Host Polymorphisms May Impact SARS-CoV-2 Infectivity

Trends Genet. 2020 Nov;36(11):813-815. doi: 10.1016/j.tig.2020.08.003. Epub 2020 Aug 10.

Abstract

Based on a broad public database compilation, we support the hypothesis that germinal polymorphisms may regulate the expression of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) cellular target itself and proteases controlling the process of its shedding or, conversely, its internalization. Consequently, a genetic influence on individual susceptibility to coronavirus disease 2019 (COVID-19) infection is strongly suspected.

Keywords: SNP; coronavirus; genetic variation; infection; pharmacogenetics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADAM17 Protein / genetics*
  • ADAM17 Protein / metabolism
  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus / physiology*
  • COVID-19
  • Coronavirus Infections / genetics*
  • Coronavirus Infections / virology
  • Disease Susceptibility
  • Humans
  • Pandemics
  • Peptidyl-Dipeptidase A / genetics*
  • Peptidyl-Dipeptidase A / metabolism
  • Pneumonia, Viral / genetics*
  • Pneumonia, Viral / virology
  • Polymorphism, Genetic / genetics*
  • Polymorphism, Single Nucleotide / genetics
  • Promoter Regions, Genetic / genetics
  • SARS-CoV-2
  • Serine Endopeptidases / genetics*
  • Serine Endopeptidases / metabolism
  • Virus Internalization
  • Virus Shedding

Substances

  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2
  • Serine Endopeptidases
  • TMPRSS2 protein, human
  • ADAM17 Protein
  • ADAM17 protein, human