AEGiS-07IAC: Complement mediates HIV-1 infection of human cells in an antibody-independent fashion.

7th International AIDS Conference

Florence, Italy — June 16-21, 1991

Complement mediates HIV-1 infection of human cells in an antibody-independent fashion.

Int Conf AIDS 1991 Jun 16-21; 7:98 (abstract no. M.A.1024)
Boyer V, Trabaud MA, Noraz N, Fischer E, Kazatchkine M, Desgranges C; Unite de recherche sur les Hepatites, la SIDA, et les retrovirus humains. INSERM U271.151, Cours A. Thomas, Lyon.

OBJECTIVE: To investigate the role of complement in HIV-1 infection of different types of cells independently of the HIV specific antibodies.

METHODS: To determine the role of complement in HIV-1 infection we incubated the HTLV-IIIB and HTLV-RF strains of HIV-1 with seronegative normal human serum under conditions which allow complement activation. The incubation of the complement-pretreated viruses was done with the human MT2 (CR2+) and U937 (CR1+ or CR3+) cell lines and with peripheral blood T cells. Infection of cells was assessed by measuring reverse transcriptase (RT) activity in supernatants at different times of culture.

RESULTS: Incubation of different cells with complement and virus resulted in enhancement of infection of the cells when low amounts of virus were used. For MT2 cells, complement activation by viral suspensions occurred through the alternative pathway and infection with suboptimal amounts of serum-opsonized HIV-1 was suppressed by blocking the C3dg receptor (CR2, CD21) on MT2 cells with monoclonal anti-CR2 antibody and rabbit Fab'2 anti-mouse Ig antibodies. Blocking of the gp120-binding site on CD4 under similar experimental conditions had no inhibitory effect on infection of MT2 cells with opsonized-virus. For U937 cells and PBL, the mechanism of complement activation by HIV-1 will be presented as well as for the coculture of PHA-activated and HIV-infected PBL from different donors.

CONCLUSION: The complement in the absence of specific antibodies enhances infection of C3 receptor bearing cells just by the interaction of opsonized virus with the CR1, CR2, or CR3 receptors. The clinical relevances of these findings remains to be determined.

Keywords: AEGIS, HIV Infections, Complement, HIV-1, Receptors, Complement 3d, Antibodies, HIV Antibodies, Antigens, CD4, Receptors, Complement 3b, HIV, RNA-Directed DNA Polymerase, T-Lymphocytes, Receptors, Complement, Receptors, HIV, Macrophage-1 Antigen, HIV Core Protein p24, HIV Envelope Protein gp120, Cell Line, Deltaretrovirus, Human, Animal, Mice, Rabbits, ICA7
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MA1024