Marschang P, Ebenbichler C F, Dierich M P
Institut für Hygiene, Innsbruck, Austria.
Int Arch Allergy Immunol. 1994;103(2):113-7. doi: 10.1159/000236616.
HIV, in contrast to animal retroviruses, is not lysed by human serum but nevertheless the virus as well as virus-infected cells activate the complement system efficiently. HIV activates the classical pathway by binding C1q to the transmembrane protein gp41. On the surface of HIV-infected cells, both the alternative and the classical pathway are activated. Complement-treated HIV has an enhanced ability to infect cells carrying receptors for C3 fragments. By this mechanism complement can target the virus to certain cells, e.g. follicular dendritic cells. HIV-infected complement-coated cells can interact with complement receptor carrying cells and thereby spread the infection or cause the destruction of the infected cells. Due to direct or indirect effects of HIV the complement system is in an activated state and the cellular expression of complement receptors as well as regulatory molecules is modified in the blood of HIV-infected patients.
与动物逆转录病毒不同，人类血清不会裂解HIV，但该病毒以及受病毒感染的细胞却能有效地激活补体系统。HIV通过将C1q与跨膜蛋白gp41结合来激活经典途径。在HIV感染细胞的表面，替代途径和经典途径都会被激活。经补体处理的HIV感染携带C3片段受体细胞的能力增强。通过这种机制，补体可将病毒靶向某些细胞，如滤泡树突状细胞。被HIV感染的补体包被细胞可与携带补体受体的细胞相互作用，从而传播感染或导致被感染细胞的破坏。由于HIV的直接或间接作用，补体系统处于激活状态，HIV感染患者血液中补体受体以及调节分子的细胞表达会发生改变。
