Enhancing role of complement in HIV infection

Mouhoub, Amal; Thiéblemont, Nathalie; Delibrias, C.; Fischer, Elizabeth; Kazatchkine, Michel D.

doi:10.1111/j.1365-2249.1994.tb06255.x

Cited by 2 publications

(2 citation statements)

References 32 publications

(16 reference statements)

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“…The aim of the present study was to analyze the role of C5a on DC during HIV-1 infection. The virus activated the C system independent of the presence of HIV-1specific antibodies [1][2][3][4] and thereby generated sufficient amounts of functional C5a to recruit iDC. In a next step, the migrating DC efficiently transferred the virus to autologous non-stimulated T cells.…”

Section: Discussionmentioning

confidence: 99%

“…HIV-induced activation of the complement (C) system mediates the N-terminal cleavage of C3, C4 and C5 [1][2][3][4][5][6], and should therefore generate the anaphylatoxins C3a, C4a and C5a. These small C fragments are involved in chemotaxis, cellular adhesion, stimulation of oxidative metabolism, release of lysosomal enzymes and mediators of inflammation, such as histamine and cytokines [7].…”

Section: Introductionmentioning

confidence: 99%

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HIV‐1 induced generation of C5a attracts immature dendriticcells and promotes infection of autologous T cells

et al. 2007

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For the recruitment of dendritic cells (DC) to the site of infection, DC express several sensors for danger signals, such as receptors for C5a. This anaphylatoxin is generated upon complement activation. As HIV-1 triggers the complement cascade, we determined whether C5a is generated by the virus and tested the functional activity of C5a in migration and infection assays. The immature (i)DC responded in migration assays to recombinant C5a and native C5a, which was generated in situ upon activation of the complement system by HIV-1. In combined migration and infection assays, a C5a-dependent enhancement of HIV-1 infection in DC-T cell cocultures was observed. These results indicate that HIV induces generation of C5a and thereby attracts iDC, which in turn promote the productive infection of autologous primary T cells.

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Section: Discussionmentioning

confidence: 99%