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HIV and complement: role of the complement system in HIV infection
P Marschang1, C F Ebenbichler, M P Dierich
1Institut für Hygiene, Innsbruck, Austria.
International Archives of Allergy and Immunology
|January 1, 1994
Summary
Human immunodeficiency virus (HIV) activates the complement system, enhancing its infectivity and targeting specific cells. This interaction modifies complement pathways and receptor expression in infected patients.
Area of Science:
- Immunology
- Virology
- Complement System Biology
Background:
- Human immunodeficiency virus (HIV) differs from animal retroviruses by resisting lysis in human serum.
- Despite resistance to lysis, HIV and HIV-infected cells effectively activate the complement system.
- Complement activation involves both classical and alternative pathways, initiated by viral components like gp41 and cell surface interactions.
Purpose of the Study:
- To investigate the intricate relationship between HIV and the human complement system.
- To elucidate the mechanisms by which HIV activates complement pathways.
- To understand how complement interaction influences HIV infectivity and cellular targeting.
Main Methods:
- Analysis of complement activation pathways (classical and alternative) by HIV and infected cells.
- Investigation of viral protein interactions (gp41) with complement components (C1q).
- Assessment of complement-opsonized HIV's infectivity for cells expressing complement receptors (e.g., C3 fragment receptors).
Main Results:
- HIV activates the classical complement pathway via gp41 binding to C1q.
- Both classical and alternative pathways are activated on the surface of HIV-infected cells.
- Complement-treated HIV exhibits enhanced infectivity, particularly for cells with C3 fragment receptors, facilitating targeting to cells like follicular dendritic cells.
- HIV-infected cells coated with complement interact with complement receptor-bearing cells, potentially spreading infection or causing cell destruction.
- HIV infection leads to a persistently activated complement system and altered expression of complement receptors and regulatory molecules in patients.
Conclusions:
- HIV actively engages and manipulates the complement system for its lifecycle.
- Complement activation by HIV can paradoxically enhance viral infectivity and mediate cellular targeting.
- The interplay between HIV and complement contributes to viral spread and pathogenesis, with significant implications for immune response modulation in infected individuals.