They find mutations that reduce cellular immunity against a primary SARS-CoV-2 infection

An investigation carried out by a team from the National Center for Microbiology (CNM) of the Carlos III Health Institute (ISC III) exposes the possible risk of immune escape in minority populations whose genetic characteristics may reduce their ability to fight disease. primary infection by SARS-CoV-2.

The work studies the cellular response mediated by CD8+ Lymphocytesimmune cells that play a central role in a first natural infection – that is, the first time the infection is suffered – rather than vaccine-induced protection, which, as two recent studies from the same center have concluded, are effective against omicron and other variants of this coronavirus.

Thus, people who do not have these mutations, have already had the disease and, in addition, are vaccinated, would not be at greater risk. These results are published today in the journal Computational Biology PLOS.

People in these subpopulations may be at higher risk of a first SARS-CoV-2 infection if they do not have the effective extra antibody response generated by vaccines.

The survey is especially useful for gaining new insights into the response to contagion in groups with limited cellular responseshow could it be some small Sub-Saharan and Far Eastern Subpopulations. People in these subpopulations may have increased risk of a first infection by SARS-CoV-2 if they do not have the effective extra antibody response generated by the vaccines.

The study reveals how massive computational analysis of virus genomes and human genetics can reveal which people or population groups are most at risk of this infection escaping infection. cellular immunity even with few mutations.

For this, algorithms were used to identify epitopes −the parts of the virus recognized by the immune system− dependent on human variants of class I histocompatibility genes (or alleles), and how mutations invalidate these epitopes in an allele-dependent human manner.

Worst ‘cards’ to fight primary infection

Antonio Javier Martin GalianoCNM scientist and lead author of the study, explains: “Genetic differences between human populations are sometimes significant, which can cause the cellular pathway of the immune system to respond differently to viral infections.”

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“Viruses such as SARS-CoV-2 generally do not mutate enough to completely evade the cellular response in most of the world’s population, but they can sometimes take advantage of specific limitations in some subpopulations,” adds the expert.

The presence of certain viral mutations would further reduce the cellular immunity of these individuals, who could still have the so-called humoral immunity −generated by antibodies−. “We can say that these people, with certain genetic characteristics, have worse initial cards to defend themselves against infection, even when they are in good initial health”, says Martín Galiano.

Viral mutations facilitate the presence of escape epitopes, capable of evading recognition by the immune system

Localized viral mutations facilitate the presence of escape epitopesthat is, the parts of the virus that the immune system recognizes to try to stop the infection increase its ability to evade this recognition and, therefore, hinder the effectiveness of the defenses.

Therefore, despite the very low probability that SARS-CoV-2 mutations cause the virus to evade the immune system’s reaction in the vast majority of the world’s immunocompetent population, there are small populations in which certain viral mutations could be selected for, the that would increase the risk of local outbreaks with worse prognosis.

“This type of work confirms that the integration of genomic, geographic and immunoinformatic information facilitates the surveillance of variants that can affect both the world population and small subpopulations”, concludes the Spanish researcher.


foix and others. (2022) “Predicted impact of viral mutational scenario on cytotoxic response against SARS-CoV-2”. Computational Biology PLOS.

Rights: Creative Commons.

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