Human immunodeficiency virus infection and the intestine

HIV is a retrovirus infecting CD4-positive cells causing profound immunosuppression, eventually clinically manifest as AIDS. The cells principally infected by HIV are T4 lymphocytes (helper) and macrophages. The eventual loss of helper cell function is the prime reason for immunodeficiency which renders the individual susceptible to opportunistic infections. HIV infection was first described in male homosexuals. However, the trend now is for seroprevalence to rise rapidly in intravenous drug abusers in the West. In addition, African AIDS is thought to be almost exclusively heterosexual in nature, a paradox which is not yet fully explained in comparison with the relatively low but increasing incidence in heterosexuals in the Western world. Virtually every organ system in the body can be affected clinically during the course of HIV infection. The gastrointestinal tract is a major target, and the physiological sequelae are an important cause of morbidity and mortality. The pathophysiology of intestinal infection is not yet fully understood, however two main mechanisms have been postulated. The first is reduced intestinal immunity resulting in chronic opportunistic infections, which themselves caused altered intestinal function. The second is that HIV itself affects the intestinal mucosa, causing malfunction. The mechanisms by which the latter occurs are controversial but may result from either direct infection of mucosal epithelial cells or macrophages within the mucosa. Reports have documented the presence of HIV genome in both epithelial argentachromaffin cells and macrophages. In addition, profound degeneration of intrinsic jejunal autonomic neurones has been demonstrated, but the functional significance of such denervation is as yet unknown. The clinical stage of HIV infection at which intestinal mucosal immunity fails is by definition when opportunistic infection occurs (that is, clinical progression to stage IV disease), namely AIDS, however a detailed knowledge of the mechanisms of intestinal immune failure are lacking.