This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Spear, G T Articles by Lint, T F Search for Related Content PubMed PubMed Citation Articles by Spear, G T Articles by Lint, T F

Neutralization of human immunodeficiency virus type 1 by complement occurs by viral lysis.

Department of Immunology/Microbiology, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612.

ABSTRACT

The ability of complement to inactivate human immunodeficiency virus (HIV) in the presence of specific antibody was evaluated. HIV was treated with complement and/or antibody, and then its titer was determined on the CD4+ H9 cell line. While complement alone had no effect on the HIV titer, complement plus subneutralizing levels of antibody resulted in titer reductions. Complement sources deficient in membrane attack component C5 or C8 did not inactivate antibody-treated HIV, suggesting that neutralization occurred via lysis. This possibility was investigated by assessing release of reverse transcriptase (RT) from the virion. Antibody plus complement, but neither reagent alone, released RT from HIV in a dose-dependent manner. Release of RT did not occur with C5- or C8-deficient sera, also indicating a requirement for membrane attack components. These studies show that complement can neutralize HIV via the classical complement pathway and that this neutralization occurs via C5b-9-mediated viral lysis. Thus, complement may play a major role in resistance to disease by lysing HIV and preventing infection of Fc- and complement receptor-positive cells, as well as CD4+ cells.

This article has been cited by other articles:

• Huber, M., von Wyl, V., Ammann, C. G., Kuster, H., Stiegler, G., Katinger, H., Weber, R., Fischer, M., Stoiber, H., Gunthard, H. F., Trkola, A. (2008). Potent Human Immunodeficiency Virus-Neutralizing and Complement Lysis Activities of Antibodies Are Not Obligatorily Linked. J. Virol. 82: 3834-3842 [Abstract] [Full Text]  
• Aasa-Chapman, M. M. I., Holuigue, S., Aubin, K., Wong, M., Jones, N. A., Cornforth, D., Pellegrino, P., Newton, P., Williams, I., Borrow, P., McKnight, A. (2005). Detection of Antibody-Dependent Complement-Mediated Inactivation of both Autologous and Heterologous Virus in Primary Human Immunodeficiency Virus Type 1 Infection. J. Virol. 79: 2823-2830 [Abstract] [Full Text]  
• Horakova, E., Gasser, O., Sadallah, S., Inal, J. M., Bourgeois, G., Ziekau, I., Klimkait, T., Schifferli, J. A. (2004). Complement Mediates the Binding of HIV to Erythrocytes. J. Immunol. 173: 4236-4241 [Abstract] [Full Text]  
• Wolbank, S., Kunert, R., Stiegler, G., Katinger, H. (2003). Characterization of Human Class-Switched Polymeric (Immunoglobulin M [IgM] and IgA) Anti-Human Immunodeficiency Virus Type 1 Antibodies 2F5 and 2G12. J. Virol. 77: 4095-4103 [Abstract] [Full Text]  
• Tacnet-Delorme, P., Boyer, V., Thielens, N. M., Hernandez, J.-F., Bally, I., Sim, R. B., Desgranges, C., Arlaud, G. J. (1999). In Vitro Analysis of Complement-Dependent HIV-1 Cell Infection Using a Model System. J. Immunol. 162: 4088-4093 [Abstract] [Full Text]  
• Zhang, L., Dailey, P. J., He, T., Gettie, A., Bonhoeffer, S., Perelson, A. S., Ho, D. D. (1999). Rapid Clearance of Simian Immunodeficiency Virus Particles from Plasma of Rhesus Macaques. J. Virol. 73: 855-860 [Abstract] [Full Text]  
• Ikeda, F., Haraguchi, Y., Jinno, A., Iino, Y., Morishita, Y., Shiraki, H., Hoshino, H. (1998). Human Complement Component C1q Inhibits the Infectivity of Cell-Free HTLV-I. J. Immunol. 161: 5712-5719 [Abstract] [Full Text]