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10.1093/cid/ciaa410

http://scihub22266oqcxt.onion/10.1093/cid/ciaa410
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32270184!7184390!32270184
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suck abstract from ncbi


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pmid32270184      Clin+Infect+Dis 2020 ; 71 (6): 1400-1409
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  • Comparative Replication and Immune Activation Profiles of SARS-CoV-2 and SARS-CoV in Human Lungs: An Ex Vivo Study With Implications for the Pathogenesis of COVID-19 #MMPMID32270184
  • Chu H; Chan JF; Wang Y; Yuen TT; Chai Y; Hou Y; Shuai H; Yang D; Hu B; Huang X; Zhang X; Cai JP; Zhou J; Yuan S; Kok KH; To KK; Chan IH; Zhang AJ; Sit KY; Au WK; Yuen KY
  • Clin Infect Dis 2020[Sep]; 71 (6): 1400-1409 PMID32270184show ga
  • BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an emerging coronavirus that has resulted in more than 2 000 000 laboratory-confirmed cases including over 145 000 deaths. Although SARS-CoV-2 and SARS-CoV share a number of common clinical manifestations, SARS-CoV-2 appears to be highly efficient in person-to-person transmission and frequently causes asymptomatic or presymptomatic infections. However, the underlying mechanisms that confer these viral characteristics of high transmissibility and asymptomatic infection remain incompletely understood. METHODS: We comprehensively investigated the replication, cell tropism, and immune activation profile of SARS-CoV-2 infection in human lung tissues with SARS-CoV included as a comparison. RESULTS: SARS-CoV-2 infected and replicated in human lung tissues more efficiently than SARS-CoV. Within the 48-hour interval, SARS-CoV-2 generated 3.20-fold more infectious virus particles than did SARS-CoV from the infected lung tissues (P < .024). SARS-CoV-2 and SARS-CoV were similar in cell tropism, with both targeting types I and II pneumocytes and alveolar macrophages. Importantly, despite the more efficient virus replication, SARS-CoV-2 did not significantly induce types I, II, or III interferons in the infected human lung tissues. In addition, while SARS-CoV infection upregulated the expression of 11 out of 13 (84.62%) representative proinflammatory cytokines/chemokines, SARS-CoV-2 infection only upregulated 5 of these 13 (38.46%) key inflammatory mediators despite replicating more efficiently. CONCLUSIONS: Our study provides the first quantitative data on the comparative replication capacity and immune activation profile of SARS-CoV-2 and SARS-CoV infection in human lung tissues. Our results provide important insights into the pathogenesis, high transmissibility, and asymptomatic infection of SARS-CoV-2.
  • |Betacoronavirus/*physiology[MESH]
  • |COVID-19[MESH]
  • |Chemokines/immunology[MESH]
  • |Coronavirus Infections/*immunology/virology[MESH]
  • |Cytokines/immunology[MESH]
  • |Humans[MESH]
  • |Immunity, Innate/*immunology[MESH]
  • |Interferons/immunology[MESH]
  • |Lung/immunology/virology[MESH]
  • |Pandemics[MESH]
  • |Pneumonia, Viral/*immunology/virology[MESH]
  • |SARS-CoV-2[MESH]
  • |Severe acute respiratory syndrome-related coronavirus/*physiology[MESH]


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