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1.
Social Behavior & Personality: an international journal ; 50(9):1-12, 2022.
Article in English | Academic Search Complete | ID: covidwho-2022447

ABSTRACT

Increasing preventive behaviors is critical to mitigating the rapid spread of COVID-19, but this can be challenging as some people are reluctant to practice these behaviors. We explored the mediating role of threat appraisal in the link between perception of COVID-19 risk exposure and preventive behavior, and the moderating effect of COVID-19 information consumption through social media. We recruited 577 people in China to complete a survey. The results show that perception of COVID-19 risk exposure was positively associated with preventive behaviors and that threat appraisal partially mediated this relationship. Moreover, COVID-19 information consumption on social media moderated the mediating effect. These results provide theoretical and practical implications to increase individuals' preventive behaviors during the COVID-19 pandemic. [ FROM AUTHOR] Copyright of Social Behavior & Personality: an international journal is the property of Society for Personality Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

2.
biorxiv; 2022.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2022.06.06.494494

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may keep patients in a clinically asymptomatic state by blocking cellular innate antiviral immunity, but the molecular mechanism remains unclear. Here, we screened the viral proteins of SARS-CoV-2 and found that the spike (S) protein inhibits the activation of interferon-stimulated genes (ISGs) and even reduces the expression of these genes to below background values. Mechanistically, the S protein interacted with STAT1, STAT2, and IRF9 and impedes the phosphorylation of STAT1/STAT2, thus preventing the formation of the interferon-stimulating gene factor 3 (ISGF3) complex and inhibiting the downstream production of Interferon-stimulated genes (ISGs). Remarkably, we also have found that the inhibitory mechanism of the S protein was conservative among SARS-CoV-2 variants and other human coronaviruses, including SARS-CoV, MERS-CoV, HCoV-229E, HCoV-NL63, and HCoV-HKU1. Truncation studies indicated that the most conserved S2 domain played a major inhibitory role. Altogether, our findings unveil a new mechanism by which SARS-CoV-2 S protein attenuated the host's antiviral immune response and provide new insights into the pathogenic mechanism of coronavirus.


Subject(s)
Coronavirus Infections , Severe Acute Respiratory Syndrome
3.
biorxiv; 2020.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2020.03.24.005702

ABSTRACT

The COVID-19 pandemic demands assimilation of all available biomedical knowledge to decode its mechanisms of pathogenicity and transmission. Despite the recent renaissance in unsupervised neural networks for decoding unstructured natural languages, a platform for the real-time synthesis of the exponentially growing biomedical literature and its comprehensive triangulation with deep omic insights is not available. Here, we present the nferX platform for dynamic inference from over 45 quadrillion possible conceptual associations extracted from unstructured biomedical text, and their triangulation with Single Cell RNA-sequencing based insights from over 25 tissues. Using this platform, we identify intersections between the pathologic manifestations of COVID-19 and the comprehensive expression profile of the SARS-CoV-2 receptor ACE2. We find that tongue keratinocytes, airway club cells, and ciliated cells are likely underappreciated targets of SARS-CoV-2 infection, in addition to type II pneumocytes and olfactory epithelial cells. We further identify mature small intestinal enterocytes as a possible hotspot of COVID-19 fecal-oral transmission, where an intriguing maturation-correlated transcriptional signature is shared between ACE2 and the other coronavirus receptors DPP4 (MERS-CoV) and ANPEP (-coronavirus). This study demonstrates how a holistic data science platform can leverage unprecedented quantities of structured and unstructured publicly available data to accelerate the generation of impactful biological insights and hypotheses. The nferX Platform Single-cell resource - https://academia.nferx.com/


Subject(s)
COVID-19
4.
arxiv; 2020.
Preprint in English | PREPRINT-ARXIV | ID: ppzbmed-2003.12773v1

ABSTRACT

The COVID-19 pandemic demands assimilation of all available biomedical knowledge to decode its mechanisms of pathogenicity and transmission. Despite the recent renaissance in unsupervised neural networks for decoding unstructured natural languages, a platform for the real-time synthesis of the exponentially growing biomedical literature and its comprehensive triangulation with deep omic insights is not available. Here, we present the nferX platform for dynamic inference from over 45 quadrillion possible conceptual associations extracted from unstructured biomedical text, and their triangulation with Single Cell RNA-sequencing based insights from over 25 tissues. Using this platform, we identify intersections between the pathologic manifestations of COVID-19 and the comprehensive expression profile of the SARS-CoV-2 receptor ACE2. We find that tongue keratinocytes and olfactory epithelial cells are likely under-appreciated targets of SARS-CoV-2 infection, correlating with reported loss of sense of taste and smell as early indicators of COVID-19 infection, including in otherwise asymptomatic patients. Airway club cells, ciliated cells and type II pneumocytes in the lung, and enterocytes of the gut also express ACE2. This study demonstrates how a holistic data science platform can leverage unprecedented quantities of structured and unstructured publicly available data to accelerate the generation of impactful biological insights and hypotheses.


Subject(s)
COVID-19
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