REGULATION OF IgE SYNTHESIS IN AIDS

Abstract

HIV infection alters the immune responses of infected persons, not only directly by infecting immune cells, resulting in the loss of CD4+ T lymphocytes but also indirectly, by triggering host immune responses to the virus. Survival of HIV infection has been improved with advances in antiretroviral therapy and in prophylaxis for opportunistic infection (OI). Some patients have more rapid progression of disease than others in spite of optimal therapy, however. It is thought that a combination of factors, including viral characteristics, genetic factors, and host immune responses, affect the person's ability to survive with HIV infection. As time of survival has increased and HIV infection has become a more chronic disease, observations relating to an increased incidence of atopic disease in persons with HIV infection have been made. The relationship between allergic rhinitis, drug reactions, asthma, skin rashes, and AIDS is reviewed elsewhere in this issue. Many investigators have reported elevated IgE levels in AIDS patients. This article reviews the normal regulation of IgE synthesis and will explore the pathophysiology behind elevated IgE levels in some patients with HIV infection. The pattern of immune response that results in elevated IgE and its relation to the length of survival for subjects with HIV infection is presented.