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32 Mutation1
Laboratories of Genomic Diversity [M. D., S. J. O.] and Molecular Immunology [H-F. D., J. J. O.], National Cancer Institute, Frederick, Maryland 21702-1201; Viral Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892 [J. J. G.]; Departments of Epidemiology [L. P. J., G. M.] and Microbiology and Molecular Immunology [J. B. M., D. V.], The Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland 21205-1999; Departments of Pathology and Infectious Diseases and Microbiology, University of Pittsburgh School of Medicine and Public Health, Pittsburgh, Pennsylvania [F. J. J.]; Intramural Research Support Program, SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201 [O. M. Z. H., M. C.]; San Francisco Department of Public Health, San Francisco, California 94102 [S. B.]; and Children’s Hospital Los Angeles, Los Angeles, California 90027 [E. G.]
Non-Hodgkin’s lymphoma (NHL) has been increasing in frequency in the industrialized world, but the environmental and genetic factors that contribute to susceptibility are not known. B-cell lymphomas represent a major cause of morbidity and mortality in HIV-infected individuals. The identification of a deletion in the CCR5 chemokine receptor gene that alters the risk for infection and progression to AIDS led us to examine a potential role of this gene in AIDS lymphoma. A matched case-control analysis was performed using all eligible NHL cases in the Multicenter AIDS Cohort Study. Patients were matched for age, study center, time AIDS-free, and slope of the CD4+ T-cell decline. The CCR5-
32 allele was found to be associated with a 3-fold lower risk of NHL among individuals after controlling for time of infection and progression toward AIDS. The CCR5 gene was not associated with a difference in risk for Kaposi’s sarcoma, another common malignancy in AIDS patients, or opportunistic infections. Costimulation of normal phorbol 12-myristate 13-acetate-treated B cells with the CCR5 ligand RANTES induced a proliferative response, indicating that RANTES is a mitogen for B cells. Taken together, these findings suggest that the CCR5 gene plays a role in the risk of NHL in HIV-infected patients, perhaps through a mechanism involving a decreased response of B cells to the mitogenic activity of RANTES.
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