The supportive role of complement in HIV pathogenesis

• Published in: Immunological reviews Vol. 180; no. 1; pp. 168 - 176
• Main Authors: Stoiber, H., Kacani, L., Speth, C., Würzner, R., Dierich, M. P.
• Format: Journal Article
• Language: English
• Published: Copenhagen Munksgaard International Publishers 01-04-2001
• Subjects: AIDS Dementia Complex - immunology; AIDS Dementia Complex - virology; AIDS-Related Opportunistic Infections - microbiology; Anaphylatoxins - physiology; Animals; Antiretroviral Therapy, Highly Active; Brain - immunology; Brain - virology; Candida albicans - chemistry; Candida albicans - immunology; Candida albicans - pathogenicity; Candidiasis - etiology; Candidiasis - microbiology; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - virology; Complement C3 - immunology; Complement C3 - metabolism; Complement Pathway, Classical; Complement System Proteins - physiology; Dendritic Cells - immunology; Dendritic Cells - virology; Disease Susceptibility; Germinal Center - immunology; HIV - metabolism; HIV - pathogenicity; HIV Infections - etiology; human immunodeficiency virus; Humans; Macrophages - virology; Molecular Mimicry; Mucous Membrane - immunology; Mucous Membrane - virology; Opsonin Proteins - immunology; Opsonin Proteins - metabolism; Phagocytosis; Protein Binding; Substance Abuse, Intravenous; Trypanosoma - chemistry; Trypanosoma - immunology; Trypanosoma - pathogenicity; Trypanosomiasis - etiology; Trypanosomiasis - parasitology; Viremia - immunology; Virulence
• ISSN: 0105-2896; 1600-065X
• DOI: 10.1034/j.1600-065X.2001.1800115.x

This review focuses on interactions of HIV with the first‐line defence of native immunity, the complement system. In all body compartments tested so far, HIV meets complement. Activation of the complement system results in deposition of C3 fragments on the viral surface, but in contrast to other pathogens, most of HIV is not or is only poorly lysed by membrane attack complexes. To survive complement‐mediated lysis, HIV has not only developed resistance mechanisms, but uses opsonisation with complement fragments for its own advantage. Opsonised virions interact with complement receptor‐expressing cells, which are either subsequently infected with high efficiency or retain viral particles on their surface, which promotes transmission of virus to other permissive cells. Our knowledge of these mechanisms has increased enormously over the past few years. A complete understanding of these complex interactions of HIV with the complement system opens new perspectives for development of alternative therapeutic strategies.
We like to thank Anke Stoiber for secretarial support. This work was supported in part by grants from the FWF (P14070‐MED; P13182‐MOB), the OENB (Jubiläumsfonds Nr. 8504), the 5th Frame Work of the EU (QLK 2‐1999‐01215), the State of Tyrol and Federal Ministeries.