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Journal of Virology, September 2006, p. 9217-9225, Vol. 80, No. 18
0022-538X/06/$08.00+0     doi:10.1128/JVI.02746-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Rhesus Macaque Polyclonal and Monoclonal Antibodies Inhibit Simian Immunodeficiency Virus in the Presence of Human or Autologous Rhesus Effector Cells

Donald N. Forthal,1* Gary Landucci,1 Kelly Stefano Cole,2 Marta Marthas,3 Juan C. Becerra,1 and Koen Van Rompay3

Division of Infectious Diseases, Department of Medicine, University of California, Irvine School of Medicine, Irvine, California 92697-4028,1 Department of Medicine, Infectious Diseases Division, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261,2 California National Primate Research Center, University of California, Davis, Davis, California 956163

Received 30 December 2005/ Accepted 30 June 2006

Although antibodies can prevent or modulate lentivirus infections in nonhuman primates, the biological functions of antibody responsible for such effects are not known. We sought to determine the role of antibody-dependent cell-mediated virus inhibition (ADCVI), an antibody function that inhibits virus yield from infected cells in the presence of Fc receptor-bearing effector cells, in preventing or controlling SIVmac251 infection in rhesus macaques (Macaca mulatta). Using CEMx174 cells infected with simian immunodeficiency virus mac251 (SIVmac251), both polyclonal and monoclonal anti-SIV antibodies were capable of potent virus inhibition in the presence of human peripheral blood mononuclear cell (PBMC) effector cells. In the absence of effector cells, virus inhibition was generally very poor. PBMCs from healthy rhesus macaques were also capable of mediating virus inhibition either against SIVmac251-infected CEMx174 cells or against infected, autologous rhesus target cells. We identified both CD14+ cells and, to a lesser extent, CD8+ cells as the effector cell population in the rhesus PBMCs. Finally, pooled, nonneutralizing SIV-antibody-positive serum, shown in a previous study to prevent infection of neonatal macaques after oral SIVmac251 challenge, had potent virus-inhibitory activity in the presence of effector cells; intact immunoglobulin G, rather than F(ab')2, was required for such activity. This is the first demonstration of both humoral and cellular ADCVI functions in the macaque-SIV model. ADCVI activity in nonneutralizing serum that prevents SIV infection suggests that ADCVI may be a protective immune function. Finally, our data underscore the potential importance of Fc-Fc receptor interactions in mediating biological activities of antibody.

* Corresponding author. Mailing address: 3044 Hewitt Hall, University of California, Irvine, Irvine, CA 92697-4028. Phone: (949) 824-3366. Fax: (714) 456-7169. E-mail: dnfortha{at}uci.edu.

Journal of Virology, September 2006, p. 9217-9225, Vol. 80, No. 18
0022-538X/06/$08.00+0     doi:10.1128/JVI.02746-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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