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© The Rockefeller University Press, 0022-1007/1998/7/233/ $5.00
The Journal of Experimental Medicine, Volume 188, Number 2, July 20, 1998 233-245

Articles

HIV-1 Antigen–specific and –nonspecific B Cell Responses Are Sensitive to Combination Antiretroviral Therapy

Lynn Morris, James M. Binley, Brian A. Clas, Sebastian Bonhoeffer, Thomas P. Astill, Rhonda Kost, Arlene Hurley, Yunzhen Cao, Martin Markowitz, David D. Ho, and John P. Moore

From the Aaron Diamond AIDS Research Center, The Rockefeller University, New York 10016

We studied how combination antiviral therapy affects B cell abnormalities associated with HIV-1 infection, namely elevated circulating immunoglobulin (Ig)G antibody-secreting cell (ASC) frequencies and hypergammaglobulinemia. Within a few weeks of starting antiviral therapy, there is a marked decline in IgG-ASC frequency in both acutely and chronically infected people, whereas the hypergammaglobulinemia often present during chronic infection is more gradually resolved. These reductions are sustained while HIV-1 replication is suppressed. HIV-1 antigen–specific B cell responses are also affected by therapy, manifested by a rapid decline in circulating gp120-specific ASCs. Anti-gp120 titers slowly decrease in chronically infected individuals and usually fail to mature in acutely infected individuals who were promptly treated with antiretroviral therapy. Long-term nonprogressors have high titer antibody responses to HIV-1 antigens, but no detectable gp120-specific IgG-ASC, and normal (or subnormal) levels of total circulating IgG-ASC. Overall, we conclude that HIV-1 infection drives B cell hyperactivity, and that this polyclonal activation is rapidly responsive to decreases in viral replication caused by combination antiviral therapy.

Key Words: hypergammaglobulinemia • human immunodeficiency virus 1 • B cells • antiretroviral therapy • antibody

Address correspondence to J.P. Moore, The Aaron Diamond AIDS Research Center, 455 1st Ave., New York, NY 10016. Phone: 212-725-0018; Fax: 212-725-1126; E-mail: jmoore{at}adarc.org

L. Morris was supported by the Department of Health, the Poliomyelitis Research Foundation, and the Medical Research Council of South Africa. Other support was provided by National Institutes of Health grants R21 AI-42721, U01 AI-41534, and MO1 RR-06102.

Lynn Morris' permanent address is National Institute for Virology, Private Bag X4, Sandringham, Johannesburg 2131, Gauteng, South Africa.

Abbreviations used: ASC, antibody-secreting cell; bDNA, branched DNA; LTNP, long-term nonprogressor.


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