Could the CCR5-Delta32 mutation be protective in SARS-CoV-2 infection?
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
34913355
PubMed Central
PMC8884372
DOI
10.33549/physiolres.934725
PII: 934725
Knihovny.cz E-resources
- MeSH
- COVID-19 genetics immunology mortality virology MeSH
- Phenotype MeSH
- Gene Frequency MeSH
- Genetic Predisposition to Disease MeSH
- Host-Pathogen Interactions MeSH
- Humans MeSH
- Mutation * MeSH
- Protective Factors MeSH
- Prevalence MeSH
- Receptors, CCR5 genetics MeSH
- Risk Factors MeSH
- SARS-CoV-2 immunology pathogenicity MeSH
- Severity of Illness Index MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Geographicals
- Europe epidemiology MeSH
- Names of Substances
- CCR5 protein, human MeSH Browser
- Receptors, CCR5 MeSH
Increasing evidence points to host genetics as a factor in COVID-19 prevalence and outcome. CCR5 is a receptor for proinflammatory chemokines that are involved in host responses, especially to viruses. The CCR5-delta32 minor allele is an interesting variant, given the role of CCR5 in some viral infections, particularly HIV-1. Recent studies of the impact of CCR5-delta32 on COVID-19 risk and severity have yielded contradictory results. This ecologic study shows that the CCR5-delta32 allelic frequency in a European population was significantly negatively correlated with the number of COVID-19 cases (p=0.035) and deaths (p=0.006) during the second pandemic wave. These results suggest that CCR5-delta32 may be protective against SARS-CoV-2 infection, as it is against HIV infection, and could be predictive of COVID-19 risk and severity. Further studies based on samples from populations of different genetic backgrounds are needed to validate these statistically obtained findings.
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