug: Silmitasertib;   Drug: SOC<br/><b>Sponsor</b>:   Chris Recknor, MD<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>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>Use of BCG Vaccine as a Preventive Measure for COVID-19 in Health Care Workers</strong> - <b>Condition</b>:   COVID 19 Vaccine<br/><b>Intervention</b>:   Biological: BCG vaccine<br/><b>Sponsors</b>:   Universidade Federal do Rio de Janeiro;   Ministry of Science and Technology, Brazil<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>Changes in Viral Load in COVID-19 After Probiotics</strong> - <b>Condition</b>:   COVID-19<br/><b>Intervention</b>:   Dietary Supplement: Dietary supplementation in patients with covid disease admitted to hospital<br/><b>Sponsors</b>:   Hospital de Sagunto;   Biopolis S.L.;   Laboratorios Heel España<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>Efficacy and Safety of Ivermectin for Treatment and Prophylaxis of COVID-19 Pandemic</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Drug: Ivermectin;   Drug: Hydroxychloroquine;   Behavioral: personal protective Measures<br/><b>Sponsor</b>:   Benha University<br/><b>Completed</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>Phase 3 Inhaled Novaferon Study in Hospitalized Patients With Moderate to Severe COVID-19</strong> - <b>Condition</b>:   Covid19<br/><b>Interventions</b>:   Biological: Novaferon;   Biological: Placebo<br/><b>Sponsor</b>:   Genova Inc.<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>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 High-dose Vitamin C Combined With Chinese Medicine Against Coronavirus Pneumonia (COVID-19)</strong> - <b>Condition</b>:   COVID-19<br/><b>Interventions</b>:   Drug: Alpha-interferon alpha, abidol, ribavirin, Buzhong Yiqi plus and minus formula, Huhuang Detoxicity Paste, Baimu Qingre Jiedu Paste, fumigation/inhalation of vitamin C;   Drug: Alpha-interferon, abidol, ribavirin, Buzhong Yiqi plus and minus formula, Huhuang Detoxicity Paste, Baimu Qingre Jiedu Paste and 5% glucose;   Drug: Alpha-interferon, abidol, ribavirin, Buzhong Yiqi plus and minus formula, Huhuang Detoxicity Paste, Baimu Qingre Jiedu Paste and high-dose vitamin C treatment<br/><b>Sponsor</b>:   Xi'an International Medical Center Hospital<br/><b>Active, not 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 on Safety and Clinical Efficacy of AZVUDINE in COVID-19 Patients (SARS-CoV-2 Infected)</strong> - <b>Condition</b>:   COVID-19<br/><b>Interventions</b>:   Drug: AZVUDINE;   Drug: AZVUDINE placebo<br/><b>Sponsors</b>:   HRH Holdngs Limited;   GALZU INSTITUTE OF RESEARCH, TEACHING, SCIENCE AND APPLIED TECHNOLOGY, Brazil;   SANTA CASA DE MISERICORDIA DE CAMPOS HOSPITAL (SCMCH), Brazil;   UNIVERSIDADE ESTADUAL DO NORTE FLUMINENSE (UENF), Brazil<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>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>A Clinical Safety Study on AT-100 in Treating Adults With Severe COVID-19 Infection</strong> - <b>Condition</b>:   Covid19<br/><b>Intervention</b>:   Biological: AT-100<br/><b>Sponsor</b>:   Airway Therapeutics, Inc.<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>
 </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>Effects of Tocilizumab in COVID-19 patients: a cohort study</strong> - CONCLUSIONS: Majority of patients demonstrated clinical improvement and were successfully discharged alive from the hospital after receiving tocilizumab. We observed a rebound effect with CRP, which may suggest the need for higher or subsequent doses to adequately manage cytokine storm. Based on our findings, we believe that tocilizumab may have a role in the early treatment of COVID-19, however larger randomized controlled studies are needed to confirm this.</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>Gallium maltolate has in vitro antiviral activity against SARS-CoV-2 and is a potential treatment for COVID-19</strong> - CONCLUSION: The in vitro activity of GaM against SARS-CoV-2, together with GaM's known anti-inflammatory activity, provide justification for testing GaM in COVID-19 patients.</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>Identification of FDA approved drugs and nucleoside analogues as potential SARS-CoV-2 A1pp domain inhibitor: An in silico study</strong> - Coronaviruses are known to infect respiratory tract and intestine. These viruses possess highly conserved viral macro domain A1pp having adenosine diphosphate (ADP)-ribose binding and phosphatase activity sites. A1pp inhibits adenosine diphosphate (ADP)-ribosylation in the host and promotes viral infection and pathogenesis. We performed in silico screening of FDA approved drugs and nucleoside analogue library against the recently reported crystal structure of SARS-CoV-2 A1pp domain. Docking...</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>Innate Inhibiting Proteins Enhance Expression and Immunogenicity of Self-Amplifying RNA</strong> - Self-amplifying RNA (saRNA) is a cutting-edge platform for both nucleic acid vaccines and therapeutics. saRNA is self-adjuvanting, as it activates types I and III interferon (IFN), which enhances the immunogenicity of RNA vaccines but can also lead to inhibition of translation. In this study, we screened a library of saRNA constructs with cis-encoded innate inhibiting proteins (IIPs) and determined the effect on protein expression and immunogenicity. We observed that the PIV-5 V and Middle East...</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>Structure-Based Screening to Discover New Inhibitors for Papain-like Proteinase of SARS-CoV-2: An In Silico Study</strong> - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) expresses a multifunctional papain-like proteinase (PLpro), which mediates the processing of the viral replicase polyprotein. Inhibition of PLpro has been shown to suppress the viral replication. This study aimed to explore new anti-PLpro candidates by applying virtual screening based on GRL0617, a known PLpro inhibitor of SARS coronavirus (SARS-CoV). The three-dimensional (3D) structure of SARS-CoV-2 PLpro was built by homology...</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 ligand selection strategy identifies chemical probes targeting the proteases of SARS-CoV-2</strong> - Activity-based probes are valuable tools for chemical biology. However, finding probes that specifically target the active site of an enzyme remains a challenging task. Here we present a ligand selection strategy that allows to rapidly tailor electrophilic probes to a target of choice and showcase its application for the two cysteine proteases of SARS-CoV-2 as proof of concept. The resulting probes were specific for the active site labelling of 3CL pro and PL pro with sufficient selectivity in a...</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 pre-exposure use of hydroxychloroquine on COVID-19 mortality: a population-based cohort study in patients with rheumatoid arthritis or systemic lupus erythematosus using the OpenSAFELY platform</strong> - BACKGROUND: Hydroxychloroquine has been shown to inhibit entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into epithelial cells in vitro, but clinical studies found no evidence of reduced mortality when treating patients with COVID-19. We aimed to evaluate the effectiveness of hydroxychloroquine for prevention of COVID-19 mortality, as opposed to treatment for the disease.</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>Spiky nanostructures for virus inhibition and infection prevention</strong> - The outbreak of a novel highly infectious virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has aroused people's concern about public health. The lack of ready-to-use vaccines and therapeutics makes the fight with these pathogens extremely difficult. To this point, rationally designed virus entry inhibitors that block the viral interaction with its receptor can be novel strategies to prevent virus infection. For ideal inhibition of the virus, the virus-inhibitor interaction...</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 SARS-CoV-2 RNA-protein interactome in infected human cells</strong> - Characterizing the interactions that SARS-CoV-2 viral RNAs make with host cell proteins during infection can improve our understanding of viral RNA functions and the host innate immune response. Using RNA antisense purification and mass spectrometry, we identified up to 104 human proteins that directly and specifically bind to SARS-CoV-2 RNAs in infected human cells. We integrated the SARS-CoV-2 RNA interactome with changes in proteome abundance induced by viral infection and linked interactome...</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>Calcium channel blocker amlodipine besylate therapy is associated with reduced case fatality rate of COVID-19 patients with hypertension</strong> - The coronavirus disease (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has now spread to &gt;200 countries posing a global public health concern. Patients with comorbidity, such as hypertension suffer more severe infection with elevated mortality. The development of effective antiviral drugs is in urgent need to treat COVID-19 patients. Here, we report that calcium channel blockers (CCBs), a type of antihypertensive drug that is widely used in clinics,...</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>Beneficial effect of Indigo Naturalis on acute lung injury induced by influenza A virus</strong> - CONCLUSION: The results showed that INAE alleviated IAV induced ALI in mice. The mechanisms of INAE were associated with its anti-influenza, anti-inflammatory and anti-oxidation properties. Indigo Naturalis might have clinical potential to treat ALI induced by IAV.</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>Action of dipeptidyl peptidase-4 inhibitors on SARS-CoV-2 main protease</strong> - In a recent publication in this journal Eleftheriou et al. proposed inhibitors of dipeptidyl peptidase-4 (DPP-4) to be functional inhibitors of the main protease (M pro ) of SARS-CoV-2. Their predictions prompted the authors to suggest linagliptin, a DPP-4 inhibitor and approved anti-diabetes drug, as a repurposed drug candidate against the ongoing COVID-19 pandemic. We used an enzymatic assay measuring inhibition of M pro catalytic activity in the presence of four different commercially...</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>"Silent hypoxaemia in COVID-19 patients"</strong> - The clinical presentation of COVID-19 due to infection with SARS-CoV-2 is highly variable with the majority of patients having mild symptoms while others develop severe respiratory failure. The reason for this variability is unclear but is in critical need of investigation. Some COVID-19 patients have been labeled with 'happy hypoxia,' in which patient complaints of dyspnoea and observable signs of respiratory distress are reported to be absent. Based on ongoing debate, we highlight key...</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>Recognition of Plausible Therapeutic Agents to Combat COVID-19: An Omics Data Based Combined Approach</strong> - Coronavirus disease-2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), has become an immense threat to global public health. In this study, more than 67,000 reference sequences including a complete genome sequence of SARS-CoV-2 isolate performed by us and several in silico techniques were merged to propose prospective therapeutics. Through meticulous analysis, several conserved and therapeutically suitable regions of SARS-CoV-2 such as RNA-dependent RNA...</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>Understanding the immunopathogenesis of COVID-19: Its implication for therapeutic strategy</strong> - Although 80% of individuals infected with the severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) recover without antiviral treatments, the other 20% progress to severe forms of pulmonary disease, suggesting that the host's immune response to the virus could influence the outcome of coronavirus disease 2019 (COVID-19). SARS-CoV-2 infects alveolar epithelial type 2 cells expressing angiotensin-converting enzyme 2, and these infected epithelial cells recruit dendritic cells, neutrophils...</p></li>
 </ul>
 <h1 data-aos="fade-right" id="from-patent-search">From Patent Search</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 19 - Chewing Gum</strong> -</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 traditional Chinese medicine composition for COVID-19 and/or influenza and preparation method thereof</strong> -</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>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).</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 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> -</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 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> -</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>"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.</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>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.</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>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.</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>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。</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>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.</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 New COVID-19 Relief Package Is Flawed but Essential</strong> - If Congress had done nothing, the U.S. would soon face a humanitarian disaster as well as an economic one. - <a href="https://www.newyorker.com/news/our-columnists/the-new-covid-19-relief-package-is-flawed-but-essential">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>What the Era of Trump and the Coronavirus May Teach America’s Children</strong> - The myths of national nobility do not exist for today’s first graders. - <a href="https://www.newyorker.com/news/daily-comment/what-the-era-of-trump-and-the-coronavirus-may-teach-americas-children">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>How Ammon Bundy Helped Foment an Anti-Masker Rebellion in Idaho</strong> - The COVID-19 pandemic has pitted establishment Republicans, who defer to public-health officials’ expertise, against hard-right libertarians. - <a href="https://www.newyorker.com/news/us-journal/how-ammon-bundy-helped-foment-an-anti-masker-rebellion-in-idaho">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Georgia Trump Fans Say the Last Election Was a Sham. Will They Vote in This One?</strong> - Kelly Loeffler and David Perdue are trying to placate the President and run for the Senate at the same time. - <a href="https://www.newyorker.com/news/us-journal/georgia-trump-fans-say-the-2020-election-was-a-sham-will-they-vote-in-this-one">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>As the Vaccine Arrives, Death and Denial Rage in a California Coronavirus Epicenter</strong> - In the San Joaquin Valley, medical professionals fear that many in the public still fail to grasp the dangers of COVID-19. - <a href="https://www.newyorker.com/science/medical-dispatch/as-the-vaccine-arrives-death-and-denial-rage-in-a-california-coronavirus-epicenter">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 viral tweet about Trump refusing to give Biden his <span class="citation">@POTUS</span> followers is wrong, even if it is on-brand</strong> -
 <figure>
 <img alt="" src="https://cdn.vox-cdn.com/thumbor/ag6_ZZDPBYBvyZDWL-ZyGsniRQc=/541x0:5490x3712/1310x983/cdn.vox-cdn.com/uploads/chorus_image/image/68569755/GettyImages_1215876854.0.jpg"/>
 <figcaption>
 President Trump speaks before signing an executive order targeting social media platforms for perceived anti-conservative bias. | Brendan Smialowski/AFP via Getty Images
 </figcaption>
 </figure></li>
 </ul>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 The confusion over what happens to Trump’s official White House Twitter accounts, briefly explained.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="hAhZ6b">
 When Joe Biden becomes president on January 20, his administration will gain control of the <a href="https://twitter.com/potus"><span class="citation">@POTUS</span></a> and <a href="https://twitter.com/whitehouse"><span class="citation">@WhiteHouse</span></a> Twitter accounts. But the combined 60 million followers of those accounts may not be going with them.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Qw48Rx">
 The transfer has become an issue between Twitter and the Biden transition team, according to <a href="https://www.wsj.com/articles/trump-will-face-different-twitter-rules-when-he-leaves-office-11608642198">the Wall Street Journal</a>. The Biden team wants to keep the followers of those accounts, as was the case for the Obama-Trump transition. Four years ago, and dealing with this issue for the first time, the Obama administration <a href="https://obamawhitehouse.archives.gov/blog/2016/10/31/digital-transition-how-presidential-transition-works-social-media-age">made it a point</a> to make the digital transition as smooth and seamless as possible. This time, Twitter has other ideas.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="PzJ81V">
 “The accounts will not automatically retain their existing followers,” Twitter spokesperson Nick Pacilio said in a statement. “Instead, Twitter will notify followers of these accounts to provide context that the content will be archived and allow them the choice to follow the Biden administration’s new accounts.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="0AdmSM">
 Twitter did not provide a reason for the change, but the Wall Street Journal article pointed out that the 2017 Twitter transition had <a href="https://www.cnbc.com/2017/01/21/twitter-unwittingly-forces-users-to-follow-potus-account-after-transition-from-obama-to-trump.html">technical issues</a>. Among them, a glitch caused people who had deliberately unfollowed the <span class="citation">@POTUS</span> account to automatically follow it again, which many people did not appreciate.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="rBHWOc">
 What might have been a minor issue blew up on — where else? — Twitter on Tuesday afternoon after a freelance journalist named Hugo Lowell tweeted that the Trump administration refused to give its followers to Biden.
 </p>
 <div id="zz8RiV">
 <blockquote class="twitter-tweet">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
 Biden transition says Trump admin has refused to transfer the <a href="https://twitter.com/POTUS?ref_src=twsrc%5Etfw"><span class="citation">@POTUS</span></a> and <a href="https://twitter.com/WhiteHouse?ref_src=twsrc%5Etfw"><span class="citation">@WhiteHouse</span></a> Twitter accounts with followers and that Biden must start from zero — reversing goodwill gesture from Obama admin in 2016.
 </p>
 — Hugo Lowell (<span class="citation">@hugolowell</span>) <a href="https://twitter.com/hugolowell/status/1341432767888957442?ref_src=twsrc%5Etfw">December 22, 2020</a>
 </blockquote>
 </div>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="49njt5">
 But that’s not true, according to Twitter, which said it was an “inaccurate characterization.” Biden digital director Rob Flaherty agreed.
 </p>
 <div id="6SXQUn">
 <blockquote class="twitter-tweet">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
 Just to be clear: this is Twitter's decision, not Trump's.<a href="https://t.co/7jqhLmbX9e">https://t.co/7jqhLmbX9e</a>
 </p>
 — Rob Flaherty (<span class="citation">@Rob_Flaherty</span>) <a href="https://twitter.com/Rob_Flaherty/status/1341481779899842561?ref_src=twsrc%5Etfw">December 22, 2020</a>
 </blockquote>
 </div>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="tqdU0I">
 The White House did not respond to a request for comment.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="FUnF1N">
 Lowell declined to comment, but he did issue a correction.
 </p>
 <div id="ew95DP">
 <blockquote class="twitter-tweet">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
 Correction: Digital Director for Joe Biden <a href="https://twitter.com/Rob_Flaherty?ref_src=twsrc%5Etfw"><span class="citation">@Rob_Flaherty</span></a> says <a href="https://twitter.com/POTUS?ref_src=twsrc%5Etfw"><span class="citation">@POTUS</span></a> and <a href="https://twitter.com/WhiteHouse?ref_src=twsrc%5Etfw"><span class="citation">@WhiteHouse</span></a> accounts being reset to zero followers is Twitter’s decision, not the Trump admin. Unclear still whether Trump admin has asked for followers to roll over as Obama did in 2016. <a href="https://t.co/T659ZZgC89">https://t.co/T659ZZgC89</a>
 </p>
 — Hugo Lowell (<span class="citation">@hugolowell</span>) <a href="https://twitter.com/hugolowell/status/1341530333074874370?ref_src=twsrc%5Etfw">December 22, 2020</a>
 </blockquote>
 </div>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="EwrFtU">
 Lowell’s incorrect tweet has gotten thousands of retweets and “Likes,” and understandably so: It is consistent with Trump’s brand to do something like this. Trump is <a href="https://www.rollingstone.com/politics/politics-news/trump-twitter-followers-obama-826471/">obsessed</a> with how many followers he has and with having more of them than anyone else, so it would make sense if he were loath to give away the tens of millions of followers acquired during his presidency to the person who beat him.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="skut04">
 Such pettiness would have also been a fitting end to the <a href="https://www.vox.com/the-highlight/22170168/trump-twitter-social-media-presidency-aoc-biden">Twitter presidency</a>. Twitter helped Trump get elected, as he used the platform to raise his profile, speak out against Obama, and spread racist birther conspiracies. The platform also enabled Trump to run a successful presidential campaign, run the country, and, finally, run an unsuccessful presidential campaign — all without changing his behavior or tone one bit.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="sLXWbv">
 It’s therefore ironic that Trump would be the victim of viral misinformation-by-tweet after being <a href="https://www.nytimes.com/2020/11/23/technology/election-misinformation-facebook-twitter.html">a misinformation superspreader</a> himself. He has lied, frequently, and then watched those lies spread across social media before making their way onto traditional media formats to be seen and heard by millions if not billions.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="u0maKp">
 President Trump has faced few consequences for his tweets. <a href="https://www.vox.com/recode/2020/5/26/21271210/twitter-fact-check-trump-tweets-mail-voting-fraud-rigged-election-misleading-statements">Only in the last year</a>, when it became apparent that there was a real chance he would lose the election, did social media platforms try to curb the misinformation he expertly used them to spread. It will be interesting to see how they treat him once his account isn’t subject to special rules for public officials; Twitter has already said it would consider taking down Trump tweets that violate its rules (currently, it only tags them with a fact-check). When he leaves office in January, Trump will still have control over his personal account, <span class="citation">@realDonaldTrump</span>, which he used far more than the official accounts and which has millions more followers than <span class="citation">@POTUS</span> and <span class="citation">@WhiteHouse</span> combined.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ZkawAr">
 So after all that, maybe it’s for the best that the official White House accounts get a fresh start and a chance to rebuild from the ground up. Hopefully, the people who followed those accounts purely out of interest in and respect for the offices — as opposed to whoever happens to be in them — will see and accept the offer to follow them again.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="mvsPe3">
 <strong>Update, December 22, 7 pm ET:</strong> Added Hugo Lowell’s correction tweet and decline to comment.
 </p>
 <ul>
 <li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The political chief at Mark Zuckerberg’s philanthropy is stepping down</strong> -
 <figure>
 <img alt="Priscilla Chan and Mark Zuckerberg speak with another person in front of a sign reading, “Chan Zuckerberg Initiative.”" src="https://cdn.vox-cdn.com/thumbor/VkWZAmCEdQT6hZpykFdKmmlovxM=/0x136:5185x4025/1310x983/cdn.vox-cdn.com/uploads/chorus_image/image/68569573/1MP_CZI.0.jpg"/>
 <figcaption>
 Courtesy of The Chan Zuckerberg Initiative
 </figcaption>
 </figure></li>
 </ul>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Mike Troncoso is a former top aide to Kamala Harris, so this move is stirring speculation about a move to the White House.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="pwcoX9">
 The political chief of Mark Zuckerberg’s philanthropy is leaving his post, Recode has learned, which is stirring some speculation that he could take on a new role with his former boss, Kamala Harris.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="BXU8CA">
 Mike Troncoso, once a top aide to Harris, is stepping down from his position as the head of the Chan Zuckerberg Initiative’s Justice and Opportunity Initiatives (JOI), CZI confirmed to Recode. The leader of JOI is one of the top positions at the organization that Zuckerberg and his wife, Priscilla Chan, founded in 2015. As the head of JOI, Troncoso oversaw one of Silicon Valley’s biggest political advocacy operations that has spent hundreds of millions of dollars pushing for immigration reform, changes to the criminal justice system, and more affordable housing.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Khq1aU">
 The departure is notable for two reasons: Zuckerberg’s political team at his philanthropy has had to <a href="https://www.vox.com/recode/2020/6/26/21303664/mark-zuckerberg-facebook-chan-zuckerberg-initiative-philanthropy-tension">navigate tricky tensions</a> that are rooted in political challenges in Zuckerberg’s day job at Facebook, challenges that will only intensify under Joe Biden. And secondly, the timing of Troncoso’s departure raises the possibility that he could be in line for a senior position staffing with Harris, which would serve as another possible link between the Biden administration and Zuckerberg, who is facing antitrust scrutiny and a skeptical public.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="sD32Ai">
 Troncoso served as chief counsel to Harris when she was California’s attorney general. He <a href="https://www.theatlantic.com/politics/archive/2020/08/kamala-harris-biden-mortgage-settlement/615394/">oversaw a major investigation</a> into the state’s banking actions during the financial crisis, one of her landmark accomplishments, and he later co-chaired her transition team when she was elected to the Senate. Harris name-checks Troncoso in her autobiography’s acknowledgments.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="TTss6u">
 Troncoso had recently told people he works with at CZI that he did not currently have plans to join the administration, according to sources, but that no decision had been made. CZI said that Troncoso planned to return to public service and is relocating with his family to the East Coast.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="CkR6JO">
 Harris has only unveiled the names of a few of her top aides. The Biden-Harris transition team didn’t return a request for comment.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="7ovCSh">
 Troncoso <a href="https://www.bloomberg.com/news/articles/2019-10-10/david-plouffe-moves-to-part-time-role-at-zuckerberg-philanthropy">succeeded David Plouffe</a>, Barack Obama’s longtime political adviser, in the role overseeing CZI’s JOI programming. While Troncoso was a lower-profile figure, he oversaw a number of high-profile political projects, such as the <a href="https://www.vox.com/recode/21508914/mark-zuckerberg-priscilla-chan-proposition-13-split-roll-california-politics">$10 million</a> that CZI spent on its ultimately unsuccessful attempt to add billions to California’s budget, CZI’s most expensive electoral play yet. Troncoso originally oversaw CZI’s work on criminal justice reform, and CZI eventually was <a href="https://www.facebook.com/zuck/posts/10111969612272851">spending about $40 million a year</a> on that effort, becoming one of the area’s largest philanthropic funders.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="9dq3PU">
 He had to navigate making these plays at a time when CZI’s co-founder, Zuckerberg, and the source of its wealth, Facebook, grew to become a greater liability. <a href="https://www.vox.com/recode/2020/6/26/21303664/mark-zuckerberg-facebook-chan-zuckerberg-initiative-philanthropy-tension">Some of that antagonism has ricocheted onto Zuckerberg’s philanthropy,</a> even though CZI is entirely distinct from Facebook. Some people who have worked at CZI have alleged that its political work is overly sensitive to what could impact Facebook, and a former JOI employee last month publicly <a href="https://rayholgado.medium.com/chan-zuckerberg-initiative-racial-discrimination-claim-4d4637f054d8">filed a discrimination complaint</a> against the organization, claiming in part that Troncoso’s team did not center racial equity enough in its political programming. <a href="https://www.theverge.com/2020/11/10/21559126/chan-zuckerberg-initiative-raymond-holgado-racial-discrimination-complaint">CZI has said</a> that it investigated these claims and they are “unsubstantiated.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="spnGLU">
 Troncoso will be succeeded at least in the interim by Osi Imeokparia, who comes from a more technical background and oversaw the JOI team’s product development.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="JeFArh">
 Like other political advocacy shops, CZI will probably have to rethink some of its programming under a new president and in a new political climate, especially its work on federal immigration reform. CZI recently <a href="https://chanzuckerberg.com/about/annual-letter/year-2020/">released an internal report card of sorts</a> on its five-year anniversary this month, which disclosed that it had spent $436 million on its JOI work during that time.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="RNBqhy">
 As part of that review, CZI also said it would spend $500 million over the next five years on initiatives focused on racial equity, something that Zuckerberg critics <a href="https://www.vox.com/recode/2020/6/1/21277108/facebook-employees-protest-mark-zuckerberg-trump-looting-shooting-george-floyd-fact-check">say he has fumbled at Facebook</a>.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="11rUqX">
 </p>
 <ul>
 <li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The new UK coronavirus mutations, explained</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 other parts of the world.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="7E5mgC">
 Health officials in the United Kingdom and around the world are worried about 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>), which has emerged in the country and was announced over the weekend. 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="e3OSDv">
 Nations are already 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>, where the new strain, known as B.1.1.7 (we’ll call it the UK variant, for simplicity’s sake), is rapidly spreading in the southeastern part of the country. Within the UK, officials are imposing <a href="https://abcnews.go.com/International/coronavirus-variant-uk-prompts-lockdown-travel-bans-evidence/story?id=74842248">stricter limits on movement and public spaces</a>.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="2QC8m1">
 Right now 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 Monday <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. “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> Tuesday.
 </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.)
 </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 only points 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="nNs6Ei">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="F6Wo93">
 “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.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="5jxoC7">
 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. Hodcraft 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="NqsUNm">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="FzgXMP">
 “It’s one scenario,” she says. “We may never know exactly what happened here.”
 </p>
 <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">77 million confirmed cases worldwide</a>.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="L2CjV5">
 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.
 </p>
 <h3 id="l7vml9">
 What can we do about Covid-19 mutants?
 </h3>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Ift3lH">
 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.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="r3201F">
 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.”
 </p>
 <div id="dHLBFg">
 <blockquote class="twitter-tweet">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" dir="ltr" lang="en">
 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>
 </blockquote></div></li>
 </ol></li>
 </ol></li>
 </ol>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="gFk3MS">
 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>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="inHwvY">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="At2rFP">
 “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.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="gtSP21">
 Overall, the CDC <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/scientific-brief-emerging-variant.html">reports</a> that the US has only sequenced 51,000 of the 17 million cases reported here (that’s .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 <em>per week</em></a>, and plans to increase that capacity further). That lack of viral genetic testing creates a big blindspot. 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>.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="EqiasJ">
 More sequencing, overall, would lead to the faster detection of new strains and faster means to contain them if they were deemed problematic.
 </p>
 <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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="hO8TOl">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ugSSo9">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="eSM0jG">
 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).
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Y5VF51">
 “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.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="wLCNdm">
 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.
 </p>
 <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>
 </blockquote>
 </div>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="x22GKL">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="XBfVdc">
 “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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="sKE4P5">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="vRxui9">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="UyAQ8q">
 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?
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="Pt4BOR">
 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.
 </p>
 <h3 id="ELyZ9T">
 Should we expect more mutations in the future?
 </h3>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="tlkzXx">
 Short answer: yes.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ArUqoF">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="ZEciZz">
 “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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="uLanYV">
 And there are some mutations we can perhaps even expect — if not in the coming weeks, over the next several years.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="pdUaUb">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="KBGZ3A">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="lZ6YS1">
 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 own ability to enter cells.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="hJ7slj">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="4VYYyZ">
 “This is all hypothetical in this particular virus, but it happens in other viruses all the time,” Neuman said.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="1Rc9ZK">
 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.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom" id="F9NmeZ">
 </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>Bishan Bedi asks DDCA to remove his name from stands, quits membership</strong> - The former India captain was angry with idea of an Arun Jaitley statue at the Feroz Shah Kotla in Delhi</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>Polls can be held electronically, come with confirmed schedule: HC to Boxing Federation of India</strong> - “A large number of associations are conducting elections through electronic form,” the court observed.</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>Warner, Abbott to miss second Test against India</strong> - Both the Australian cricketers were outside the team's bio-secure hub to get treatment for their respective groin and calf injuries.</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>Messi passes Pele as top scorer at a single club</strong> - The Argentine scored his 644th goal for Barcelona</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>Indian Super League | Four goals but no winner</strong> - Odisha FC and NorthEast United FC (NEUFC) slugged it out in an eventful Indian Super League (ISL) contest which ended 2-2 at Bambolim on Tuesday. Odis</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>‘Khaps’ spearhead farmers agitation in Haryana</strong> - State has witnessed a late surge in agitation</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>National Herald case | Subramanian Swamy delaying proceedings: Sonia, Rahul Gandhi tell court</strong> - Sonia Gandhi and Rahul made the submission before the court while opposing an application filed by Subramanian Swamy, seeking summoning of various documents and witnesses in the case.</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>Rajinikanth’s ‘Annaatthe’ shoot postponed after few crew members test positive for coronavirus</strong> - “Superstar Rajinikanth and other crew members have tested negative,” Sun Pictures said through a message on its official twitter page</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>Gujarat HC discharges NCP MLA Kandhal Jadeja in Arms Act case</strong> - The case was lodged against Jadeja in Porbandar after he was allegedly caught with weapons in 1998.</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>High Court rejects Yediyurappa’s plea to quash proceedings in illegal land denotification case</strong> - Declining to quash the case against Mr. Yediyurappa on Tuesday, Justice Michael Cunha directed the Lokayukta special court to monitor the investigation ordered by the courts with regard to the misconduct of MPs, MLAs involved in criminal offences.</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-19: Scuffles as hauliers face 'a few days' at UK border</strong> - France has eased its travel ban but lorry drivers need a negative Covid test to travel from the UK.</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: Johnson and EU chief in 'close contact' over trade deal push</strong> - Fishing and competition rules remain sticking points in push for pre-Christmas trade agreement.</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>France police shootings: Three officers killed by gunman who is later found dead</strong> - Police were investigating domestic violence in a village, and the suspect has now been found dead.</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>Erdogan attacks Europe court's order for Demirtas's release</strong> - Turkey's president condemns a call by Europe's rights court to free a jailed Kurdish political leader.</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>Macron's dog Nemo in video plea to be kind to pets</strong> - The French president's pooch sends the Christmas message "adopt with awareness!"</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>Rocket Report: SN9 rolls to the launch pad, SLS “wet dress” test ends early</strong> - "It has surely been a year of challenges." - <a href="https://arstechnica.com/?p=1731449">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>The omnibus bill was packed with energy and environment policy</strong> - DOE gets a long list of clean energy R&amp;D projects. - <a href="https://arstechnica.com/?p=1731609">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Let’s Encrypt comes up with workaround for abandonware Android devices</strong> - When you haven't been updated since 2016, expiring certificates are a problem. - <a href="https://arstechnica.com/?p=1731408">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Leonardo da Vinci’s drawings have unique microbiomes, study finds</strong> - Research could help slow down deterioration of aging artwork, unmask counterfeits - <a href="https://arstechnica.com/?p=1724965">link</a></p></li>
 <li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Congress creates new copyright court that could make trolling easier</strong> - Congress also made streaming pirated works a felony. - <a href="https://arstechnica.com/?p=1731441">link</a></p></li>
 </ul>
 <h1 data-aos="fade-right" id="from-jokes-subreddit">From Jokes Subreddit</h1>
 <ul>
 <li><strong>I got my covid test results and I'm so confused.. it was just the number 83...</strong> - <!-- SC_OFF -->
 <div class="md">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 On the plus side my IQ test came back positive
 </p>
 </div>
 <!-- SC_ON -->
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">  submitted by   <a href="https://www.reddit.com/user/childsy441"> /u/childsy441 </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kidg19/i_got_my_covid_test_results_and_im_so_confused_it/">[link]</a></span>   <span><a href="https://www.reddit.com/r/Jokes/comments/kidg19/i_got_my_covid_test_results_and_im_so_confused_it/">[comments]</a></span></p></li>
 <li><strong>An Italian guy is out picking up women in Rome. While at his favorite bar, he manages to attract one rather attractive-looking blonde.</strong> - <!-- SC_OFF -->
 <div class="md">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 They go back to his place, and sure enough, they go at it. After a long while, he climaxes. Then he rolls over, lights up a cigarette and asks her, “So… you finish?”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 After a short pause, she replies, “No.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Surprised, but pleasantly, he puts out his cigarette, rolls back on top of her, and has his way with her again, this time lasting even longer than the first. Again he rolls over, lights a cigarette, and asks, “So… you finish?”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 And again, after a short pause, she just says “No.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Stunned, but still acting reflexively on his macho pride, he once again puts out the cigarette and entertains his companion du jour. This time, with all the strength he can muster up, he barely manages to end the task, but he does, after expending quite a lot of time and energy.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Barely able to roll over, he reaches for his cigarette, lights it again, and then asks tiredly, “So… you finish?”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 “No. I’m Swedish.”
 </p>
 </div>
 <!-- SC_ON -->
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">  submitted by   <a href="https://www.reddit.com/user/YZXFILE"> /u/YZXFILE </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/ki3me5/an_italian_guy_is_out_picking_up_women_in_rome/">[link]</a></span>   <span><a href="https://www.reddit.com/r/Jokes/comments/ki3me5/an_italian_guy_is_out_picking_up_women_in_rome/">[comments]</a></span></p></li>
 <li><strong>A young lady in the maternity ward is asked by the midwife if she would like her husband to be present at the birth of her child.</strong> - <!-- SC_OFF -->
 <div class="md">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 “I'm afraid I don't have a husband" she replies. "Okay do you have a boyfriend?" asks the Midwife. "No, no boyfriend either".
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 "Do you have a partner then?" "No, I'm not attached to anyone. I'll be having my baby on my own".
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 After the birth the midwife again speaks to the young woman. “You have a healthy bouncing baby girl, but I must warn you before you see her that the baby is black.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 “Well,” replies the girl "I was very down on my luck, with no money and nowhere to live, and so I accepted a job in a porn film. The lead man was black.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 "Oh, I'm very sorry" says the midwife, “that's really none of my business and I'm sorry that I have to ask you these awkward questions but I must also tell you that the baby has blonde hair.” “Well, yes" the girl again replies "you see the co-star in the movie was this Swedish guy.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 "Oh, I'm sorry" the midwife repeats "that's really none of my business either and I hate to pry further but your baby also has slanted eyes.” Yes,” continues the girl "there was a little Chinese man in the movie also, I really had no choice.”
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 At this, the midwife again apologizes, collects the baby and presents her to the girl, who immediately proceeds to give the baby a slap on the butt.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 The baby starts crying and the mother exclaims "Thank god for that!"
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 “What do you mean?" says the midwife, shocked.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 "Well,” says the girl extremely relieved "I had this horrible feeling that she was going to bark..."
 </p>
 </div>
 <!-- SC_ON -->
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">  submitted by   <a href="https://www.reddit.com/user/nothinlefttochoose"> /u/nothinlefttochoose </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kib4cd/a_young_lady_in_the_maternity_ward_is_asked_by/">[link]</a></span>   <span><a href="https://www.reddit.com/r/Jokes/comments/kib4cd/a_young_lady_in_the_maternity_ward_is_asked_by/">[comments]</a></span></p></li>
 <li><strong>My SUV needs all 4 tires replaced at a total cost of $800. That's more than the stimulus they gave us and so the wife freaked out a little.</strong> - <!-- SC_OFF -->
 <div class="md">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 I told her that it's no big deal and we can just rent a SUV for a day and it would only cost $50.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 She said I was an idiot and that we would need an SUV for more then 24 hours.
 </p>
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Then I explained to her that it's more then enough time for me to swap the tires.
 </p>
 </div>
 <!-- SC_ON -->
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">  submitted by   <a href="https://www.reddit.com/user/Doobiem87"> /u/Doobiem87 </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kib747/my_suv_needs_all_4_tires_replaced_at_a_total_cost/">[link]</a></span>   <span><a href="https://www.reddit.com/r/Jokes/comments/kib747/my_suv_needs_all_4_tires_replaced_at_a_total_cost/">[comments]</a></span></p></li>
 <li><strong>Why did the mermaid wear seashells?</strong> - <!-- SC_OFF -->
 <div class="md">
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
 Because she grew out of b shells
 </p>
 </div>
 <!-- SC_ON -->
 <p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">  submitted by   <a href="https://www.reddit.com/user/ilandedhereyesterday"> /u/ilandedhereyesterday </a> <br/> <span><a href="https://www.reddit.com/r/Jokes/comments/kiqncm/why_did_the_mermaid_wear_seashells/">[link]</a></span>   <span><a href="https://www.reddit.com/r/Jokes/comments/kiqncm/why_did_the_mermaid_wear_seashells/">[comments]</a></span></p></li>
 </ul>
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 <li> <a href="#covid-19">Covid-19</a>
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 <h2 id="daily-dose">Daily Dose</h2>
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+<ul id="daily-dose-list"><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>
 <h2 id="covid-19">Covid-19</h2>
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+<ul id="covid-19-list"><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>
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