Antiretroviral therapy (ART) limits the level of HIV infection in the blood to very low levels. Them
A team of researchers from George UniversityWashington found that ART can only suppress the infection and prevent its further transmission. But HIV changes the genetic behavior of immune cells, and here it is powerless. Pro-inflammatory genes in these cells continue to be expressed.
Thus, regardless of whether it containscell protein of the human immunodeficiency virus or is free from it after ARS, then it is likely to be constantly exposed to inflammation. “Inflammation is a critical component of many, if not most, diseases associated with controlled HIV infection. Basically, we're talking about cardiovascular and neurocognitive disorders,” explains Michael Bukrinski, lead researcher and professor of microbiology at George Washington University.
Scientists cultured some immune cells inlaboratory and then divided them into two groups. The cells were first exposed to an HIV protein called Nef. They received the same dose of Nef that is seen in cells from patients with controlled HIV infection (the amount of virus is so low that it cannot be detected in a viral load test).
The researchers then exposed cells from both groupsexposure to a bacterial toxin to record the difference in their immune response. They noticed high levels of inflammatory proteins (cytokines) and also identified activated pro-inflammatory genes in the first group of cells.
On the other hand, immune cells that do notexposed to Nef, no similar behavior was observed. These data support immunological memory (or trained immunity) resulting from HIV infection and its role in inflammation.
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Credit: CDC/C. Goldsmith, P. Feorino, E. L. Palmer, W. R. McManus