[Gastrointestinal manifestations of HIV infection]

The intestinal (in particular rectal) mucosa is the main portal of entry for HIV in homosexual men, who represent the vast majority of HIV-infected patients in Europe and North America. There are several possibilities for HIV to reach the CD4-positive T cells, macrophages and follicular-dendritic cells in the intestinal mucosa. HIV may be transported through M-cells directly to mucosal lymph follicles. Alternatively HIV may infect enterocytes via Fc-receptor by antibody-bound HIV or via a CD4-independent receptor. By successive budding on the basolateral side of the enterocytes HIV may be released into the lamina propria. The loss and functional impairment of activated CD4-positive lamina propria T-cells could be responsible for both the decreased immune defense and altered structure and function of the mucosa. The common intestinal symptoms in HIV-infected patients may be caused by a variety of mechanisms. The high number of secondary opportunistic or non-opportunistic infections and secondary malignancies of the gut may be responsible for the observed symptoms. However, the pathogenic relevance of some of these pathogens is questionable since there is often no correlation between symptoms and presence of the pathogen. In addition, there is a considerable percentage of symptomatic patients without identifiable microorganisms. Yet unidentified pathogens, small intestinal bacterial overgrowth, damage of intestinal nerve fibres, or secretory diarrhea may contribute to the pathogenesis of gastrointestinal symptoms. The findings of a pathogen-negative diarrhea, of HIV-infected mononuclear cells in the gut, and of epithelial hypoproliferation and enterocyte dysmaturation is in agreement with the hypothesis that there is an enteropathy caused by HIV itself.