Virus Stopper: Herpes drug dampens HIV infection

An antiviral drug commonly taken for genital herpes seems to suppress HIV, the AIDS virus, in people harboring both pathogens, a study in West Africa finds. The report bolsters the notion that the two viruses have some biological interplay and suggests that herpes drugs might slow the spread of HIV.

Researchers identified 136 women in Burkina Faso who were infected with both genital herpes and HIV. The AIDS virus hadn’t depleted immune cells in any of these women enough to make them candidates for drug treatment, and none was receiving any herpes drug. The researchers randomly assigned half the women to receive the herpes drug valacyclovir in daily pills and the other women to get a placebo. Physicians examined the volunteers over the subsequent 3 months, taking vaginal and cervical swabs, and obtained blood samples every other week.

Women getting valacyclovir were less than half as likely as the others to have HIV show up in genital-tract swabs. Participants receiving the drug also had significantly less HIV in their blood, epidemiologist Nicolas Nagot of the London School of Hygiene and Tropical Medicine and his team report in the Feb. 22 New England Journal of Medicine (NEJM).

Those two findings suggest that herpes treatment “is likely to reduce HIV progression in [dually] infected people as well as reduce the likelihood of HIV transmission to uninfected partners,” says Ronald Gray, a physician and epidemiologist at Johns Hopkins Medical Institutions in Baltimore.

Scientists cite two mechanisms by which herpes might exacerbate an HIV infection, and hence envision how curbing herpes would slow the course of HIV.

Proteins that form part of the herpesvirus structure may “activate HIV-replication genes, a sort of viral-viral interaction,” Nagot says. Herpes proteins seem to reawaken HIV and probably contributed to the higher blood concentrations of HIV in untreated people in the new study, physician Lawrence Corey of the University of Washington in Seattle says in NEJM.

Other evidence suggests that the inflammatory reaction triggered by a herpes infection causes white blood cells to rush to herpes-and-HIV-infected tissue. That influx includes CD4 T cells, immune cells that HIV infects. Suddenly, “you’ve got more HIV targets,” Gray says.

The result is a depletion of these immune cells. Earlier work showed that HIV-positive people who are also infected with tuberculosis decline faster than those not dually infected, apparently because CD4 T cells were exposed to HIV as they fought the TB microbes. By the same token, past work has shown that men dually infected with HIV and gonorrhea or chlamydia have less HIV in their semen when treated with antibiotics that fight the bacteria.

The new study “has direct clinical implications, suggesting that HIV replication can be reduced with antiviral therapy directed solely at [genital] herpes,” Corey says.

Study participants getting valacyclovir shed less HIV from their genital tissues than did women not getting the drug, but “whether this translates into a reduction of transmission is unclear,” Nagot says.

The question might be answered by an ongoing study of couples in which one person has HIV and herpes and the other is HIV negative. Scientists are seeking to determine whether treatment for herpes affects transmission between individuals.

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