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Journal of Virology, August 2001, p. 6953-6961, Vol. 75, No. 15
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.15.6953-6961.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Antibody from Patients with Acute Human Immunodeficiency Virus (HIV) Infection Inhibits Primary Strains of HIV Type 1 in the Presence of Natural-Killer Effector Cells

Donald N. Forthal,1,* Gary Landucci,1 and Eric S. Daar2

Division of Infectious Diseases, Department of Medicine, University of California, Irvine College of Medicine, Irvine,1 and Cedars-Sinai Burns & Allen Research Institute, Division of Infectious Diseases, Department of Medicine, and UCLA School of Medicine, Los Angeles,2 California

Received 26 February 2001/Accepted 26 April 2001

The partial control of viremia during acute human immunodeficiency virus type 1 (HIV-1) infection is accompanied by an HIV-1-specific cytotoxic T-lymphocyte (CTL) response and an absent or infrequent neutralizing antibody response. The control of HIV-1 viremia has thus been attributed primarily, if not exclusively, to CTL activity. In this study, the role of antibody in controlling viremia was investigated by measuring the ability of plasma or immunoglobulin G from acutely infected patients to inhibit primary strains of HIV-1 in the presence of natural-killer (NK) effector cells. Antibody that inhibits virus when combined with effector cells was present in the majority of patients within days or weeks after onset of symptoms of acute infection. Furthermore, the magnitude of this effector cell-mediated antiviral antibody response was inversely associated with plasma viremia level, and both autologous and heterologous HIV-1 strains were inhibited. Finally, antibody from acutely infected patients likely reduced HIV-1 yield in vitro both by mediating effector cell lysis of target cells expressing HIV-1 glycoproteins and by augmenting the release of beta -chemokines from NK cells. HIV-1-specific antibody may be an important contributor to the early control of HIV viremia.

* Corresponding author. Mailing address: Division of Infectious Diseases, Department of Medicine, University of California, Irvine Medical Center, Building 11, 101 City Dr., Orange, CA 92868. Phone: (714) 456-7701. Fax: (714) 456-7169. E-mail: dnfortha{at}uci.edu.

Journal of Virology, August 2001, p. 6953-6961, Vol. 75, No. 15
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.15.6953-6961.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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