Heterozygous mutation of the CCR5 gene in HIV-infected individuals with lymphomas

The chemokine receptor CCR5, encoded by appropriate gene, is expressed by CD4+ cells, being a membrane co-receptor for HIV-1. Homozygous carriers of CCR5 mutation (CCR5-32 deletion) are resistant to HIV-1 infection. The heterozygous mutation (hetero-CCR5-32) does not affect susceptibility, but such patients have a late onset of AIDS. The role of this heterozygous mutation is unclear in HIV-infected individuals with lymphomas. Hence, the purpose of our study was to evaluate the impact of carrying hetero-CCR5-32 on the epidemiology and course of lymphoma in patients with HIV infection, as well as the impact on treatment outcomes. We studied 39 patients with lymphomas and HIV, for whom the CCR5 gene mutation status was determined. We identify the five (13%) HIV-infected patients with lymphomas who had a heterozygous mutation of CCR5 gene (hetero-CCR5-32), others -34 (87%) HIV-infected patients with lymphomas had wild-type genotype (WT/WT). We observed the significant prevalence of Burkitt lymphoma in hetero-CCR5-32 cohort, but no difference in clinical course and outcomes of the lymphomas. We may assume that heterozygous mutation of CCR5 gene predisposes for delayed progression from HIV infection to AIDS among infected individuals. Thus, we see in this cohort more often lymphomas not related to the low CD4+ cell level, i.e., Burkitt lymphoma. We suppose that a study in a larger cohort will help to discover the pathogenetic features of lymphomas in patients with HIV thus clarifying the role of CCR5 gene mutation status.