Viral load in infection determines the evolution of HIV – 01/10/2024 – Health

Viral load in infection determines the evolution of HIV – 01/10/2024 – Health

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HIV (human immunodeficiency virus) is known to recombine and thus manage to escape the hosts’ immune system, also evading the action of drugs and antibodies.

This is one of the reasons why it is so difficult to obtain an anti-HIV vaccine, precisely because the same infected individual can carry dozens of different variants.

But the relationship between recombinant forms of HIV in the human body and viral load during infection has never been fully understood. Until now.

A new study has identified an association between the highest viral load in an individual and the rate of virus recombination. This would be one of the agents of viral evolution.

The research, written by Elena Romero, from the Department of Genomic Sciences at the University of Washington, and Alison Feder, from the Fred Hutchinson Cancer Center (Seattle), was published this Wednesday (10) in the journal Molecular Biology and Evolution.

The authors started with a hypothesis based on studies observed in laboratory animals and organs in plaques, where the co-infection of multiple variants of the virus in cells favors the recombination of these different forms of the virus. Recombination is the mixing of genetic material from two or more strains of HIV, resulting in greater genetic variability.

The other way to increase diversity is through mutations that occur with the replication of the virus in cells, which occurs at rates already well known to scholars.

According to research, in individuals with a higher viral load, the variety of HIV populations in different cells (called virions) contributes to the emergence of new variants. This helps determine the evolution of the virus, with the emergence of forms that can more effectively escape the action of antiretroviral cocktails.

The study found a recombination rate in individuals with a high viral load up to six times higher than that observed in normal virus samples.

They then compared the viral load of ten people living with HIV for 6 to 12 years and who had the virus rate in their bodies measured periodically. Participant 1, indicated as the one with the highest viral load, presented the greatest genetic variety of HIV strains in the body; the same was observed with participants 3, 4 and 7, who also had high viral loads.

It is important to note that people living with HIV also have a different viral load in their bodies over time, which will depend, for example, on whether the virus is controlled by antiviral drugs, the time since infection, among others.

The technique presented in the study can help in the development of new, more effective tests for detecting viral load and HIV variants present in the body.

Confirming observations from other in vitro (laboratory) studies, the research is the first evidence of how intra-host variation (within the same individual) is a determining factor in viral recombination in humans.

The researchers reinforce, however, that the association found is correlational, but it is not possible to determine a causal association, since the factors that lead to genetic variability cannot be explained solely by the number of copies of HIV.

The study also included a small number of participants (10), who, although not undergoing treatment, have the virus controlled in their bodies, which may also point to avenues for research into HIV remission.

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