The Lipoprotein Profile in HIV Infected Patients

Infection can change plasma lipoproteins by increasing the triglycerides and decreasing the cholesterol plasma levels. This process is thought to be the result of alterations in lipoprotein metabolism produced by cytokines that mediate the immune response, including tumor necrosis factor, interleukin-1 and the interferons. The acquired immunodeficiency syndrome (AIDS) has been shown to be accompanied by increased plasma triglyceride levels and a trend toward decreased plasma cholesterol levels. Plasma low density lipoprotein (LDL) patterns are also changed by infection and patients with AIDS have increased levels of small dense LDL particles. Decreases in high density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I, and an increase in lipoprotein (a) [Lp(a)] are the usual lipidic disorders during HIV infection, even in those patients with CD, lymphocyte counts above 400 cells/ mm(3). Plasma lipoproteins possess well-recognized transport functions. Certain classes of these lipoproteins can also regulate selected metabolic functions of a variety of cell types. Among these bioregulatory properties is the regulation of lymphocyte function and regulation of immune response. Thus, a number of immune functions may be significantly influenced by the lipoprotein alterations present in AIDS. Furthermore, the decreased HDL-C and increased triglycerides and Lp(a) are associated with an increased risk of myocardial infarction and some cardiovascular events have been reported in HIV positive individuals. This paper describes lipoprotein alterations during HIV infection, and evaluates their relationship to immune function and atherogenic profile.