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Journal of Virology, May 2007, p. 5024-5035, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02444-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Antiviral Antibodies Are Necessary for Control of Simian Immunodeficiency Virus Replication{triangledown}

Christopher J. Miller,1,2* Meritxell Genescà,1,2 Kristina Abel,1,2 David Montefiori,3 Donald Forthal,4 Kristen Bost,1,2 Jun Li,2 David Favre,5 and Joseph M. McCune5

Center for Comparative Medicine,1 California National Primate Research Center, University of California, Davis, Davis, California 95616,2 Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710,3 Department of Medicine, Division of Infectious Diseases, School of Medicine, University of California, Irvine, Orange, California 92868,4 Department of Medicine, Division of Experimental Medicine, San Francisco General Hospital, University of California, San Francisco, California 941105

Received 6 November 2006/ Accepted 21 February 2006

To better define the role of B cells in the control of pathogenic simian immunodeficiency virus (SIV) replication, six rhesus monkeys were depleted of B cells by intravenous infusion of rituximab (anti-CD20) 28 days and 7 days before intravaginal SIVmac239 inoculation and every 21 days thereafter until AIDS developed. Although the blood and tissues were similarly depleted of B cells, anti-SIV immunoglobulin G (IgG) antibody responses were completely blocked in only three of the six animals. In all six animals, levels of viral RNA (vRNA) in plasma peaked at 2 weeks and declined by 4 weeks postinoculation (PI). However, the three animals prevented from making an anti-SIV antibody response had significantly higher plasma vRNA levels through 12 weeks PI (P = 0.012). The remaining three B-cell-depleted animals made moderate anti-SIV IgG antibody responses, maintained moderate plasma SIV loads, and showed an expected rate of disease progression, surviving to 24 weeks PI without developing AIDS. In contrast, all three of the B-cell-depleted animals prevented from making anti-SIV IgG responses developed AIDS by 16 weeks PI (P = 0.0001). These observations indicate that antiviral antibody responses are critical in maintaining effective control of SIV replication at early time points postinfection.

* Corresponding author. Mailing address for Christopher J. Miller: CNPRC, UC, Davis, One Shields Ave., Davis, CA 95616. Phone: (530) 752-0447. Fax: (530) 754-4411. E-mail: cjmiller{at}ucdavis.edu. Mailing address for Joseph M. McCune: Division of Experimental Medicine, Department of Medicine, San Francisco General Hospital, Bldg. 3, Rm. 601, 1001 Potrero Ave., San Francisco, CA 94110. E-mail: mike.mccune{at}ucsf.edu

{triangledown} Published ahead of print on 28 February 2007.

Journal of Virology, May 2007, p. 5024-5035, Vol. 81, No. 10
0022-538X/07/$08.00+0     doi:10.1128/JVI.02444-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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