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7th International AIDS ConferenceFlorence, Italy — June 16-21, 1991 |
Int Conf AIDS 1991 Jun 16-21; 7:99 (abstract no. M.A.1028)
Haeffner-Cavaillon N, Thieblemont N, Weiss L, Ziegler-Heitbrock HW, Kazatchkine MD; Hopital Brousais, Paris, France
OBJECTIVE: To study the role of complement in the facilitation of viral entry into monocyte/macrophages.
METHODS: Glycosylated recombinant gp160 of HIV-1; monocytic cell lines Mono Mac 6 (CD4 antigen-negative) and THP1 (low expression of CD4 antigen); HTLV IIIB strain of HIV-1; LAV II strain of HIV-2.
RESULTS: Incubation of recombinant gp160 with normal human serum resulted in dose and time-dependent activation of the classical complement pathway and deposition of neoantigens of cleaved C3 on the glycoprotein. No binding of C3 to gp160 occurred in C2- and Clq-deficient sera. Binding of human anti-gp160 IgG to the protein enhanced its ability to activate the classical pathway. Opsonization of HIV-1 and HIV-2 with HIV-seronegative normal human serum enhanced infection of the two monocytic cell lines that were tested, as assessed by the higher amount of p24 measured in supernatants of infected cells and the earlier time point at which p24 was detected following infection of the cells.
DISCUSSION: The gp160 envelope glycoprotein of HIV-1 activates the classical complement pathway in the absence of antibody, resulting in binding of C3b/C3bi to the viral particle. Opsonization with complement of HIV-1 and HIV-2 results in an early and enhanced infection of the CD4-negative Mono Mac6 cell line and of THP1 cells. Thus, complement facilitates entry of HIV into monocytes.
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