Schneider T, Ullrich R, Zeitz M
Abteilung für Innere Medizin mit Schwerpunkt Gastroenterologie, Medizinische Klinik und Poliklinik, Klinikum Steglitz der Freien Universität Berlin.
Z Gastroenterol. 1994 Mar;32(3):174-81.
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.
肠道(尤其是直肠)黏膜是同性恋男性中HIV的主要进入门户,而同性恋男性占欧洲和北美绝大多数HIV感染患者。HIV有多种途径可接触到肠道黏膜中的CD4阳性T细胞、巨噬细胞和滤泡树突状细胞。HIV可能通过M细胞直接转运至黏膜淋巴滤泡。或者,HIV可能通过抗体结合的HIV经由Fc受体或通过不依赖CD4的受体感染肠上皮细胞。通过在肠上皮细胞基底外侧连续出芽,HIV可能释放到固有层。活化的固有层CD4阳性T细胞的丢失和功能受损可能是免疫防御下降以及黏膜结构和功能改变的原因。HIV感染患者常见的肠道症状可能由多种机制引起。肠道大量的继发性机会性或非机会性感染以及继发性恶性肿瘤可能是观察到的症状的原因。然而,其中一些病原体的致病相关性值得怀疑,因为症状与病原体的存在之间往往没有关联。此外,有相当比例的有症状患者未发现可识别的微生物。尚未明确的病原体、小肠细菌过度生长、肠神经纤维损伤或分泌性腹泻可能导致胃肠道症状的发病机制。病原体阴性腹泻、肠道中HIV感染的单核细胞以及上皮细胞增殖不足和肠上皮细胞发育异常的发现与HIV本身引起肠病的假说一致。