New anti-cancer drugs will help kill HIV cells

The study of the possibilities of clinical trials for the treatment of cancer gives all grounds to assume their effectiveness in the fight against latent HIV infection in patients undergoing antiretroviral therapy (ART), a suppressive virus.

Despite the fact that antiretroviral therapy helps to significantly reduce the level of mortality from HIV globally, the search for medicines for the complete elimination of this disease continues.

A group of scientists from the SBP Institute of Medical Research (La Hoya, California) used anti-cancer drugs of the SMAC class of mimetics (imitators of the secondary mitochondrial caspase-endogenous protein stimulating apoptosis of cancer cells) to suppress "sleeping" cells of the human immunodeficiency virus in HIV-infected treatment with the help of antiretroviral drugs that only slow the progression of HIV infection.

Standard antiretroviral drugs work to prevent the multiplication of HIV cells and give the body's immune system the ability to prevent other infections. However, HIV has never been completely eradicated by ART. And the problem of HIV treatment is that after stopping the use of antiretroviral drugs, some of the resting virus cells are activated, causing a new active stage of the disease.

According to one of the leaders of a new study by Dr. Lars Paschet, scientists are looking for methods for purifying cells in which the immunodeficiency virus "slumbers". The specialists named this approach "shock-striking", but so far no special success has been achieved in its development. The drugs created today - the agents of reversible latency (LRA) - do not give the expected effect, and in some cases stimulate immunity, which leads to death of patients.

The information about the results of a new study published in the American scientific journal Cell Host & Microbe says that scientists have established a link between the increase in HIV activity and the absence of the gene BIRC2 encoding the endogenous inhibitor of programmed cell death (apoptosis), the protein cIAP1. Since anti-cancer SMAC mimetics block the BIRC2 gene, researchers were interested in the potential for these drugs to make the dormant virus "wake up." This would allow him to identify him and subject him to an attack of the immune system.

As scientists note, the virus of immunodeficiency manages to escape from the immune system due to "tightly twisted" DNA. They suggested that SMAC mimetics can be combined with a preparation of the class of histone deacetylase inhibitors Panobinostat (Panobinostat), whose action is to untwist this DNA.

Researchers tested SMAC mimetic BOO-0637142 in combination with Panobinostat on cells taken from HIV-infected patients undergoing ART. And this combination of drugs has awakened HIV cells without activating the immune system. The test with another anticancer SMAC mimetic LCL161 (which only undergoes clinical trials in oncologists) has shown the same result.

Dr. Samit Chanda, co-author of the study, notes that SMAC mimetics plus histone deacetylase inhibitors are a double hit for HIV, much more powerful than reversible latency agents (LRAs). And this gives all grounds to assume that research will be a new step towards addressing the problem of HIV latency.

The immediate plans of the researchers are to combine their efforts with the pharmaceutical company to conduct an appropriate study of the safety and efficacy of combining these drugs on clinical models, before initiating the trial on patients.

In July this year, Medical News Today reported a study that found that HIV cells after antiretroviral therapy are less active than previously thought: only once a week (the results of this study were published in the journal Pathogens).

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