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Kit-San Yuen

Researcher at University of Hong Kong

Publications -  29
Citations -  2926

Kit-San Yuen is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Interferon & Epstein–Barr virus. The author has an hindex of 17, co-authored 27 publications receiving 2197 citations. Previous affiliations of Kit-San Yuen include Li Ka Shing Faculty of Medicine, University of Hong Kong.

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Zoonotic origins of human coronaviruses.

TL;DR: An overview of the existing knowledge about the seven HCoVs is presented, with a focus on the history of their discovery as well as their zoonotic origins and interspecies transmission, and the current CoV disease 2019 (COVID-19) epidemic is discussed.
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SARS-CoV-2 and COVID-19: The most important research questions

TL;DR: Nine most important research questions concerning virus transmission, asymPTomatic and presymptomatic virus shedding, diagnosis, treatment, vaccine development, origin of virus and viral pathogenesis are highlighted.
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Severe acute respiratory syndrome coronavirus ORF3a protein activates the NLRP3 inflammasome by promoting TRAF3-dependent ubiquitination of ASC

TL;DR: It is shown that the SARS‐CoV open reading frame 3a (ORF3a) accessory protein activates the NLRP3 inflammasome by promoting TNF receptor‐associated factor 3 (TRAF3)–mediated ubiquitination of apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC).
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A tug-of-war between severe acute respiratory syndrome coronavirus 2 and host antiviral defence: lessons from other pathogenic viruses.

TL;DR: Current understanding of the induction of a proinflammatory cytokine storm by other highly pathogenic human coronaviruses, their adaptation to humans and their usurpation of the cell death programmes are summarized.
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Middle East Respiratory Syndrome Coronavirus 4a Protein Is a Double-Stranded RNA-Binding Protein That Suppresses PACT-Induced Activation of RIG-I and MDA5 in the Innate Antiviral Response

TL;DR: These findings suggest a new mechanism through which MERS-CoV employs a viral double-stranded RNA-binding protein to circumvent the innate antiviral response by perturbing the function of cellular double-Stranded RNA -binding protein PACT.