186 lines
46 KiB
HTML
186 lines
46 KiB
HTML
<!DOCTYPE html>
|
||
<html lang="" xml:lang="" xmlns="http://www.w3.org/1999/xhtml"><head>
|
||
<meta charset="utf-8"/>
|
||
<meta content="pandoc" name="generator"/>
|
||
<meta content="width=device-width, initial-scale=1.0, user-scalable=yes" name="viewport"/>
|
||
<title>02 July, 2022</title>
|
||
<style type="text/css">
|
||
code{white-space: pre-wrap;}
|
||
span.smallcaps{font-variant: small-caps;}
|
||
span.underline{text-decoration: underline;}
|
||
div.column{display: inline-block; vertical-align: top; width: 50%;}
|
||
</style>
|
||
<title>Covid-19 Sentry</title><meta content="width=device-width, initial-scale=1.0" name="viewport"/><link href="styles/simple.css" rel="stylesheet"/><link href="../styles/simple.css" rel="stylesheet"/><link href="https://unpkg.com/aos@2.3.1/dist/aos.css" rel="stylesheet"/><script src="https://unpkg.com/aos@2.3.1/dist/aos.js"></script></head>
|
||
<body>
|
||
<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>Transcriptional Profiles Analysis of COVID-19 and Malaria Patients Reveals Potential Biomarkers in Children</strong> -
|
||
<div>
|
||
The clinical presentation overlap between malaria and COVID-19 poses special challenges for rapid diagnosis in febrile children. In this study, we collected RNA-seq data of children with malaria and COVID-19 infection from the public databases as raw data in fastq format paired end files. A group of six, five and two biological replicates of malaria, COVID-19 and healthy donors respectively were used for the study. We conducted differential gene expression analysis to visualize differences in the expression profiles. Using edgeR, we explored particularly the expressed genes in different phenotype groups relative to the healthy samples where 1084 genes and 2495 genes were differentially expressed in the malaria samples and COVID-19 samples respectively. Highly expressed genes in the COVID-19 samples were associated with biological processes such as cell division (CCDC124) and SLC12A5-AS1 a lncRNA gene associated with NK-cell while in the malaria samples were associated with biological processes such as immune response (CTSL), T cell activation (RSAD2) and proteolysis (LAP3). By comparing both malaria and COVID-19, the overlaps of 62 differentially expressed genes patterns were identified. Among the shared genes, the hemoglobin complexes and lipid mediators are highly expressed. We found six genes such as CYB5R3, RSAD2, ALOX15, HBQ1, HBM and PNPLA2 associated with malaria and COVID-19 diseases in children, which can be further validated as potential biomarkers. Our study provided new insights for further investigation of the biological pattern in hosts with malaria and COVID-19 coinfection.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2022.06.30.498338v1" target="_blank">Transcriptional Profiles Analysis of COVID-19 and Malaria Patients Reveals Potential Biomarkers in Children</a>
|
||
</div></li>
|
||
<li><strong>The coevolutionary mosaic of bat betacoronavirus emergence risk</strong> -
|
||
<div>
|
||
Pathogen evolution is one of the least predictable components of disease emergence, particularly in nature. Here, building on principles established by the geographic mosaic theory of coevolution, we develop a quantitative, spatially-explicit framework for mapping the evolutionary risk of viral emergence. Driven by interest in diseases like SARS, MERS, and COVID-19, we examine the global biogeography of bat-origin betacoronaviruses, and find that coevolutionary principles suggest geographies of risk that are distinct from the hotspots and coldspots of host richness. Further, our framework helps explain patterns like a unique pool of merbecoviruses in the Neotropics, a recently-discovered lineage of divergent nobecoviruses in Madagascar, and–most importantly–hotspots of diversification in southeast Asia, sub-Saharan Africa, and the Middle East that correspond to the site of previous zoonotic emergence events. Our framework may help identify hotspots of future risk that have also been previously overlooked, like west Africa and the Indian subcontinent, and may more broadly help researchers understand how host ecology shapes the evolution and diversity of pandemic threats.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://ecoevorxiv.org/8mgv6/" target="_blank">The coevolutionary mosaic of bat betacoronavirus emergence risk</a>
|
||
</div></li>
|
||
<li><strong>The 1968 Influenza Pandemic and COVID-19 Outcomes</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
Past pandemic experience can affect health outcomes in future pandemics. This paper focuses on the last major influenza pandemic in 1968 (H3N2), which killed up to 100,000 people in the US. We find that places with high influenza mortality in 1968 experienced 1-4% lower COVID-19 death rates. Our identification strategy isolates variation in COVID-19 rates across people born before and after 1968. In places with high 1968 influenza incidence, older cohorts experience lower COVID-19 death rates relative to younger ones. The relationship holds using county and patient-level data, as well as in hospital and nursing home settings. Results do not appear to be driven by systemic or policy-related factors, instead suggesting an individual-level response to prior influenza pandemic exposure. The findings merit investigation into potential biological and immunological mechanisms that account for these differences–and their implications for future pandemic preparedness.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2021.10.23.21265403v2" target="_blank">The 1968 Influenza Pandemic and COVID-19 Outcomes</a>
|
||
</div></li>
|
||
<li><strong>Outcomes of laboratory-confirmed SARS-CoV-2 infection during resurgence driven by Omicron lineages BA.4 and BA.5 compared with previous waves in the Western Cape Province, South Africa</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
Objective: We aimed to compare clinical severity of Omicron BA.4/BA.5 infection with BA.1 and earlier variant infections among laboratory-confirmed SARS-CoV-2 cases in the Western Cape, South Africa, using timing of infection to infer the lineage/variant causing infection. Methods: We included public sector patients aged ≥20 years with laboratory-confirmed COVID-19 between 1-21 May 2022 (BA.4/BA.5 wave) and equivalent prior wave periods. We compared the risk between waves of (i) death and (ii) severe hospitalization/death (all within 21 days of diagnosis) using Cox regression adjusted for demographics, comorbidities, admission pressure, vaccination and prior infection. Results: Among 3,793 patients from the BA.4/BA.5 wave and 190,836 patients from previous waves the risk of severe hospitalization/death was similar in the BA.4/BA.5 and BA.1 waves (adjusted hazard ratio (aHR) 1.12; 95% confidence interval (CI) 0.93; 1.34). Both Omicron waves had lower risk of severe outcomes than previous waves. Prior infection (aHR 0.29, 95% CI 0.24; 0.36) and vaccination (aHR 0.17; 95% CI 0.07; 0.40 for boosted vs. no vaccine) were protective. Conclusion: Disease severity was similar amongst diagnosed COVID-19 cases in the BA.4/BA.5 and BA.1 periods in the context of growing immunity against SARS-CoV-2 due to prior infection and vaccination, both of which were strongly protective.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.28.22276983v2" target="_blank">Outcomes of laboratory-confirmed SARS-CoV-2 infection during resurgence driven by Omicron lineages BA.4 and BA.5 compared with previous waves in the Western Cape Province, South Africa</a>
|
||
</div></li>
|
||
<li><strong>Reducing land use-induced spillover risk by fostering landscape immunity: policy priorities for conservation practitioners</strong> -
|
||
<div>
|
||
Anthropogenic land use change is the major driver of zoonotic pathogen spillover from wildlife to humans. In response to the global spread of the SARS-CoV-2 virus (the agent of COVID-19 disease), there have been renewed calls for landscape conservation as a disease preventive measure. While protected areas are a vital conservation tool for wildlands, more than 50% of habitable land is now human-modified and thus requires strategic, site-based measures to prevent land use-induced spillover, especially by managing landscape immunity and the dynamics of animal-human proximity. Crisis is a conversation starter for reimagining and recommitting ourselves to what is most vital and generative. Here we provide a brief overview of zoonotic spillover concepts and dynamics from a conservation practitioner perspective and outline a landscape-oriented policy agenda to minimize the risk of future large-scale zoonoses outbreaks. Among other things, we need to recognize human health as a vital ecological service, ensure ecological resilience, and facilitate public investment in biosecurity to sustain economic viability and human well-being. Landscape management approaches to spillover risk reduction are part of a toolkit that includes ecological, veterinary, and medical interventions, disease surveillance, and wildlife trade policy measures.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://ecoevorxiv.org/7gd6a/" target="_blank">Reducing land use-induced spillover risk by fostering landscape immunity: policy priorities for conservation practitioners</a>
|
||
</div></li>
|
||
<li><strong>Social sharing of emotion during the collective crisis of COVID-19</strong> -
|
||
<div>
|
||
We collected data from two sources—social media and online surveys—to investigate the emotional consequences of social sharing during the COVID-19 pandemic. Study 1 tracked and analysed emotionality of tweets published within a month of the crisis and found that the more frequently users tweeted about COVID-19, the less negativity they expressed in their later tweets. Study 2 focused on immediate consequences of sharing COVID-related events and found a selective attenuating effect of sharing on participants’ negative feelings about their personal experience. Participants generally perceived their feelings about an event to have improved when that event was shared, but perceived improvement was less when the event was a news story (especially when it was shared remotely) than when it was a personal experience. Overall, both of our studies suggested that social sharing is linked with emotional recovery and therefore appears to be an adaptive response to a persistent collective crisis.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://osf.io/9p3wh/" target="_blank">Social sharing of emotion during the collective crisis of COVID-19</a>
|
||
</div></li>
|
||
<li><strong>Inhibitory effects of GT0918 on acute lung injury and the molecular mechanisms of anti-inflammatory response</strong> -
|
||
<div>
|
||
Coronavirus disease 2019 (COVID-19) has caused the public health crisis in the whole world. Anti-androgens block severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry and protect against severe clinical COVID-19 outcomes. GT0918, a second-generation androgen receptor antagonist, accelerated viral clearance and increased recovery rate in outpatients, reduced mortality rate and shortened hospital stay in hospitalized COVID-19 patients. GT0918 also had an effective trend for severe COVID-19 patient treatment. But the mechanism of GT0918 treatment for severe COVID-19 patient is unknown. Here, we found GT0918 decreased the expression and secretion of proinflammatory cytokines through NF-{kappa}B signaling. The acute lung injury induced by LPS or Poly(I:C) was also attenuated in GT0918-treated mice. Moreover, GT0918 increased the NRF2 protein level. GT0918 induced proinflammatory cytokines downregulation was partially dependent on NRF2. In conclusion, our data showed GT0918 reduced cytokine release and suppressed inflammatory responses through inhibiting NF-{kappa}B signaling and activating NRF2. GT0918 is not only effective for treatment of mild to moderate COVID-19 patients, but also a potential therapeutic drug for severe COVID-19 patients.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2022.06.29.498191v1" target="_blank">Inhibitory effects of GT0918 on acute lung injury and the molecular mechanisms of anti-inflammatory response</a>
|
||
</div></li>
|
||
<li><strong>Influenza and pneumococcal vaccination and the risk of COVID-19: A systematic review and meta-analysis</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
A number of studies have investigated the potential non-specific effects of some routinely administered vaccines (e.g. influenza, pneumococcal) on COVID-19 related outcomes, with contrasting results. In order to elucidate this discrepancy, we conducted a systematic review and meta-analysis to assess the association between seasonal influenza vaccination and pneumococcal vaccination with SARS-CoV-2 infection and its clinical outcomes. PubMed and medRxiv databases were searched, up until November 2021. Random effects model was used in the meta-analysis to pool odds ratio (OR) and adjusted estimates with their 95% confidence intervals (CIs). Heterogeneity was quantitatively assessed using the Cohran9s Q and the I2 index. Sub-group analysis, sensitivity analysis and assessment of publication bias were performed for all outcomes. In total 38 observational studies were included in the meta-analysis and there was substantial heterogeneity. Influenza and pneumococcal vaccination were associated with lower risk of SARS-Cov-2 infection (OR: 0.80, 95% CI: 0.75-0.86 and OR: 0.70, 95% CI: 0.57-0.88, respectively). Regarding influenza vaccination, it seems that the majority of studies did not properly adjust for all potential confounders, so when the analysis was limited to studies that adjusted for age, sex, comorbidities and socioeconomic indices, the association diminished. This is not the case regarding the pneumococcal vaccination, for which even after adjustment for such factors the association persisted. Regarding harder endpoints such as ICU admission and death, current data do not support the association. Possible explanations are discussed, including trained immunity, inadequate matching for socioeconomic indices and possible coinfection.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.30.22277089v1" target="_blank">Influenza and pneumococcal vaccination and the risk of COVID-19: A systematic review and meta-analysis</a>
|
||
</div></li>
|
||
<li><strong>RT-LAMP-CRISPR-Cas13a technology as a promising diagnostic tool for the SARS-CoV-2 virus</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
At the end of 2019, the new coronavirus, SARS-CoV-2, began a pandemic that persists to date and which has caused more than 6.2 million deaths. In the last couple of years, researchers have made great efforts to develop a diagnostic technique that maintains high levels of sensitivity and specificity, since an accurate and early diagnosis is required to minimize the prevalence of SARS-CoV-2 infection. In this context, CRISPR-Cas systems are proposed as promising tools for development in diagnostic techniques due to their high specificity, highlighting that Cas13 endonuclease discriminates single nucleotide changes and displays a collateral activity against single stranded RNA molecules. With the aim of improve the sensitivity of the diagnosis, this technology is usually combined with isothermal pre-amplification reactions (SHERLOCK, DETECTR). Basing on this, we have developed an RT-LAMP-CRISPR-Cas13a for SARS-CoV-2 virus detection in nasopharyngeal samples without using RNA extraction kit that exhibited 100 % specificity and 83 % sensitivity, as well as a positive predictive value of 100 % and a negative predictive value of 100%, 81%, 79.1% and 66.7 % in <20 Ct, 20-30 Ct, >30 Ct and total Ct values, respectively.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.29.22277060v1" target="_blank">RT-LAMP-CRISPR-Cas13a technology as a promising diagnostic tool for the SARS-CoV-2 virus</a>
|
||
</div></li>
|
||
<li><strong>Severity of Omicron (B.1.1.529) and Delta (B.1.1.617.2) SARS-CoV-2 infection among hospitalised adults: a prospective cohort study</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
Limited data exist assessing severity of disease in adults hospitalised with Omicron SARS-CoV-2 variant infections, and to what extent patient-factors, including vaccination and pre-existing disease, affect variant-dependent disease severity. This prospective cohort study of all adults (≥18 years of age) hospitalised at acute care hospitals in Bristol, UK assessed disease severity using 3 different measures: FiO2 >28%, World Health Organization (WHO) outcome score >5, and hospital length of stay (LOS) >3 days following admission for Omicron or Delta variant infection. Independent of other variables, including vaccination, Omicron variant infection was associated with a statistically lower severity compared to Delta; risk reductions were 58%, 67%, and 16% for FiO2, WHO score, and LOS, respectively. Younger age and vaccination with two or three doses were also independently associated with lower COVID-19 severity. Despite lower severity relative to Delta, Omicron infection still resulted in substantial patient and public health burden following admission.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.29.22277044v1" target="_blank">Severity of Omicron (B.1.1.529) and Delta (B.1.1.617.2) SARS-CoV-2 infection among hospitalised adults: a prospective cohort study</a>
|
||
</div></li>
|
||
<li><strong>Vitamin D and the ability to produce 1,25(OH)2D are critical for protection from viral infection of the lungs.</strong> -
|
||
<div>
|
||
Vitamin D supplementation has been linked to improved outcomes from respiratory virus infection, and the COVID19 pandemic has renewed interest in understanding the potential role of vitamin D in protecting the lung from viral infections. Therefore, we evaluated the role of Vitamin D using animal models of pandemic H1N1 influenza and SARS-CoV-2 infection. In mice, dietary induced vitamin D deficiency resulted in lung inflammation that was present prior to infection. Vitamin D sufficient (D+) and deficient (D-) wildtype (WT) and D+ and D- Cyp27B1 (Cyp) knockout (KO, cannot produce 1,25(OH)2D) mice were infected with pandemic H1N1. D- WT, D+ Cyp KO, and D- Cyp KO mice all exhibited significantly reduced survival compared to D+ WT mice. Importantly, survival was not the result of reduced viral replication as influenza M gene expression in the lungs was similar for all animals. Based on these findings, additional experiments were performed using the mouse and hamster models of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. In these studies, high dose vitamin D supplementation reduced lung inflammation in mice but not hamsters. A trend to faster weight recovery was observed in 1,25(OH)2D treated mice that survived SARS-CoV-2 infection. There was no effect of vitamin D on SARS-CoV-2 N gene expression in the lung of either mice or hamsters. Therefore, vitamin D deficiency enhanced disease severity, while vitamin D sufficient/supplementation reduced inflammation following infections with H1N1 influenza and SARS-CoV-2.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2022.06.29.498158v1" target="_blank">Vitamin D and the ability to produce 1,25(OH)2D are critical for protection from viral infection of the lungs.</a>
|
||
</div></li>
|
||
<li><strong>Limitations of models for guiding policy in the COVID-19 pandemic</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
At the outset of the COVID-19 epidemic in the UK, infectious disease modellers advised the government that unless a lockdown was imposed, most of the population would be infected within a few months and critical care capacity would be overwhelmed. This paper investigates the quantitative arguments underlying these predictions, and draws lessons for future policy. The modellers assumed that within age bands all individuals were equally susceptible and equally connected, leading to predictions that more than 80% of the population would be infected in the first wave of an unmitigated epidemic. Models that relax this unrealistic assumption to allow for selective removal of the most susceptible and connected individuals predict much smaller epidemic sizes. In most European countries no more than 10% of the population was infected in the first wave, irrespective of what restrictions were imposed. The modellers assumed that about 2% of those infected would require critical care, far higher than the proportion who entered critical care in the first wave, and failed to identify the key role of nosocomial transmission in overloading health systems. Model-based forecasts that only a lockdown could suppress the epidemic relied on a survey of contact rates in 2006, with no information on the types of contact most relevant to aerosol transmission or on heterogeneity of contact rates. In future epidemics, modellers should communicate the uncertainties associated with their assumptions and data, especially when these models are used to recommend policies that have high societal costs and are hard to reverse. Recognition of the gap between models and reality also implies a need to rebalance in favour of greater reliance on rapid studies of real-world transmission, robust model criticism, and acceptance that when measurements contradict model predictions it is the model that needs to be changed.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.30.22277091v1" target="_blank">Limitations of models for guiding policy in the COVID-19 pandemic</a>
|
||
</div></li>
|
||
<li><strong>CASP4/11 contributes to pulmonary inflammation and disease exacerbation in COVID-19</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
Infection with SARS-CoV-2 induces COVID-19, an inflammatory disease that is usually self-limited, but depending on patient conditions may culminate with critical illness and patient death. The virus triggers activation of intracellular sensors, such as the NLRP3 inflammasome, which promotes inflammation and aggravates the disease. Thus, identification of host components associated with NLRP3 inflammasome is key for understanding the physiopathology of the disease. Here, we reported that SARS-CoV-2 induces upregulation and activation of human Caspase-4/CASP4 (mouse Caspase-11/CASP11) and this process contributes to inflammasome activation in response to SARS-CoV-2. CASP4 was expressed in lung autopsy of lethal cases of COVID-19 and CASP4 expression correlates with expression of inflammasome components and inflammatory mediators such as CASP1, IL1B, IL18 and IL6. In vivo infections performed in transgenic hACE2 humanized mouse, deficient or sufficient for Casp11, indicate that hACE2 Casp11-/- mice were protected from disease development, with reduced body weight loss, reduced temperature variation, increased pulmonary parenchymal area, reduced clinical score of the disease and reduced mortality. Collectively, our data establishes that CASP4/11 contributes to disease pathology and contributes for future immunomodulatory therapeutic interventions to COVID-19.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.29.22277067v1" target="_blank">CASP4/11 contributes to pulmonary inflammation and disease exacerbation in COVID-19</a>
|
||
</div></li>
|
||
<li><strong>Tradeoff between speed and infectivity in pathogen evolution</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
Given the present pandemic and the constantly arising new variants of SARS-CoV-2, there is an urgent need to understand the factors driving disease evolution. Here, we investigate the tradeoff between the speed at which a disease progresses and its reproductive number. Using SEIR and agent-based models, we show that in the exponential growth phase of an epidemic, there will be an optimal duration of new disease variants, balancing the advantage of developing fast with the advantage of infecting many new people. In the endemic state this optimum disappears, and lasting longer is always advantageous for the disease. However, if we take into account the possibility of quarantining the infected, this leads to a new optimum disease duration emerging. This work thereby comments on the observation of ever shorter generation times in the evolution of variants of SARS-CoV-2 from the original strain to the Alpha, Delta, and finally Omicron variants.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2022.06.30.22277094v1" target="_blank">Tradeoff between speed and infectivity in pathogen evolution</a>
|
||
</div></li>
|
||
<li><strong>Trapping virus-loaded aerosols using granular protein nanofibrils and iron oxyhydroxides nanoparticles</strong> -
|
||
<div>
|
||
The ongoing COVID-19 pandemic has revealed that developing effective therapeutics against viruses might be outpaced by emerging variants, waning immunity, vaccine skepticism/hesitancy, lack of resources, and the time needed to develop virus-specific therapeutics, emphasizing the importance of non-pharmaceutical interventions as the first line of defense against virus outbreaks and pandemics. However, fighting the spread of airborne viruses has proven extremely challenging, much more if this needs to be achieved on a global scale and in an environmentally-friendly manner. Here, we introduce an aerosol filter made of granular material based on whey protein nanofibrils and iron oxyhydroxides nanoparticles. The material is environmentally-friendly, biodegradable, and composed mainly of a dairy industry byproduct. It features remarkable filtration efficiencies between 95.91% and 99.99% for both enveloped and non-enveloped viruses, including SARS-CoV-2, the influenza A virus strain H1N1, enterovirus 71, bacteriophage {Phi}6, and bacteriophage MS2. The developed material is safe to handle and recycle, with a simple baking step sufficient to inactivate trapped viruses. The high filtration efficiency, virtually-zero environmental impact, and low cost of the material illuminate a viable role in fighting current and future pandemics on a global scale.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2022.06.29.498082v1" target="_blank">Trapping virus-loaded aerosols using granular protein nanofibrils and iron oxyhydroxides nanoparticles</a>
|
||
</div></li>
|
||
</ul>
|
||
<h1 data-aos="fade-right" id="from-clinical-trials">From Clinical Trials</h1>
|
||
<ul>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Immuno-bridging Study of COVID-19 Protein Subunit Recombinant Vaccine</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Biological: COVID-19 Protein Subunit Recombinant Vaccine; Biological: Active Comparator<br/><b>Sponsors</b>: PT Bio Farma; Fakultas Kedokteran Universitas Indonesia; Faculty of Medicine Universitas Diponegoro; Faculty of Medicine Universitas Andalas; Faculty of Medicine Universitas Hassanudin<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>A Study to Learn About the Study Medicines (Called Nirmatrelvir/Ritonavir) in People 12 Years Old or Older With COVID-19 Who Are Immunocompromised</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: Nirmatrelvir; Drug: Ritonavir; Drug: Placebo for nirmatrelvir; Drug: Placebo for ritonavir<br/><b>Sponsor</b>: Pfizer<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 Randomized Controlled Trial of a Digital, Self-testing Strategy for COVID-19 Infection in South Africa.</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Device: Abbott Panbio rapid antigen self-tests; Other: COVIDSmart CARE! app<br/><b>Sponsors</b>: McGill University Health Centre/Research Institute of the McGill University Health Centre; University of Cape Town Lung 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>Discussing COVID-19 Vaccines in Private Facebook Groups</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Behavioral: Gist messages on COVID-19 vaccination; Behavioral: COVID-19 vaccine information<br/><b>Sponsor</b>: George Washington 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>Immunogenicity and Safety Study of One Booster Dose of Trivalent COVID-19 Vaccine (Vero Cell), Inactivated</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Biological: Trivalent COVID-19 Vaccine (Vero Cell), Inactivated, Prototype Strain, Delta Strain and Omicron Strain; Biological: COVID-19 Vaccine (Vero Cell), Inactivated<br/><b>Sponsors</b>: Sinovac Biotech (Colombia) S.A.S.; Sinovac Life Sciences Co., Ltd.<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>Home-Based Exercise Tele-Rehabilitation After COVID-19</strong> - <b>Condition</b>: Post SARS-CoV2 (COVID-19)<br/><b>Intervention</b>: Other: Tele-exercise<br/><b>Sponsors</b>: VA Office of Research and Development; Baltimore Veterans Affairs Medical Center; Salem Veterans Affairs Medical Center<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>IMM-BCP-01 in Mild to Moderate COVID-19</strong> - <b>Conditions</b>: SARS-CoV2 Infection; COVID-19<br/><b>Interventions</b>: Drug: IMM-BCP-01; Drug: Placebo<br/><b>Sponsors</b>: Immunome, Inc.; United States Department of Defense<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>A Study to Evaluate the Safety, Tolerability, and Immunogenicity of SARS-CoV-2 Variant (COVID-19 Omicron) mRNA Vaccine (Phase 1)</strong> - <b>Condition</b>: COVID-19<br/><b>Intervention</b>: Biological: ABO1009-DP<br/><b>Sponsor</b>: Suzhou Abogen Biosciences Co., Ltd.<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 Study to Evaluate Safety, Tolerability, and Immunogenicity of SARS-CoV-2 Variant (COVID-19) mRNA Vaccines</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Biological: ABO1009-DP; Biological: ABO-CoV.617.2; Other: Placebo<br/><b>Sponsor</b>: Suzhou Abogen Biosciences Co., Ltd.<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>Can Intensive Insulin Therapy Improve Outcomes of COVID-19 Patients</strong> - <b>Conditions</b>: COVID-19; Dysglycemia<br/><b>Interventions</b>: Drug: Insulin; Drug: Subcutaneous Insulin<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>Mesenchymal Stromal Cells for the Treatment of Patients With COVID-19.</strong> - <b>Conditions</b>: COVID-19 Pneumonia; COVID-19<br/><b>Interventions</b>: Biological: Mesenchymal stem cell; Other: Placebo<br/><b>Sponsors</b>: Paulo Brofman; Conselho Nacional de Desenvolvimento Científico e Tecnológico<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>A Study to Evaluate Immunogenicity and Safety of MVC-COV1901 Vaccine Compared With AZD1222</strong> - <b>Condition</b>: COVID-19 Vaccine<br/><b>Interventions</b>: Biological: MVC-COV1901; Biological: AZD1222<br/><b>Sponsor</b>: Medigen Vaccine Biologics Corp.<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>Laser Therapy on Tension-type Cephalea and Orofacial Pain in Post-covid-19 Patients</strong> - <b>Conditions</b>: Tension-Type Headache; Orofacial Pain; COVID-19<br/><b>Intervention</b>: Radiation: Photobimodulation<br/><b>Sponsor</b>: University of Nove de Julho<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>Study of Self-Amplifying Messenger Ribonucleic Acid (samRNA) Vaccines Against COVID-19 in Healthy Adults and People Living With Human Immunodeficiency Virus (HIV)</strong> - <b>Conditions</b>: COVID-19; SARS-CoV-2<br/><b>Interventions</b>: Drug: GRT-R912, samRNA-Spikebeta-TCE11; Drug: GRT-R914, samRNA-Spikebeta-TCE9; Drug: GRT-R918, samRNA-SpikeOmicron-N-TCE11<br/><b>Sponsor</b>: Gritstone bio, Inc.<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>A Phase 1b Study of a Q-Griffithsin Intranasal Spray for Broad-spectrum Coronavirus Prophylaxis</strong> - <b>Condition</b>: COVID-19 Prevention<br/><b>Interventions</b>: Drug: Q-Griffithsin 3.0; Drug: Q-Griffithsin 6.0<br/><b>Sponsors</b>: Kenneth Palmer; United States Department of Defense<br/><b>Recruiting</b></p></li>
|
||
</ul>
|
||
<h1 data-aos="fade-right" id="from-pubmed">From PubMed</h1>
|
||
<ul>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Rapid Assessment of Biological Activity of Ag-Based Antiviral Coatings for the Treatment of Textile Fabrics Used in Protective Equipment Against Coronavirus</strong> - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its variants have rapidly spread worldwide, causing coronavirus disease (COVID-19) with numerous infected cases and millions of deaths. Therefore, developing approaches to fight against COVID-19 is currently the most priority goal of the scientific community. As a sustainable solution to stop the spread of the virus, a green dip-coating method is utilized in the current work to prepare antiviral Ag-based coatings to treat cotton…</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 pilot phase Ib/II study of whole-lung low dose radiation therapy (LDRT) for the treatment of severe COVID-19 pneumonia: First experience from Africa</strong> - CONCLUSION: LDRT was feasible, safe and shows promise in the management of severe COVID-19 pneumonia including in patients progressing on conventional systemic treatment. Additional phase II trials are warranted to identify patients most likely to benefit from LDRT.</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 novel platform for attenuating immune hyperactivity using EXO-CD24 in Covid-19 and beyond</strong> - A small but significant proportion of Covid19 patients develop life-threatening cytokine storm. We have developed a new anti-inflammatory drug, EXO-CD24, a combination of an immune checkpoint (CD24) and a delivery platform (exosomes). CD24 inhibits the NF-kB pathway and the production of cytokines/chemokines. EXO-CD24 discriminates Damage- from Pathogen-Associated Molecular Patterns (DAMPs and PAMPs) therefore does not interfere with viral clearance. EXO-CD24 was produced and purified from…</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>Antiviral effects of coinage metal-based nanomaterials to combat COVID-19 and its variants</strong> - The world has been suffering from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, and millions of people have been infected through human-to-human transmission and lost their lives within months. Although multidisciplinary scientific approaches have been employed to fight against this deadly pandemic, various mutations and diverse environments keep producing constraints in treating SARS-CoV-2. Indeed, the efficacy of the developed vaccines has been limited, and…</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>Cepharanthine: A Promising Old Drug against SARS-CoV-2</strong> - Recently, the inhibiting effects of a clinically approved drug Cepharanthine on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have attracted widespread attention and discussion. However, the public does not understand the relevant research progress very well. This paper aims to introduce a brief history of studies on the effects of cepharanthine against SARS-CoV-2, including “discovery of anti-SARS-CoV-2 activity of cepharanthine in vitro”, "potential mechanisms of cepharanthine…</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>Therapeutic role of traditionally used Indian medicinal plants and spices in combating COVID-19 pandemic situation</strong> - The coronavirus disease (COVID-19) caused by SARS-CoV-2 is a big challenge and burning issue to the scientific community and doctors worldwide. Globally, COVID-19 has created a health disaster and adversely affects the economic growth. Although some vaccines have already emerged, no therapeutic medication has yet been approved by FDA for the treatment of COVID-19 patients. Traditionally, we have been using different medicinal plants like neem, tulsi, tea, and many spices like garlic, ginger,…</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 basis for inhibition of SARS-CoV-2 by the feline drug GC376</strong> - No abstract</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>Artemisinin inhibits neutrophil and macrophage chemotaxis, cytokine production and NET release</strong> - Immune cell chemotaxis to the sites of pathogen invasion is critical for fighting infection, but in life-threatening conditions such as sepsis and Covid-19, excess activation of the innate immune system is thought to cause a damaging invasion of immune cells into tissues and a consequent excessive release of cytokines, chemokines and neutrophil extracellular traps (NETs). In these circumstances, tempering excessive activation of the innate immune system may, paradoxically, promote recovery. Here…</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 a 2-week interruption in methotrexate treatment versus continued treatment on COVID-19 booster vaccine immunity in adults with inflammatory conditions (VROOM study): a randomised, open label, superiority trial</strong> - BACKGROUND: Immunosuppressive treatments inhibit vaccine-induced immunity against SARS-CoV-2. We evaluated whether a 2-week interruption of methotrexate treatment immediately after the COVID-19 vaccine booster improved antibody responses against the S1 receptor-binding domain (S1-RBD) of the SARS-CoV-2 spike protein compared with uninterrupted treatment in patients with immune-mediated inflammatory diseases.</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 adverse inflammatory response of tobacco smoking in COVID-19 patients: biomarkers from proteomics and metabolomics</strong> - Whether tobacco smoking affects the occurrence and development of COVID-19 is still a controversial issue, and potential biomarkers to predict the adverse outcomes of smoking in the progression of COVID-19 patients have not yet been elucidated. To further uncover their linkage and explore the effective biomarkers, three proteomics and metabolomics databases (i.e. smoking status, COVID-19 status, and basic information of population) from human serum proteomic and metabolomic levels were…</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 many facets of CD26/dipeptidyl peptidase 4 and its inhibitors in disorders of the CNS - a critical overview</strong> - Dipeptidyl peptidase 4 is a serine protease that cleaves X-proline or X-alanine in the penultimate position. Natural substrates of the enzyme are glucagon-like peptide-1, glucagon inhibiting peptide, glucagon, neuropeptide Y, secretin, substance P, pituitary adenylate cyclase-activating polypeptide, endorphins, endomorphins, brain natriuretic peptide, beta-melanocyte stimulating hormone and amyloid peptides as well as some cytokines and chemokines. The enzyme is involved in the maintenance of…</p></li>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Identification of repurposing therapeutics toward SARS-CoV-2 main protease by virtual screening</strong> - SARS-CoV-2 causes the current global pandemic coronavirus disease 2019. Widely-available effective drugs could be a critical factor in halting the pandemic. The main protease (3CLpro) plays a vital role in viral replication; therefore, it is of great interest to find inhibitors for this enzyme. We applied the combination of virtual screening based on molecular docking derived from the crystal structure of the peptidomimetic inhibitors (N3, 13b, and 11a), and experimental verification revealed…</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>Spatially Patterned Neutralizing Icosahedral DNA Nanocage for Efficient SARS-CoV-2 Blocking</strong> - Broad-spectrum anti-SARS-CoV-2 strategies that can inhibit the infection of wild-type and mutant strains would alleviate their threats to global public health. Here, we propose an icosahedral DNA framework for the assembly of up to 30 spatially arranged neutralizing aptamers (IDNA-30) to inhibit viral infection. Each triangular plane of IDNA-30 is composed of three precisely positioned aptamers topologically matching the SARS-CoV-2 spike trimer, thus forming a multivalent spatially patterned…</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>An Overview on Immunity Booster Foods in Coronavirus Disease (COVID-19)</strong> - The present COVID-19 pandemic is highly terrible for the respiratory system and is caused by severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2). It has affected millions of people globally and over 511.9 million cases and 6.2 million deaths have been reported across the world. Various drugs have been repurposed, however, no specific medicine has been approved by the FDA to combat this disease till date. In this condition, researchers have attracted to natural and safe products to…</p></li>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>C910 chemical compound inhibits the traffiking of several bacterial AB toxins with cross-protection against influenza virus</strong> - The development of anti-infectives against a large range of AB-like toxin-producing bacteria includes the identification of compounds disrupting toxin transport through both the endolysosomal and retrograde pathways. Here, we performed a high-throughput screening of compounds blocking Rac1 proteasomal degradation triggered by the Cytotoxic Necrotizing Factor-1 (CNF1) toxin, which was followed by orthogonal screens against two toxins that hijack the endolysosomal (diphtheria toxin) or retrograde…</p></li>
|
||
</ul>
|
||
<h1 data-aos="fade-right" id="from-patent-search">From Patent Search</h1>
|
||
|
||
|
||
<script>AOS.init();</script></body></html> |