Our new study reveals that our immune system does more than defend against viruses. In certain cases, it induces mutations within viruses that make them easier to recognize later on. The findings have been published in Nature Communications.
During the COVID-19 pandemic, an unprecedented amount of genetic data became available on the SARS-CoV-2 virus, allowing researchers to analyse in exceptional detail how the pathogen changed over time. The study shows that a substantial portion of mutations in the viral genome are not random errors or viral strategies, but are instead caused by the human body’s own APOBEC enzymes.
These enzymes are part of the early, non-specific immune response, and they can chemically modify the genetic material of viruses. According to our results, the mutations they introduce do not typically weaken immune recognition — in fact, they often enhance it. They generate changes in viral proteins that are more easily detected by HLA molecules, the immune system’s key antigen-presenting components that reveal hidden, infected cells to T-cells.
We analysed thousands of SARS-CoV-2 protein variants and found that APOBEC-associated mutations lead to better HLA binding and stronger T-cell activation — ultimately improving the effectiveness of the immune response.
The phenomenon is not limited to the coronavirus: similar APOBEC-driven patterns have been observed in other viruses as well. As HLA types vary significantly among individuals, the findings may also open new avenues in personalized medicine.
