tetano
Editor, Senior Moderator
Dev Growth Differ
. 2021 Feb 17.
doi: 10.1111/dgd.12717. Online ahead of print.
Genetic variation analyses indicate conserved SARS-CoV-2-host interaction and varied genetic adaptation in immune-response factors in modern human evolution
Ji-Won Lee[SUP] 1 [/SUP], In-Hee Lee[SUP] 2 [/SUP], Takanori Sato[SUP] 1 [/SUP], Sek Won Kong[SUP] 2 3 [/SUP], Tadahiro Iimura[SUP] 1 [/SUP]
Affiliations
Abstract
Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is a pandemic as of early 2020. Upon infection, SARS-CoV-2 attaches to its receptor of angiotensin-converting enzyme 2 (ACE2) on the surface of host cells and then is internalized into host cells via enzymatic machineries. This subsequently stimulates immune response factors. Since the host-immune response and severity of COVID-19 vary among individuals, genetic risk factors for severe COVID-19 cases have been investigated. Our research group recently conducted a survey of genetic variants among SARS-CoV-2-interacting molecules across populations, noting near absence of difference in allele frequency spectrum between populations in these genes. Recent genome-wide association studies have identified genetic risk factors for severe COVID-19 cases in a segment of chromosome 3 that involves six genes encoding three immune-regulatory chemokine receptors and another three molecules. The risk haplotype seemed to be inherited from Neanderthals, suggesting genetic adaptation against pathogens in modern human evolution. Therefore, SARS-CoV-2 uses highly conserved molecules as its virion interaction, whereas its immune-response appears to be genetically biased in individuals to some extent. We herein review the molecular process of SARS-CoV-2 infection with adding our further survey of genetic variants of its related immune effectors. We also discuss aspects of modern human evolution.
Keywords: COVID-19; genetic variant; human evolution.
. 2021 Feb 17.
doi: 10.1111/dgd.12717. Online ahead of print.
Genetic variation analyses indicate conserved SARS-CoV-2-host interaction and varied genetic adaptation in immune-response factors in modern human evolution
Ji-Won Lee[SUP] 1 [/SUP], In-Hee Lee[SUP] 2 [/SUP], Takanori Sato[SUP] 1 [/SUP], Sek Won Kong[SUP] 2 3 [/SUP], Tadahiro Iimura[SUP] 1 [/SUP]
Affiliations
- PMID: 33595856
- DOI: 10.1111/dgd.12717
Abstract
Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 is a pandemic as of early 2020. Upon infection, SARS-CoV-2 attaches to its receptor of angiotensin-converting enzyme 2 (ACE2) on the surface of host cells and then is internalized into host cells via enzymatic machineries. This subsequently stimulates immune response factors. Since the host-immune response and severity of COVID-19 vary among individuals, genetic risk factors for severe COVID-19 cases have been investigated. Our research group recently conducted a survey of genetic variants among SARS-CoV-2-interacting molecules across populations, noting near absence of difference in allele frequency spectrum between populations in these genes. Recent genome-wide association studies have identified genetic risk factors for severe COVID-19 cases in a segment of chromosome 3 that involves six genes encoding three immune-regulatory chemokine receptors and another three molecules. The risk haplotype seemed to be inherited from Neanderthals, suggesting genetic adaptation against pathogens in modern human evolution. Therefore, SARS-CoV-2 uses highly conserved molecules as its virion interaction, whereas its immune-response appears to be genetically biased in individuals to some extent. We herein review the molecular process of SARS-CoV-2 infection with adding our further survey of genetic variants of its related immune effectors. We also discuss aspects of modern human evolution.
Keywords: COVID-19; genetic variant; human evolution.