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.
Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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ADAM17 Protein / genetics*
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ADAM17 Protein / metabolism
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Angiotensin-Converting Enzyme 2
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Betacoronavirus / physiology*
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COVID-19
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Coronavirus Infections / genetics*
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Coronavirus Infections / virology
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Disease Susceptibility
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Humans
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Pandemics
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Peptidyl-Dipeptidase A / genetics*
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Peptidyl-Dipeptidase A / metabolism
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Pneumonia, Viral / genetics*
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Pneumonia, Viral / virology
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Polymorphism, Genetic / genetics*
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Polymorphism, Single Nucleotide / genetics
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Promoter Regions, Genetic / genetics
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SARS-CoV-2
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Serine Endopeptidases / genetics*
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Serine Endopeptidases / metabolism
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Virus Internalization
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Virus Shedding
Substances
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Peptidyl-Dipeptidase A
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ACE2 protein, human
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Angiotensin-Converting Enzyme 2
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Serine Endopeptidases
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TMPRSS2 protein, human
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ADAM17 Protein
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ADAM17 protein, human