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Reduced risk of AIDS lymphoma in individuals heterozygous for the CCR5-Delta 32 mutation

  1. Author:
    Dean, M.
    Jacobson, L. P.
    McFarlane, G.
    Margolick, J. D.
    Jenkins, F. J.
    Howard, O. M. Z.
    Dong, H. F.
    Goedert, J. J.
    Buchbinder, S.
    Gomperts, E.
    Vlahov, D.
    Oppenheim, J. J.
    O'Brien, S. J.
    Carrington, M.

  2. Author Address

    O'Brien SJ NCI, Lab Genom Divers Frederick, MD 21702 USA NCI, Lab Genom Divers Frederick, MD 21702 USA NCI, Lab Mol Immunol Frederick, MD 21702 USA NCI, Viral Epidemiol Branch Bethesda, MD 20892 USA Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Epidemiol Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Microbiol Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Hyg & Publ Hlth, Dept Mol Immunol Baltimore, MD 21205 USA Univ Pittsburgh, Sch Med & Publ Hlth, Dept Pathol Pittsburgh, PA USA Univ Pittsburgh, Sch Med & Publ Hlth, Dept Infect Dis & Microbiol Pittsburgh, PA USA NCI, Intramural Res Support Program, SAIC Frederick, Frederick Canc Res & Dev Ctr Frederick, MD 21702 USA San Francisco Dept Publ Hlth San Francisco, CA 94102 USA Childrens Hosp Los Angeles Los Angeles, CA 90027 USA
    1. Year: 1999
  2. Journal: Cancer Research
    1. 59
    2. 15
    3. Pages: 3561-3564
  4. Type of Article: Article
  1. Abstract:

    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-Delta 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. [References: 29]

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