AIDSWEEKLY Plus; Monday, September 7 & 14, 1998
Daniel J. DeNoon, Senior Editor
Such strategies would block or down-regulate the CCR5 chemokine receptor needed for macrophage-tropic (M-tropic) HIV-1 strains to infect cells. M-tropic strains are responsible for the vast majority of HIV infections.
People homozygous for a naturally occurring mutation that inactivates the CCR5 receptor resist HIV infection and appear healthy. Researchers are thus seeking a drug or immune therapy that would reproduce this condition. But a new study shows that people with the CCR5-delta32/delta32 mutation are at increased risk of hypertension, and that they appear to have increased risk of liver damage when infected with hepatitis C virus.
"CCR5-delta32/delta32 homozygotes had an increased prevalence of hypertension, modestly increased lymphocyte counts, and higher hepatic enzyme levels in the presence of HCV infection," reported Thomas R. O'Brien of the National Cancer Institute, Bethesda, Maryland, and colleagues.
O'Brien et al. announced the findings in a presentation to the 12th World AIDS Conference, held June 28-July 3, 1998, in Geneva, Switzerland.
The researchers reviewed the clinical records of 312 HIV uninfected hemophilic or gay men enrolled in prospective cohort studies of HIV incidence. Fifteen subjects were found to be homozygous for the CCR5-delta32 mutation (i.e., they inherited the mutant gene from both parents).
The only outstanding clinical difference between the delta32 homozygotes and other age-matched study participants was a 2.8-fold higher incidence of hypertension. None of the subjects had severe hypertension.
The patients with the double mutation also had 20 percent higher total lymphocyte counts. And among hemophilia patients with hepatitis C virus (HCV), the delta32 homozygotes had 117 percent higher hepatic enzyme (ALT) levels, although their HCV serum titers did not differ from subjects with normal CCR5 genes.
The authors suggested caution as researchers develop drugs that affect normal chemokine receptors.
"These possible phenotypic expressions of CCR5-delta32/delta32 homozygosity should be considered in the development of therapeutic modalities that mimic this genotype," they warned.
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