Complement-dependent control of viral dynamics in pathogenesis of human immunodeficiency virus and simian immunodeficiency virus infection

Since the first contact with the host, human immunodeficiency virus (HIV) e xploits the complement system to reach maximal spread of infection. HIV has adapted many strategies to avoid complement-mediated lysis and uses the op sonization with complement fragments for attachment to complement receptors (CR). From the pathogen's perspective, binding to CR-expressing cells is r emarkably beneficial, bringing together virus and activated target cells th at are highly susceptible to infection. Moreover, complement-mediated trapp ing on CR+ cells permits HIV to infect surrounding cells even in the presen ce of an excess of neutralizing antibodies. Thus, complement activation ini tiates the assumption of power over the host's immune system by HIV and thu s augments viral spread and replication throughout the body. On the other h and, natural hosts of primate lentiviruses, such as sooty mangabeys, Africa n green monkeys and chimpanzees, are generally considered to be resistant t o the development of AIDS, despite persistent viral replication. This revie w focuses on the possible link between the resistance to disease and specie s-specific diversity in function of human and monkey complement system. (C) 2001 Elsevier Science Ltd. All rights reserved.