The study, published today in PLOS Genetics by Dr David Morris and Professor Timothy Vyse from the School of Basic & Medical Biosciences, suggests that genetic predisposition for systemic lupus erythematosus (SLE) may have a protective factor.
Researchers compared the genetics of severe COVID-19 with those of SLE using multiple analyses, including an approach that can focus on specific areas of the genome. The authors then accessed data on genes and the structure of the genome obtained from several biomedical databases to understand the biology of the shared genetics.
The researchers found that TYK2, a gene associated with both SLE and severe COVID-19, provides protection against viral infection. However, this also increases risk for autoimmune disease. Future studies will be needed to fully understand
Our results indicate that there are shared genetic effects between the autoimmune disease SLE and the clinical consequences of COVID-19. The locus with the most evidence of shared association (TYK2) is involved in interferon production, a process that is important in response to viral infection and known to be dysregulated in SLE patients. In seeking to uncover the mechanisms underlying these relationships it was apparent that the functional effects of the risk and protective genotypes are complex.– Co-lead author Dr David Morris the School of Basic & Medical Biosciences
Study lead Professor Timothy Vyse added: “This is an exciting result made possible by the large genetic studies in COVID-19 and Lupus, and opens the door to our understanding of how the biology of the immune system is calibrated to protect us against infection from viruses and other infectious agents, but at the risk of developing autoimmune disease.”