Immunologic Response to HIV Infection: Main Immunopathological Alterations

Abstract

The intense degradation of defense cells caused by the human immunodeficiency virus (HIV) in an organism and the speed at which the viral genome mutates to escape the initial immune response are the prime difficulties in combating opportunistic diseases and in creating an efficient vaccine for this virus. The common opportunistic diseases observed for HIV positive patients include tuberculosis, candidiasis and toxoplasmosis. One of the risk factors is the decrease in CD4+ T-lymphocyte count and the high plasmatic viral load, rendering the organism susceptible to these pathogens. Despite the effectiveness of antiretroviral therapy, this does not provide total elimination of the virus, only eliminating the virus present in the plasma. On treatment withdrawal, the infected latent CD4+ T-cells can re-establish the infection, conferring a large barrier to definitive HIV cure. Current studies have evaluated the inhibition of class I histone diacetylase (HDAC) enzymes as a strategy to induce the viral gene expression and, consequently, the gradual emptying of latent reservoirs of the virus, improving the action of antiretroviral therapy. Thus, the monitoring of immune activation and counting of CD4+ T-lymphocytes are of fundamental importance to the prognosis of HIV patients, along with early diagnoses of opportunistic diseases, in order to avoid complications from these diseases.