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Factors Associated with Emerging and Re-emerging of SARS-CoV-2 Variants
Austin N Spratt; Saathvik K Kannan; Lucas T Woods; Gary A Weisman; Thomas D Quinn; Christian L Lorson; Anders Sonnerborg; Siddappa N Byrareddy; Kamal Singh.
Afiliação
  • Austin N Spratt; Christopher S. Bond Life Sciences Center, University of Missouri,
  • Saathvik K Kannan; Christopher S. Bond Life Sciences Center, University of Missouri
  • Lucas T Woods; Department of Biochemistry, University of Missouri, Columbia
  • Gary A Weisman; Department of Biochemistry, University of Missouri, Columbia
  • Thomas D Quinn; Department of Biochemistry, University of Missouri, Columbia
  • Christian L Lorson; Department of Veterinary Pathobiology, University of Missouri, Columbia
  • Anders Sonnerborg; Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, Huddinge 14186, Stockholm, Sweden
  • Siddappa N Byrareddy; University of Nebraska Medical Center
  • Kamal Singh; University of Missouri
Preprint em En | PREPRINT-BIORXIV | ID: ppbiorxiv-436850
ABSTRACT
Global spread of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has triggered unprecedented scientific efforts, as well as containment and treatment measures. Despite these efforts, SARS-CoV-2 infections remain unmanageable in some parts of the world. Due to inherent mutability of RNA viruses, it is not surprising that the SARS-CoV-2 genome has been continuously evolving since its emergence. Recently, four functionally distinct variants, B.1.1.7, B.1.351, P.1 and CAL.20C, have been identified, and they appear to more infectious and transmissible than the original (Wuhan-Hu-1) virus. Here we provide evidence based upon a combination of bioinformatics and structural approaches that can explain the higher infectivity of the new variants. Our results show that the greater infectivity of SARS-CoV-2 than SARS-CoV can be attributed to a combination of several factors, including alternate receptors. Additionally, we show that new SARS-CoV-2 variants emerged in the background of D614G in Spike protein and P323L in RNA polymerase. The correlation analyses showed that all mutations in specific variants did not evolve simultaneously. Instead, some mutations evolved most likely to compensate for the viral fitness.
Licença
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Texto completo: 1 Coleções: 09-preprints Base de dados: PREPRINT-BIORXIV Idioma: En Ano de publicação: 2021 Tipo de documento: Preprint
Texto completo: 1 Coleções: 09-preprints Base de dados: PREPRINT-BIORXIV Idioma: En Ano de publicação: 2021 Tipo de documento: Preprint