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Role of complement in HIV infection
H Stoiber1, A Clivio, M P Dierich
1Institut für Hygiene, Innsbruck, Austria. Stoiber.hygiene@uibk.ac.at
Annual Review of Immunology
|January 1, 1997
Summary
Human Immunodeficiency Virus (HIV) uses complement regulatory molecules to evade immune destruction, enhancing its infectivity. Blocking these interactions offers a potential therapeutic strategy against HIV.
Area of Science:
- Immunology
- Virology
- Molecular Biology
Background:
- Human Immunodeficiency Virus (HIV) activates the human complement system in plasma, even without antibodies.
- Complement activation, if unchecked, leads to viral lysis (virolysis), which is detrimental to HIV.
Purpose of the Study:
- To investigate how HIV evades complement-mediated destruction.
- To explore the role of complement regulatory molecules in HIV pathogenesis.
- To identify potential therapeutic targets for overcoming HIV's resistance to complement.
Main Methods:
- Analysis of complement regulatory molecules on HIV virions.
- Investigation of HIV's interaction with complement components like factor H.
- Testing the efficacy of monoclonal antibodies against factor H recruitment.
Main Results:
- HIV incorporates complement regulatory molecules, such as Decay-Accelerating Factor (DAF/CD55) and factor H, to resist complement-mediated lysis.
- HIV leverages complement interactions to enhance infectivity, facilitate follicular localization, and broaden its target cell range.
- Monoclonal antibodies that inhibit factor H binding to HIV can overcome viral resistance to complement lysis.
Conclusions:
- HIV employs sophisticated strategies involving complement regulatory proteins to ensure its survival and propagation.
- Targeting the interaction between HIV and factor H presents a promising therapeutic avenue for combating HIV infection.