In human plasma, HIV activates the complement system, even in the absence of specific antibodies. Complement activation would, however, be harmful to the virus if the reactions were allowed to go to completion, since their final outcome would be virolysis. This is avoided by complement regulatory molecules, which either are included in the virus membrane upon budding from the infected cells (e.g. DAF/CD55) or are secondarily attached to HIV envelope glycoproteins as in the case of factor H. By using this strategy of interaction with complement components, HIV takes advantage of human complement activation for enhancement of infectivity, for follicular localization, and for broadening its target cell range at the same time that it displays an intrinsic resistance against the lytic action of human complement. This intrinsic resistance to complement-mediated virolysis can be overcome by monoclonal antibodies inhibiting recruitment of human factor H to the virus surface, suggesting a new therapeutic principle.


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  • Article Type: Review Article
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