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Blood, Vol. 93 No. 6 (March 15), 1999:
pp. 1838-1842
RAPID COMMUNICATION
Chemokine and Chemokine Receptor Gene Variants and Risk of
Non-Hodgkin's Lymphoma in Human Immunodeficiency Virus-1-Infected
Individuals
Charles S. Rabkin,
Quan-en Yang,
James J. Goedert,
Giao Nguyen,
Hiroaki Mitsuya, and
Shizuko Sei
From the Viral Epidemiology Branch, HIV and AIDS Malignancy Branch,
and Experimental Retrovirology Section, National Cancer Institute,
Bethesda, MD; the HIV Clinical Interface Laboratory, Science
Applications International Corp-National Cancer Institute, Frederick,
MD; and the Department of Internal Medicine II, Kumamoto University
School of Medicine, Kumamoto, Japan.
Normal B-lymphocyte maturation and proliferation are regulated by
chemotactic cytokines (chemokines), and genetic polymorphisms in
chemokines and chemokine receptors modify progression of human immunodeficiency virus-1 (HIV-1) infection. Therefore, 746 HIV-1-infected persons were examined for associations of previously
described stromal cell-derived factor 1 (SDF-1) chemokine and CCR5 and
CCR2 chemokine receptor gene variants with the risk of B-cell
non-Hodgkin's lymphoma (NHL). The SDF1-3'A chemokine variant,
which is carried by 37% of whites and 11% of blacks, was associated
with approximate doubling of the NHL risk in heterozygotes and roughly
a fourfold increase in homozygotes. After a median follow-up of 11.7 years, NHL developed in 6 (19%) of 30 SDF1-3'A/3'A
homozygotes and 22 (10%) of 202 SDF1-+/3'A heterozygotes,
compared with 24 (5%) of 514 wild-type subjects. The acquired
immunodeficiency syndrome (AIDS)-protective chemokine receptor variant
CCR5- 32 was highly protective against NHL, whereas the
AIDS-protective variant CCR2-64I had no significant effect. Racial
differences in SDF1-3'A frequency may contribute to the lower
risk of HIV-1-associated NHL in blacks compared with whites. SDF-1
genotyping of HIV-1-infected patients may identify subgroups
warranting enhanced monitoring and targeted interventions to reduce the
risk of NHL.
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