The authors of the study point out that between 4% and 13% of people originating from the African continent have this genetic variant.
An international group of researchers discovered that a genetic variant present in people of African descent infected with HIV-1 can slow the growth of the viruswhich means that the infection caused by it does not get even worse, Murdoch University (Australia) reports this week.
HIV is a virus that weakens the human immune system by destroying cells known as linfocitos CD4, which are responsible for fighting infections caused by other viruses, bacteria and germs. This infectious agent can cause Acquired Immune Deficiency Syndrome (AIDS) when not treated in time, so infected people can contract serious diseases and cancers.
Until 2021, around 38.4 million people with HIV were counted in the world. Despite the fact that medicines to treat the virus have improved considerably since it was first detected, they were reported in the same year at least 650,000 deaths from AIDS-related illnesses.
A new study, recently published in the journal Nature, described the finding of a genetic variant that clustered around a gene on chromosome 1, called ‘CHD1L’, which appears to slow down the replication and transmission of the virus. According to the scientists, this gene is associated with low levels of the virus (viral load) in the most chronic period of infection. In turn, they mentioned that this is the first HIV-related genetic variant found in more than 25 years of research.
How was this genetic variant discovered?
This revelation came to light after evaluating the genetic factors that determine viral load control in 3,879 patients of African descent who are carriers of HIV-1, the most common type of the virus. The authors of the report detail that among he 4% and 13% of people originating from the African continent have this genetic variant.
Although it is still unknown how CHD1L controls the viral load, specialists are confident that further research on this gene may help the development of new treatments for people infected with HIV.
In subsequent experiments, HIV replication was found to increase as a result of CHD1L knockout in macrophages, which are cells specialized for detecting and destroying bacteria and viruses. However, there was no effect on T cells, another type of immune cell, in which HIV also often replicates.
“Although experimental studies suggest that CHD1L is capable of limiting HIV infection in some cell types ‘in vitro’, further research is required to understand the mechanisms underlying our observations,” the researchers concluded.