A new study by the HUN-REN Biological Research Center in Szeged shows that our immune system not just defends against viruses, but it can trigger mutations that make them easier to detect later. This discovery could open up new perspectives in the development of vaccines and personalized therapies, the HUN-REN Hungarian Research Network reported on its website.
During the COVID-19 pandemic, a huge amount of genetic data has been collected on the SARS-CoV-2 virus, allowing researchers to study the pathogen’s changes over time in detail. Previous research has shown that certain mutations in SARS-CoV-2 serve to evade immunological recognition, i.e., to make the virus “invisible.” However, the current study, published in the journal Nature Communications, observed the opposite effect through a special mechanism. HUN-REN researchers have found that a significant proportion of the mutations occurring in the virus’s genetic material are caused by molecules in our body called APOBECs.
APOBEC enzymes are part of the early, non-specific immune response and are capable of altering the genetic code of viruses.
In fact, the new research has found that the mutations caused by these molecules generally do not weaken but strengthen the subsequent immune response.
This is because they create protein changes that are more easily detected by the immune system, meaning that the rapid immune response helps the subsequent specific response to work more effectively.
Fact
A significant proportion of SARS-CoV-2 mutations were not a result of chance, but by a family of proteins in the human immune system that play an important role in defense, the APOBEC3 enzymes. These enzymes chemically modify the virus’s genetic material: they replace a building block called cytosine (C) with uracil (U), thereby altering the virus’s proteins.
The researchers examined the proteins of thousands of SARS-CoV-2 variants and found that APOBEC-related mutations lead to better HLA binding (the process by which viral fragments are displayed to immune cells) and stronger T-cell activation (when the immune system switches on its defense against a virus), resulting in better overall immune recognition. This result was confirmed by an analysis of a large database of over 17,000 British COVID-19 patients.
“This discovery sheds light on a completely new phenomenon in the relationship between our body and viruses: the immune system not only responds to viruses, but also exerts a kind of genetically encoded pressure on them, that makes them easier to recognize in the long term,” explained Gergő Balogh, the study’s first author.
The phenomenon can be observed not only in relation to the coronavirus, but also to other viruses, and due to individual HLA differences, it may open up new possibilities in personalized medicine.
The mutation patterns created by APOBEC activity can predict, even in the early stages of a pandemic, what new protein variants may appear in the virus. This knowledge could be crucial in vaccine development and the design of personalized therapies.
The research was led by Máté Manczinger and Gergő Balogh with the professional support of academics Csaba Pál and Balázs Papp, while the experimental work was supervised by Gábor Szebeni.
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Via hun-ren.hu, Featured image: Pixabay
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