193 lines
50 KiB
HTML
193 lines
50 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>18 March, 2021</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>How do Good and Bad News Impact Mood During the Covid-19 Pandemic? The Role of Similarity</strong> -
|
||
<div>
|
||
How do media reports about the Covid-19 pandemic influence our mood? Building on the social comparison theory, we predicted that reading negative news affecting a similar group would result in an impaired mood. In contrast, reading negative news about a dissimilar group should lead to improved mood. To test this, 150 undergraduate students read positive or negative news about the well-being of a similar or dissimilar group during the pandemic. As predicted, a mood assimilation effect occurred for similar groups, whilst a contrast effect occurred for a dissimilar group. This pattern went so far that undergraduates reported the best mood after learning that the elder generation suffered from Covid-19. This finding seems worrying and calls for future research.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://osf.io/sy2kd/" target="_blank">How do Good and Bad News Impact Mood During the Covid-19 Pandemic? The Role of Similarity</a>
|
||
</div></li>
|
||
<li><strong>Social network factors in university student well-being and resilience during a large-scale stressor</strong> -
|
||
<div>
|
||
The transition to college is a challenging time during which many students suffer declines in well-being. Social connections play a key role in supporting mental health, but only tell part of the story of social life on campus. For instance, the personalities of one’s friends and neighbors on campus contribute to a “social microclimate.” Here, we quantify the collective impact of individual, social network, and community factors in the well-being of a first-year college cohort during (i) their first academic term and (ii) a stressor (the COVID-19 pandemic). Students who maintained supportive connections and belonged to emotionally stable and tight-knit microclimates reported greater well-being in their first academic term, and less anxiety when exposed to stress during the COVID-19 pandemic, highlighting the importance of both personal relationships and community factors in supporting mental health.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://psyarxiv.com/pha3j/" target="_blank">Social network factors in university student well-being and resilience during a large-scale stressor</a>
|
||
</div></li>
|
||
<li><strong>Anti-Asian Discrimination and Antiracist Bystander Behaviors amid the COVID-19 Outbreak</strong> -
|
||
<div>
|
||
Anti-Asian racism is a public health concern, and it has escalated during the coronavirus disease 2019 (COVID-19) outbreak. Bystanders—individuals who witness acts of racism—can help by discouraging perpetrations of discrimination (and other forms of interpersonal violence), offering help and support to victims, and reinforcing (antiracist) prosocial norms. Yet, little is known about who engages in antiracist bystander intervention behaviors in response to discriminatory events, and who engages in proactive bystander behaviors in general. In the current study, 456 US community adults of diverse ethnic backgrounds (18-85 years, Mage = 48.8, 52.0% women, 212 Asian Americans) reported on their experiences with discrimination, attitudes about the acceptability of discrimination, and engagement in proactive and reactive bystander behaviors. About 40% of the Asian American participants experienced COVID-related discrimination during a one-week period. Among individuals who witnessed anti-Asian discrimination during the COVID-19 outbreak, 45% of them engaged in any antiracist reactive bystander interventions. More frequent everyday discrimination experiences predicted greater odds of reactive bystander behaviors, over and above ethnicity, gender, and attitudes about the acceptability of discrimination. Initial evidence supported the utility of a new measure assessing bystander behaviors in response to racial discrimination. Prior exposure to discrimination may contribute to individuals’ active engagement in antiracist bystander behaviors. Future research directions on antiracist bystander actions and allyship are discussed.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://psyarxiv.com/eaz3k/" target="_blank">Anti-Asian Discrimination and Antiracist Bystander Behaviors amid the COVID-19 Outbreak</a>
|
||
</div></li>
|
||
<li><strong>Pneumolysis: a fundamental concept in COVID-19 lung disease</strong> -
|
||
<div>
|
||
Background COVID-19 severe lung compromise often evolves to life-threatening hypoxia. The experience led to the implementation of standardized protocols assuming similarity to SARS-CoV. Impulsive use of ventilators ended in up to 88% fatality. Methods COVID-19 pathophysiology and histopathological lung biopsy photomicrographs are analyzed. Results Pneumolysis is defined as progressive alveolar-capillary destruction resulting from the CoV-2 attack on pneumocytes. The histopathological results show the presence of Masson bodies, alveolar coating cells with nuclear atypia, reactive pneumocytes, reparative fibrosis, intra-alveolar hemorrhage, moderate inflammatory infiltrates, microabscesses, microthrombus, hyaline membrane remnants, and emphysema. The three theoretical pathophysiological stages of progressive hypoxemia (silent hypoxemia, gasping, and death zone) are depicted. Conclusion Silent hypoxemia suddenly evolves to critical hypoxemia. This, as a consequence of progressive pneumolysis + inflammation + overexpressed immunity + autoimmunity + HAPE-type edema resulting in acute pulmonary insufficiency. The proposed treatment (based on Tolerance to Hypoxia and the Hemoglobin factor) includes: prompt oxygen administration, inflammation and immunity reaction control, antibiotics, rehydration & anticoagulation.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://osf.io/g9m6x/" target="_blank">Pneumolysis: a fundamental concept in COVID-19 lung disease</a>
|
||
</div></li>
|
||
<li><strong>Epigallocatechin Gallate from Green Tea Effectively Blocks Infection of SARS-CoV-2 and New Variants by Inhibiting Spike Binding to ACE2 Receptor</strong> -
|
||
<div>
|
||
As the COVID-19 pandemic rages on, the new SARS-CoV-2 variants have emerged in the different regions of the world. These newly emerged variants have mutations in their spike (S) protein that may confer resistance to vaccine-elicited immunity and existing neutralizing antibody therapeutics. Therefore, there is still an urgent need of safe, effective, and affordable agents for prevention/treatment of SARS-CoV-2 and its variant infection. Here, we demonstrated that green tea beverage (GTB) or its major ingredient, epigallocatechin gallate (EGCG), were highly effective in inhibiting infection of live SARS-CoV-2 and human coronavirus (HCoV OC43). In addition, infection of the pseudoviruses with spikes of the new variants (UK-B.1.1.7, SA-B.1.351, and CA-B.1.429) was efficiently blocked by GTB or EGCG. Among the 4 active green tea catechins at noncytotoxic doses, EGCG was the most potent in the action against the viruses. The highest inhibitory activity was observed when the viruses or the cells were pre-incubated with EGCG prior to the infection. Mechanistic studies revealed that EGCG blocked infection at the entry step through interfering with the engagement of the receptor binding domain (RBD) of the viral spikes to angiotensin-converting enzyme 2 (ACE2) receptor of the host cells. These data support further clinical evaluation and development of EGCG as a novel, safe, and cost-effective natural product for prevention/treatment of SARS-CoV-2 transmission and infection.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2021.03.17.435637v1" target="_blank">Epigallocatechin Gallate from Green Tea Effectively Blocks Infection of SARS-CoV-2 and New Variants by Inhibiting Spike Binding to ACE2 Receptor</a>
|
||
</div></li>
|
||
<li><strong>SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway</strong> -
|
||
<div>
|
||
Pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induces inflammatory cytokines and chemokines including IL-6, IL-1b, TNFa, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and neucleocapsid (N) proteins. When stimulated with extracellular S protein, human lung epithelial cells A549 also produce inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly are non-inflammatory, but elicit an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-kB pathway in a MyD88-dependent manner. Further, such an activation of the NF-kB pathway is abrogated in Tlr2-deficient macrophages. Consistently, administration of S protein induces IL-6, TNF-a, and IL-1b in wild-type, but not Tlr2-deficient mice. Together these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2021.03.16.435700v1" target="_blank">SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway</a>
|
||
</div></li>
|
||
<li><strong>Longitudinal characterization of humoral and cellular immunity in hospitalized COVID-19 patients reveal immune persistence up to 9 months after infection</strong> -
|
||
<div>
|
||
Background: Insights into early, specific humoral and cellular responses to infection with SARS-CoV-2, as well as the persistence and magnitude of resulting immune memory is important amidst the ongoing pandemic. The combination of humoral and cellular immunity will most likely contribute to protection from reinfection or severe disease. Methods: Here, we conducted a longitudinal study on hospitalized moderate and severe COVID-19 patients from the acute phase of disease into convalescence at five- and nine-months post symptom onset. Utilizing flow cytometry, serological assays as well as B cell and T cell FluoroSpot assays, we assessed the magnitude and specificity of humoral and cellular immune memory during and after human SARS-CoV-2 infection. Findings: During acute COVID-19, we observed an increase in germinal center activity, a substantial expansion of antibody-secreting cells, and the generation of SARS-CoV-2-neutralizing antibodies. Despite gradually decreasing antibody levels, we show persistent, neutralizing antibody titers as well as robust specific memory B cell responses and polyfunctional T cell responses at five- and nine-months after symptom onset in both moderate and severe COVID-19 patients. Long-term SARS-CoV-2 specific responses were marked by preferential targeting of spike over nucleocapsid protein. Conclusions: Our findings describe the initiation and, importantly, persistence of cellular and humoral SARS-CoV-2 specific immunological memory in hospitalized COVID-19 patients long after recovery, likely contributing towards protection against reinfection.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2021.03.17.435581v1" target="_blank">Longitudinal characterization of humoral and cellular immunity in hospitalized COVID-19 patients reveal immune persistence up to 9 months after infection</a>
|
||
</div></li>
|
||
<li><strong>Identification of ACE2 mutations that modulate SARS-CoV-2 spike binding across multiple mammalian species</strong> -
|
||
<div>
|
||
Understanding how SARS-CoV-2 interacts with different mammalian angiotensin-converting enzyme II (ACE2) cell entry receptors will help elucidate determinants of intra- and cross-species virus transmission, facilitate development of effective new vaccines for both humans and livestock animals, and guide livestock farming and coronavirus screening procedures to ensure food supply security. In this work we applied laboratory directed evolution to several mammalian ACE2s with the goal of identifying conserved ACE2 mutations that increase spike binding affinity across multiple species. We found the Gln42Leu mutation increased ACE2-spike binding for human as well as four of four other mammalian ACE2s, while the Leu79Ile mutation had a similar effect for human and three of three mammalian ACE2 orthologs. These results are especially notable given the residues’ high levels of representation, i.e., 83% for Gln42 and 56% for Leu79, among annotated mammalian ACE2s. We also found that substitutions at ACE2 position 34, which is relatively variable across mammalian ACE2s, increased binding for multiple ACE2 orthologs. Taken together, these results speak strongly to the plausibility of SARS-CoV-2 strains with increased ability to cross species transmission barriers. Our results can guide further computational and experimental studies to develop biomedical technologies and animal husbandry practices that help protect both humans and livestock from existing and future SARS-CoV-2 variants.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2021.03.16.435705v1" target="_blank">Identification of ACE2 mutations that modulate SARS-CoV-2 spike binding across multiple mammalian species</a>
|
||
</div></li>
|
||
<li><strong>Structural basis of anti-SARS-CoV-2 activity of hydroxychloroquine: specific binding to NTD/CTD and disruption of LLPS of N protein</strong> -
|
||
<div>
|
||
SARS-CoV-2 is the coronavirus causing the catastrophic pandemic which already led to >120 millions of infections and >2.6 millions of deaths. Hydroxychloroquine (HCQ) has been shown to own promising potential in clinically combating SARS-CoV-2 but the underlying mechanisms still remain almost unknown. So far, all action sites are proposed on the host cells, and in particular no specific viral target protein has been experimentally identified. In this study, by use of DIC microscopy and NMR spectroscopy, for the first time we have decoded that HCQ specifically binds to both N-terminal domain (NTD) and C-terminal domain (CTD) of SARS-CoV-2 nucleocapsid (N) protein to inhibit their interactions with nucleic acids (NAs), as well as to disrupt its NA-induced liquid- liquid phase separation (LLPS) essential for the viral life cycle including the package of gRNA and N protein into new virions. These results suggest that HCQ may achieve its anti-SARS-CoV-2 activity by interfering in several key steps of the viral life cycle. The study not only provides a structural basis for the anti-SARS-CoV-2 activity of HCQ, but also indicates that SARS-CoV-2 N protein and its LLPS represent key targets for further optimization and development of anti-SARS-CoV-2 drugs.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://osf.io/yx6k2/" target="_blank">Structural basis of anti-SARS-CoV-2 activity of hydroxychloroquine: specific binding to NTD/CTD and disruption of LLPS of N protein</a>
|
||
</div></li>
|
||
<li><strong>Characterisation of a novel ACE2-based therapeutic with enhanced rather than reduced activity against SARS-CoV2 variants</strong> -
|
||
<div>
|
||
The human angiotensin-converting enzyme 2 acts as the host cell receptor for SARS-CoV-2 and the other members of the Coronaviridae family SARS-CoV-1 and HCoV-NL63. Here we report the biophysical properties of the SARS-CoV-2 spike variants D614G, B.1.1.7 and B.1.351 with affinities to the ACE2 receptor and infectivity capacity, revealing weaknesses in the developed neutralising antibody approaches. Furthermore, we report a pre-clinical characterisation package for a soluble receptor decoy engineered to be catalytically inactive and immunologically inert, with broad neutralisation capacity, that represents an attractive therapeutic alternative in light of the mutational landscape of COVID-19. This construct efficiently neutralised four SARS-CoV-2 variants of concern. The decoy also displays antibody-like biophysical properties and manufacturability, strengthening its suitability as a first-line treatment option in prophylaxis or therapeutic regimens for COVID-19 and related viral infections.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2021.03.17.435802v1" target="_blank">Characterisation of a novel ACE2-based therapeutic with enhanced rather than reduced activity against SARS-CoV2 variants</a>
|
||
</div></li>
|
||
<li><strong>ACE2 polymorphisms interplay with the apelinergic peptide system: potential tools for COVID-19 diagnosis and treatment</strong> -
|
||
<div>
|
||
ACE2 polymorphisms have been previously linked to increased susceptibility to multiple diseases and are currently linked to SARS CoV-2 susceptibility and complications. Notably, ACE2 transcribed or regulated proteins include the activity of metaloproteinsase-2 and apelin-13 and 36, might be linked to abnormal immune responses and complications. Furthermore, potential genetic or serological tests might be developed to detect the higher vulnerable groups to SARS CoV-2 complications and/or mortality. Furthermore, we hypothesize that diabetic and obese patients suffer from exhausted and/or abnormally functioning apelinergic peptides that predispose them to a higher severe COVID-19 risk. Moreover, infusion of apelin-13 to treat selected critical cases of COVID-19, especially those complaining of refractory advanced heart failure not responding to other drugs, might be considered for clinical trials.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://osf.io/enjxt/" target="_blank">ACE2 polymorphisms interplay with the apelinergic peptide system: potential tools for COVID-19 diagnosis and treatment</a>
|
||
</div></li>
|
||
<li><strong>Examining face-mask usage as an effective strategy to control COVID-19 spread</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
The COVID-19 global crisis is facilitated by high virus transmission rates and high percentages of asymptomatic and presymptomatic infected individuals. Containing the pandemic hinged on combinations of social distancing and face mask use. Here we examine the efficacy of these measures, using an agent-based modeling approach that evaluates face masks and social distancing in realistic confined spaces scenarios. We find face masks are more effective than social distancing. Importantly, combining face masks with even moderate social distancing provides optimal protection. The finding that widespread usage of face masks limits COVID-19 outbreaks can inform policies to reopening of social functions.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2020.08.12.20173047v3" target="_blank">Examining face-mask usage as an effective strategy to control COVID-19 spread</a>
|
||
</div></li>
|
||
<li><strong>Discovery of TMPRSS2 inhibitors from virtual screening</strong> -
|
||
<div>
|
||
The SARS-CoV-2 pandemic has prompted researchers to pivot their efforts to finding anti-viral compounds and vaccines. In this study, we focused on the human host cell transmembrane protease serine 2 (TMPRSS2), which plays an important role in the viral life cycle by cleaving the spike protein to initiate membrane fusion. TMPRSS2 is an attractive target and has received attention for the development of drugs against SARS and MERS. Starting with comparative structural modeling and binding model analysis, we developed an efficient pharmacophore-based approach and applied a large-scale in silico database screening for small molecule inhibitors against TMPRSS2. The hits were evaluated in the TMPRSS2 biochemical assay and the SARS-CoV-2 pseudotyped particle (PP) entry assay. A number of novel inhibitors were identified, providing starting points for further development of drug candidates for the treatment of COVID-19.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.28.424413v2" target="_blank">Discovery of TMPRSS2 inhibitors from virtual screening</a>
|
||
</div></li>
|
||
<li><strong>Identification of a High-frequency Intra-host SARS-CoV-2 spike Variant with Enhanced Cytopathic and Fusogenic Effect</strong> -
|
||
<div>
|
||
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a virus that is continuously evolving. Although its RNA-dependent RNA polymerase exhibits some exonuclease proofreading activity, viral sequence diversity can be produced by replication errors and host factors. A diversity of genetic variants can be observed in the intra-host viral population structure of infected individuals. Most mutations will follow a neutral molecular evolution and won’t make significant contributions to variations within and between infected hosts. Herein, we profiled the intra-sample genetic diversity of SARS-CoV-2 variants using high-throughput sequencing datasets from 15,289 infected individuals and infected cell lines. Most of the genetic variations observed, including C->U and G->U, were consistent with errors due to heat-induced DNA damage during sample processing and/or sequencing protocols. Despite high mutational background, we identified recurrent intra-variable positions in the samples analyzed, including several positions at the end of the gene encoding the viral Spike (S) protein. Strikingly, we observed a high-frequency C->A missense mutations resulting in the S protein lacking the last 20 amino acids (S{Delta}20). We found that this truncated S protein undergoes increased processing and increased syncytia formation, presumably due to escaping M protein retention in intracellular compartments. Our findings suggest the emergence of a high-frequency viral sublineage that is not horizontally transmitted but potentially involved in intra-host disease cytopathic effects.
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.biorxiv.org/content/10.1101/2020.12.03.409714v2" target="_blank">Identification of a High-frequency Intra-host SARS-CoV-2 spike Variant with Enhanced Cytopathic and Fusogenic Effect</a>
|
||
</div></li>
|
||
<li><strong>Show us the Data: Global COVID-19 Wastewater Monitoring Efforts, Equity, and Gaps</strong> -
|
||
<div>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
A year since the declaration of the global coronavirus disease 2019 (COVID-19) pandemic there have been over 110 million cases and 2.5 million deaths. Using methods to track community spread of other viruses such as poliovirus, environmental virologists and those in the wastewater based epidemiology (WBE) field quickly adapted their existing methods to detect SARS-CoV-2 RNA in wastewater. Unlike COVID-19 case and mortality data, there was not a global dashboard to track wastewater monitoring of SARS-CoV-2 RNA worldwide. This study describes the development of the COVIDPoops19 dashboard to disseminate information regarding sites, universities, research institutions and private laboratories in countries that are involved in WBE for SARS-CoV-2. Methods to assemble the dashboard combined standard literature review, direct submissions, and daily, social media keyword searches. Over 200 universities, 1,000 sites, and 50 countries with 59 dashboards monitor wastewater for SARS-CoV-2 RNA. However, monitoring is inequitably distributed in high-income countries and data are not widely shared publicly or accessible to researchers to inform public health actions, meta-analysis, better coordinate, and determine equitable distribution of monitoring sites. For WBE to be used to its full potential during COVID-19 and beyond, show us the data.
|
||
</p>
|
||
</div>
|
||
<div class="article-link article-html-link">
|
||
🖺 Full Text HTML: <a href="https://www.medrxiv.org/content/10.1101/2021.03.14.21253564v1" target="_blank">Show us the Data: Global COVID-19 Wastewater Monitoring Efforts, Equity, and Gaps</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>Dose-Ranging Study to Assess the Safety and Efficacy of Melatonin in Outpatients Infected With COVID-19</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: Melatonin; Drug: Placebo<br/><b>Sponsors</b>: State University of New York at Buffalo; National Center for Advancing Translational Science (NCATS)<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 the Efficacy and Safety of Brilacidin in Hospitalized Participants With COVID-19</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: Brilacidin; Drug: Placebo; Drug: Standard of Care (SoC)<br/><b>Sponsor</b>: Innovation Pharmaceuticals, 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>Evaluation of ADG20 for the Treatment of Mild or Moderate COVID-19</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: ADG20; Drug: Normal saline<br/><b>Sponsor</b>: Adagio 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>A Study to Evaluate the Safety and Efficacy of OT-101+Artemisinin in Hospitalized COVID-19 Subjects</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: OT-101; Drug: Artemisinin; Drug: Placebo<br/><b>Sponsor</b>: Oncotelic 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>Study of mRNA Vaccine Formulation Against COVID-19 in Healthy Adults 18 Years of Age and Older</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Biological: SARS-CoV-2 mRNA vaccine formulation 1; Biological: SARS-CoV-2 mRNA vaccine formulation 2; Biological: SARS-CoV-2 mRNA vaccine formulation 3; Biological: Placebo (0.9% normal saline)<br/><b>Sponsor</b>: Sanofi Pasteur, a Sanofi Company<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>Trial to Determine the Efficacy/Safety of Plitidepsin vs Control in Patients With Moderate COVID-19 Infection</strong> - <b>Condition</b>: COVID-19 Infection<br/><b>Interventions</b>: Drug: Plitidepsin; Drug: Dexamethasone; Drug: Remdesivir<br/><b>Sponsor</b>: PharmaMar<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>Safety and Immunogenicity Study of a SARS-CoV-2 (COVID-19) Variant Vaccine (mRNA-1273.351) in Naïve and Previously Vaccinated Adults</strong> - <b>Conditions</b>: COVID-19; COVID-19 Immunisation<br/><b>Interventions</b>: Biological: mRNA-1273; Biological: mRNA-1273.351<br/><b>Sponsors</b>: National Institute of Allergy and Infectious Diseases (NIAID); ModernaTX, 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>Safety and Tolerability of Emricasan in Symptomatic Outpatients Diagnosed With Mild-COVID-19</strong> - <b>Condition</b>: Covid19<br/><b>Interventions</b>: Drug: Emricasan; Other: Placebo<br/><b>Sponsor</b>: Histogen<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 of Reinforcing Standard Therapy in COVID-19 Patients With Repeated Transfusion of Convalescent Plasma</strong> - <b>Condition</b>: Covid19<br/><b>Interventions</b>: Other: Convalescent Plasma with antibody against SARS-CoV-2.; Other: Standard treatment for COVID-19<br/><b>Sponsors</b>: Hospital Son Llatzer; Fundació d’investigació Sanitària de les Illes Balears<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>Diagnostic Performance of the ID Now™ COVID-19 Screening Test Versus Simplexa™ COVID-19 Direct Assay</strong> - <b>Condition</b>: Covid19<br/><b>Intervention</b>: Diagnostic Test: ID Now™ COVID-19 Screening Test<br/><b>Sponsor</b>: Groupe Hospitalier Paris Saint Joseph<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>A Phase 2 Study of Human Monoclonal Antibodies, BRII-196 and BRII-198</strong> - <b>Condition</b>: COVID-19<br/><b>Interventions</b>: Drug: BRII-196 and BRII-198; Drug: Placebo<br/><b>Sponsors</b>: Brii Biosciences Limited; TSB Therapeutics (Beijing) 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>Off-the-shelf NK Cells (KDS-1000) as Immunotherapy for COVID-19</strong> - <b>Condition</b>: Covid19<br/><b>Interventions</b>: Biological: KDS-1000; Other: Placebo<br/><b>Sponsor</b>: Kiadis Pharma<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 Assess if a Medicine Called Bamlanivimab is Safe and Effective in Reducing Hospitalization Due to COVID-19</strong> - <b>Condition</b>: Covid19<br/><b>Interventions</b>: Biological: Bamlanivimab; Other: Standard of Care<br/><b>Sponsors</b>: Fraser Health; Fraser Health Authrority Department of Evaluation and Research Services; Surrey Memorial Hospital Clinical Research Unit; Centre for Health Evaluation and Outcome Sciences; Surrey Hospitals Foundation; BC Support Unit; University of British Columbia; Ministry of Health, British Columbia<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>Effects of Telerehabilitation After Discharge in COVID-19 Survivors</strong> - <b>Condition</b>: Covid19<br/><b>Intervention</b>: Other: Telerehabilitation<br/><b>Sponsor</b>: Hacettepe 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>Corticosteroids for COVID-19</strong> - <b>Condition</b>: Covid19<br/><b>Interventions</b>: Drug: Prednisone; Device: Point of Care testing device for C-reactive protein<br/><b>Sponsor</b>: University of Alberta<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>Etoricoxib may inhibit cytokine storm to treat COVID-19</strong> - The worldwide spread of COVID-19 has caused an unprecedented disaster. The emergence of COVID-19-mediated cytokine storm is one of the most important contributors to the development of acute and severe illness in patients. At present, there is an urgent need for drugs that can inhibit cytokine storm to treat COVID-19. In the absence of specific drugs and vaccines, it is important to screen existing drugs as potential treatments. This article introduces a potential repositioning of the existing…</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>(1)H, (13)C and (15)N Backbone chemical shift assignments of the n-terminal and central intrinsically disordered domains of SARS-CoV-2 nucleoprotein</strong> - The nucleoprotein (N) from SARS-CoV-2 is an essential cofactor of the viral replication transcription complex and as such represents an important target for viral inhibition. It has also been shown to colocalize to the transcriptase-replicase complex, where many copies of N decorate the viral genome, thereby protecting it from the host immune system. N has also been shown to phase separate upon interaction with viral RNA. N is a 419 amino acid multidomain protein, comprising two folded,…</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>Immunity, virus evolution, and effectiveness of SARS-CoV-2 vaccines</strong> - Phylogenetic and pathogenesis studies of the severe acute respiratory syndrome-related coronaviruses (SARS-CoVs) strains have highlighted some specific mutations that could confer the RNA genome fitness advantages and immunological resistance for their rapid spread in the human population. The analyses of 30 kb RNA SARS-CoVs genome sequences, protein structures, and functions have provided us a perspective of how host-virus protein-protein complexes act to mediate virus infection. The open…</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>CCR5Delta32 deletion as a protective factor in Czech first-wave COVID-19 subjects</strong> - Infection by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease (COVID-19), has spread widely around the globe. Significant inter-individual differences have been observed during the course of the infection, which suggests that genetic susceptibility may be a contributing factor. CC chemokine receptor 5 (CCR5), which acts as a co-receptor for the entry of HIV-1 into cells, is promising candidate whose can have an influence on 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>Immunoinformatics and Molecular Docking Studies Predicted Potential Multiepitope-Based Peptide Vaccine and Novel Compounds against Novel SARS-CoV-2 through Virtual Screening</strong> - CONCLUSION: Our investigations predicted epitopes and the reported molecules that may have the potential to inhibit the SARS-CoV-2 virus. These findings can be a step towards the development of a peptide-based vaccine or natural compound drug target against 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>Clofazimine broadly inhibits coronaviruses including SARS-CoV-2</strong> - COVID-19 pandemic is the third zoonotic coronavirus (CoV) outbreak of the century after severe acute respiratory syndrome (SARS) in 2003¹ and Middle East respiratory syndrome (MERS) since 2012². Treatment options for CoVs are largely lacking. Here we show that clofazimine, an anti-leprosy drug with a favourable safety profile³, possesses pan-coronaviral inhibitory activity, and can antagonize SARS-CoV-2 and MERS-CoV replication in multiple in vitro systems. The FDA-approved molecule was found 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>A brief review on potential application of mesenchymal stem cell and secretome in combating mortality and morbidity in COVID-19 patients</strong> - Coronavirus disease 2019 (COVID-19) caused by novel Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV2), is typically associated with severe respiratory distress and has claimed more than 525,000 lives already. The most fearful aspect is the unavailability of any concrete guidelines and treatment or protective strategies for reducing mortality or morbidity caused by this virus. Repurposing of drugs, antivirals, convalescent plasma and neutralizing antibodies are being considered for…</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>Human coronaviruses and therapeutic drug discovery</strong> - CONCLUSIONS: During the spread of COVID-19 outbreak, great efforts have been made in therapeutic drug discovery against the virus, although the pharmacological effects and adverse reactions of some drugs under study are still unclear. However, well-designed high-quality studies are needed to further study the effectiveness and safety of these potential drugs so as to provide valid recommendations for better control of the COVID-19 pandemic.</p></li>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>COVIDENZA - A prospective, multicenter, randomized PHASE II clinical trial of enzalutamide treatment to decrease the morbidity in patients with Corona virus disease 2019 (COVID-19): a structured summary of a study protocol for a randomised controlled trial</strong> - OBJECTIVES: The main goal of the COVIDENZA trial is to evaluate if inhibition of testosterone signalling by enzalutamide can improve the outcome of patients hospitalised for COVID-19. The hypothesis is based on the observation that the majority of patients in need of intensive care are male, and the connection between androgen receptor signalling and expression of TMPRSS2, an enzyme important for SARS-CoV-2 host cell internalization.</p></li>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>A review: Mechanism of action of antiviral drugs</strong> - Antiviral drugs are a class of medicines particularly used for the treatment of viral infections. Drugs that combat viral infections are called antiviral drugs. Viruses are among the major pathogenic agents that cause number of serious diseases in humans, animals and plants. Viruses cause many diseases in humans, from self resolving diseases to acute fatal diseases. Developing strategies for the antiviral drugs are focused on two different approaches: Targeting the viruses themselves or the host…</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>Computational approach to decipher cellular interactors and drug targets during co-infection of SARS-CoV-2, Dengue, and Chikungunya virus</strong> - The world is reeling under severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, and it will be frightening if compounded by other co-existing infections. The co-occurrence of the Dengue virus (DENV) and Chikungunya virus (CHIKV) has been into existence, but recently the co-infection of DENV and SARS-CoV-2 has been reported. Thus, the possibility of DENV, CHIKV, and SARS-CoV-2 co-infection could be predicted in the future with enhanced vulnerability. It is essential to elucidate…</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>Seroconversion stages COVID19 into distinct pathophysiological states</strong> - COVID19 is a heterogeneous medical condition involving diverse underlying pathophysiological processes including hyperinflammation, endothelial damage, thrombotic microangiopathy, and end-organ damage. Limited knowledge about the molecular mechanisms driving these processes and lack of staging biomarkers hamper the ability to stratify patients for targeted therapeutics. We report here the results of a cross-sectional multi-omics analysis of hospitalized COVID19 patients revealing that…</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>Repurposing CFDA-approved drug carrimycin as an antiviral agent against human coronaviruses, including the currently pandemic SARS-CoV-2</strong> - COVID-19 pandemic caused by SARS-CoV-2 infection severely threatens global health and economic development. No effective antiviral drug is currently available to treat COVID-19 and any other human coronavirus infections. We report herein that a CFDA-approved macrolide antibiotic, carrimycin, potently inhibited the cytopathic effects (CPE) and reduced the levels of viral protein and RNA in multiple cell types infected by human coronavirus 229E, OC43, and SARS-CoV-2. Time-of-addition 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>The serotonin reuptake inhibitor Fluoxetine inhibits SARS-CoV-2 in human lung tissue</strong> - To circumvent time-consuming clinical trials, testing whether existing drugs are effective inhibitors of SARS-CoV-2, has led to the discovery of Remdesivir. We decided to follow this path and screened approved medications “off-label” against SARS-CoV-2. Fluoxetine inhibited SARS-CoV-2 at a concentration of 0.8 µg/ml significantly in these screenings, and the EC50 was determined with 387 ng/ml. Furthermore, Fluoxetine reduced viral infectivity in precision-cut human lung slices showing its…</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>Unique and complementary suppression of cGAS-STING and RNA sensing- triggered innate immune responses by SARS-CoV-2 proteins</strong> - The emergence of SARS-CoV-2 has resulted in the COVID-19 pandemic, leading to millions of infections and hundreds of thousands of human deaths. The efficient replication and population spread of SARS-CoV-2 indicates an effective evasion of human innate immune responses, although the viral proteins responsible for this immune evasion are not clear. In this study, we identified SARS-CoV-2 structural proteins, accessory proteins, and the main viral protease as potent inhibitors of host innate…</p></li>
|
||
</ul>
|
||
<h1 data-aos="fade-right" id="from-patent-search">From Patent Search</h1>
|
||
<ul>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Peptides and their use in diagnosis of SARS-CoV-2 infection</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU319943278">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>A PROCESS FOR SUCCESSFUL MANAGEMENT OF COVID 19 POSITIVE PATIENTS</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU319942709">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Sars-CoV-2 vaccine antigens</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU318283136">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>SARS-COV-2 BINDING PROTEINS</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU318004130">link</a></p></li>
|
||
<li data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Gerät zur Unterstützung und Verstärkung natürlicher Lüftung</strong> -
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">
|
||
</p><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom">Lüftungssystem für einen mit öffnbaren Fenstern (16) ausgestatteten Gebäuderaum, gekennzeichnet dadurch, dass es ein Gehäuse (18) und einen Ventilator (20) aufweist, wobei durch das Gehäuse eine vom Ventilator erzeugte Luftströmung strömen kann, wobei das Gehäuse dafür eine Einströmöffnung (24) für Luft und eine Ausströmöffnung (22) für Luft enthält, wobei eine der beiden Öffnungen der Form eines Öffnungsspalts (26) zwischen einem Fensterflügel (12) und einem Blendrahmen (14) des Fensters (16) angepasst ist.</p></li>
|
||
</ul>
|
||
<img alt="embedded image" id="EMI-D00000"/>
|
||
<p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"></p>
|
||
<ul>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=DE319927546">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>X射线图像识别方法、装置、计算机设备及存储介质</strong> - 本申请涉及一种X射线图像识别方法、装置、计算机设备和存储介质。通过获取X射线图像，将X射线图像作为训练样本；构建多注意力交互网络，多注意力交互网络包括卷积批处理标准化网络、特征提取网络和输出网络；其中特征提取网络包括多注意力交互特征提取模块和批标准化模块，特征提取网络通过学习通道之间的相关性，多通道之间的信息交互来达到增强模型的识别能力。利用训练样本对多注意力交互网络进行训练，得到X射线图像识别模型；获取待测X射线图像；将待测X射线图像输入到X射线图像识别模型中，得到X射线图像的类别。本方法减少了网络的参数量和计算量，提高了模型的泛化能力。 - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=CN319953046">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>利用HEK293细胞制备新型冠状病毒核衣壳蛋白的方法</strong> - 本发明提供一种利用HEK293细胞制备新型冠状病毒核衣壳蛋白的方法，包括：1）构建新冠病毒核衣壳蛋白（N蛋白）重组表达载体；2）用重组表达载体转染HEK293细胞；3）体外培养细胞，从培养上清中分离纯化N蛋白。利用HEK293表达系统可在短时间内获得大量新冠病毒N蛋白，通过一步亲和层析法可获得纯度高达98%以上的N蛋白。与大肠杆菌相比，采用HEK293表达系统制备的N蛋白在与抗体的结合活性及新冠抗体胶体金检测方面均表现出极大优势，且HEK293表达系统制备的N蛋白其蛋白空间构象接近于病毒N基因在宿主体内的蛋白表达构象，具有更高的免疫诊断和抗体制备的准确性，将其用于制作诊断试剂和疫苗前景广阔。 - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=CN319953048">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>Compositions and methods for detecting SARS-CoV-2 spike protein</strong> - - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=AU317343760">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>偶联新型冠状病毒S2蛋白的磁珠及其制备方法与应用</strong> - 本发明提供偶联新型冠状病毒S2蛋白的磁珠及其制备方法与应用。所述偶联新型冠状病毒S2蛋白的磁珠是将表面修饰有链霉亲和素的磁珠与生物素标记的新型冠状病毒S2蛋白结合制得的。本发明还提供偶联后磁珠的冻干过程，以及偶联后磁珠的酵母展示scFv文库的筛选。该磁珠具有结合能力强，特异性好，稳定性高，便于操作的特点，既可用于新冠病毒S2抗体的富集，也可用于表达S2抗体的酵母细胞的淘选。利用本发明磁珠进行S2蛋白抗体的富集和表达S2蛋白抗体的细胞筛选，可将低浓度的特异性抗体捕获后进行浓缩，提高了灵敏度。在酵母展示scFv文库细胞筛选上，比流式细胞分选方法所需周期短，可快速筛出目标克隆酵母细胞，提高筛选效率。 - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=CN319952963">link</a></p></li>
|
||
<li><p data-aos="fade-left" data-aos-anchor-placement="bottom-bottom"><strong>靶向SARS-CoV-2的抗体及其制备方法和应用</strong> - 本发明提供了靶向SARS‑CoV‑2的抗体及其制备方法和应用，该抗体包含VH和VL，所述VH包含以下CDR：氨基酸序列如SEQ ID NO:1、2、3所示的VH CDR1、VH CDR2、VH CDR3；所述VL包含以下的CDR：氨基酸序列如SEQ ID NO:4、5、6所示的VL CDR1、VL CDR2、VL CDR3。该抗体能够高亲和且特异地结合SARS‑CoV‑2的S蛋白的RBD，抑制RBD蛋白与受体ACE2蛋白的结合，高效地抑制SARS‑CoV‑2感染细胞，同时对潜在的免疫逃逸突变的假病毒具有很好的中和活性，从而可有效应用于SARS‑CoV‑2病毒及相关疾病的诊断、预防和治疗中。 - <a href="https://patentscope.wipo.int/search/en/detail.jsf?docId=CN319687581">link</a></p></li>
|
||
</ul>
|
||
|
||
|
||
<script>AOS.init();</script></body></html> |