Influence of inflammatory markers on HIV pathogenesis

Abstract

HIV infection can now be treated effectively with combination antiretroviral medications, and mortalities due to AIDS have been greatly reduced. The increase in the number of deaths and incidences of heart and liver diseases in people whose CD4 counts are above 200 is evidence that there is more happening inside the body than just the cell counts and viremia. HIV infection induces chronic inflammation and immune activation which predisposes patients to cardiovascular diseases (CVD). The objective of this study was to determine the prevalence of risk factors for CVD among HIV-infected people, and to investigate any association between such risk factors, stage of HIV disease, and use of antiretroviral therapies among HIV-positive outpatients at an HIV treatment clinic in Harare, Zimbabwe. To achieve this there was need to look at the lipid profiles, markers of inflammation and markers of endothelial dysfunction, to get a picture of what will be taking place with or without optimal virologic control by HAART. We compared three groups namely HIV unexposed and uninfected, HIV patients on highly active antiretroviral therapy (HAART) and HIV infected but HAART naïve. The population was controlled for traditional risk factors that are confounding factors of CVD. All participants had average lipid and glucose values within normal ranges, but there was a small difference between the ART and ART naive- for total cholesterol (TC) and high-density lipoprotein (HDL).IL-6 levels were elevated in HIV infected patients compared to healthy controls, and higher in HAART naïve patients than those on HAART. We did not find significant differences in TNF-α levels by HIV or ART status There were high levels of plasmatic VCAM and ICAM in HAART naïve patients compared to those on HAART. Results showed that HIV infection leads to an inflamed environment and endothelial damage, which is optimally controlled by HAART but still does not normalise. These markers of immune activation together with information on lipid profiles can be used to predict the risk for CVD in HIV patients. Framingham risk showed 1.4% prevalence of high CHD risk within the next ten years.