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) exploits the complement system to reach maximal spread of infection. HIV has adapted many strategies to avoid complement-mediated lysis and uses the opsonization with complement fragments for attachment to complement receptors (CR). From the pathogen's perspective, binding to CR-expressing cells is remarkably beneficial, bringing together virus and activated target cells that are highly susceptible to infection. Moreover, complement-mediated trapping on CR+ cells permits HIV to infect surrounding cells even in the presence of an excess of neutralizing antibodies. Thus, complement activation initiates the assumption of power over the host's immune system by HIV and thus augments viral spread and replication throughout the body. On the other hand, natural hosts of primate lentiviruses, such as sooty mangabeys, African green monkeys and chimpanzees, are generally considered to be resistant to the development of AIDS, despite persistent viral replication. This review focuses on the possible link between the resistance to disease and species-specific diversity in function of human and monkey complement system.