Genetic variability in the human immune system may affect susceptibility to and severity of infection by SARS-CoV-2, a novel coronavirus which causes the COVID-19 disease, according to new research.
Colorized scanning electron micrograph of an apoptotic cell (green) heavily infected with SARS-COV-2 virus particles (yellow), isolated from a patient sample. Image credit: NIAID.
Individual genetic variation may explain differences in the strength of immune responses.
Certain immune system genes, called human leukocyte antigen (HLA) genes that are involved in recognizing pathogens, vary from person to person.
Variations can influence how well the immune system recognizes a given pathogen.
Poor recognition of SARS-CoV-2 could cause a person to be more vulnerable to the virus.
“In particular, understanding how variation in HLA — a component of the immune system containing multiple genes — may affect the course of COVID-19 could help identify individuals at higher risk from the disease,” said lead author Dr. Austin Nguyen from Oregon Health & Science University and colleagues.
Individual HLA, haplotype, and full genotype variability likely influence the capacity to respond to SARS-CoV-2 infection, according to the team.
Certain alleles in particular could be associated with more severe infection, as has previously been shown with the SARS-CoV coronavirus.
“This is the first study to report global distributions of HLA types and haplotypes with potential epidemiological ramifications in the setting of the current pandemic,” the researchers said.
“HLA typing can be fast and inexpensive.”
“Pairing HLA typing with COVID-19 testing where feasible could improve assessment of viral severity in the population.”
“Following the development of a vaccine against SARS-CoV-2, individuals with high-risk HLA types could be prioritized for vaccination.”
The findings will be published in the Journal of Virology.
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Austin Nguyen et al. 2020. Human leukocyte antigen susceptibility map for SARS-CoV-2. Journal of Virology, in press; doi: 10.1101/2020.03.22.20040600
This article is based on text provided by the American Society for Microbiology.
