Revista de SIDA e investigación clínica

A New Controversial Pathophysiology Confirms that HIV does not Kill the CD4+ T-Cell But Mutates Its Physiological Behavior Becoming an Unaccountable CD8+ T-Cell

Abstract

Salah Sh, Ghaleb HA, Sara Saad and Nada Sherif

HIV pathogenesis is known to cause a progressive depilation of CD4+ T-cell cell population in close association with progressive impairment of cellular immunity and increase the susceptibility to infection. This new study is giving a new explanation about the mode of action of this virus. We assume that there is an alteration in the physiological behavior of CD4+ T-cells causing it to mutate to CD8+ T-cells and that CD4+ T-cell are neither destroyed nor lost during the infection. Twelve consenting adults took part in a randomized control trail, six were tested positive for HIV and had never received any antiretroviral therapy while the other six were tested negative. Blood samples withdrawn from participants were tested for total CD4+ T-cells and CD8+ T-cells .Infected cells from HIV positive patients were stimulated with a purified recombinant HIV-1 p17 matrix as a viral protein along with other immunological assays. The collected data showed that the sum of both CD4+ T-cells and CD8+ T-cells did not change in HIV positive patients, although there were a decrease in CD4+ T-cells and an increase in CD8+ T-cell count. Our study confirms that CD8+ T-cells is responsible for the increase in scope of HIV and the susceptibility to (OI), we assumed that this resulted from the duplication in cell signals of both newly formed (mutant) and originally found CD8+ T-cells causing a complete cellular discrepancy. According to our findings a new area of medications could arise to be a promising therapeutical modality for treating HIV-1 infection.