The reduced pathogenicity of rSARS-CoV-2 Nsp1 mutants highlights the potential for targeting Nsp1 for rational design of viral inhibitors and development of live-attenuated vaccine strategies as effective prophylactic and therapeutic treatments to combat SARS-CoV-2 and possibly other CoV infections.
The infant mouse model is used to define the role of the accessory protein ORF8 in SARS-CoV-2 spread and reveal how a SARS-CoV-2 accessory protein can exploit mucosal antiviral responses to increase host contagiousness.
G. Ciabattoni, Stacey Bartlett, M. McGrath et al.· bioRxiv· 0 citations
Evaluating the drug resistance mechanisms of multiple SARS-CoV-2 non-structural proteins, including the main protease and the RNA-dependent RNA polymerase, as well as PLPro, EndoU, and Mac1, which contribute to viral replication and counter host innate immune responses are discussed.
A genome engineering technology is used to change a single amino acid in the viruses’ main protease enzyme to match that of circulating Omicron isolates to demonstrate antiviral efficacy of approved drugs and uncover mutants with reduced drug sensitivity.
It is found that the mutations induce distinct transcriptional and translational alterations: rN-Alpha drives a stealth-like infection characterized by sustained translation efficiency and specific evasion of the 2’-5’-oligoadenylate synthetase (OAS) innate immune sensor, whereas rN-Delta and rN-BA trigger a highly ele...
J. Berger, Jonas Schröder, Timothy K. Soh et al.· bioRxiv· 0 citations
SARS-CoV-2 evolution enhanced viral fitness and immune evasion, extending the COVID-19 pandemic and resulting in millions of excess deaths. Viral diversity is generated within infected individuals, yet the timing and interplay of viral and immunological forces that drive transmissible evolution are incompletely underst...
Katherine Owens, Pierce E. Radecki, S. Tempia et al.· bioRxiv· 0 citations
The data uncover a direct, enzyme-based mechanism by which SARS-CoV-2 can suppress influenza virus replication during coinfection and provide a molecular explanation for the sharp, global decline in influenza activity observed during the COVID-19 pandemic.
Liubing Du, Xiaoyu Cai, Zi-Tao Peng et al.· Virologica Sinica· 0 citations
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