Issue: June 2012
May 29, 2012
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Acyclovir slowed HIV progression in those coinfected with HSV-2

Issue: June 2012

Recent data show that acyclovir reduced the rate of HIV-1 disease progression among those coinfected with HIV and herpes simplex virus type 2, especially among those with a high baseline viral load.

Researchers led by Steven J. Reynolds, MD, from Johns Hopkins University School of Medicine and Makerere University School of Public Health in Uganda conducted a randomized, double blind, placebo-controlled trial of acyclovir in Rakai, Uganda. Those coinfected with HIV-1 and HSV-2 were recruited between May 2007 and November 2008. Patients were excluded if they had AIDS-defining illness or active genital ulcer disease or if they were receiving ART.

“Herpes simplex virus type 2 is a common, chronic condition affecting HIV patients,” Reynolds told Infectious Disease News. “Suppressive therapy with acyclovir may reduce symptoms of recurrence and also delay the need to starting ART.”

Steven J. Reynolds, MD

Steven J. Reynolds

The study included 440 participants who were randomly assigned to acyclovir 400 mg orally twice daily or placebo. The participants were followed for 24 months, and 403 participants completed the study intervention up to month 24. Primary outcome measure was a CD4 cell count of less than 250 cells/mcL or initiation of ART.

Adherence to the study drug was similar to placebo, and no safety issues related to acyclovir were identified. Among the participants, 110 in the placebo group and 95 in the treatment group reached the primary endpoint (HR=0.75; 95% CI, 0.58-0.99).

In a post-hoc analysis stratified by HIV viral load, disease progression in those with less than 50,000 copies/mL at baseline was not significantly different (HR=0.9; 95% CI, 0.54-1.5). In participants with a viral load of 50,000 copies/mL or more at baseline, HIV progression was significantly reduced in the treatment group (HR=0.62; 95% CI, 0.43-0.96).

“Future research in this area should evaluate the impact of more potent anti-herpes therapy such as valacylovir on reducing HIV disease progression,” Reynolds said.

In an accompanying editorial, Georges M. Verjans, PhD, and Charles A. Boucher, MD, PhD, of the department of virology at Erasmus Medical Center in Rotterdam, Netherlands, posed questions about the use of acyclovir or valacyclovir in this population and discussed the possible mechanisms by which acyclovir suppresses HIV.

“The usefulness of acyclovir for patients with both HIV and HSV-2 should be tested further to assess the value of higher dosing and to confirm the absence of long-term toxic effects and drug-resistant HIV,” they concluded.

References:

Reynolds SJ. Lancet Infect Dis. 2012;12:441-448.

Disclosures:

The researchers and Drs. Verjans and Boucher report no relevant financial disclosures.