The finding rebuts earlier scientific assumptions that Valacyclovir (Valtrex) required the presence of the other infection to benefit patients with HIV-1, researchers said.
The result not only means that Valacyclovir can be used effectively with a broader range of HIV-1 patients, but also suggests promising new avenues for the development of HIV-fighting drugs.
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This insight is particularly significant given that some forms of HIV-1 have become resistant to existing medications.
"These results demonstrated that the mechanism by which Valacyclovir acts against HIV is not only through the presence of HSV-2," said senior author Benigno Rodriguez, associate professor of medicine and infectious diseases, Case Western Reserve University School of Medicine in US.
Rodriguez said studies by these groups helped illuminate exactly how the medication decreases HIV-1 levels.
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Valacyclovir is activated in virus-infected cells, and then blocks the ability of HIV to reproduce. HIV-1 can lead to the immune deficiency known as AIDS.
Scientists previously thought that Valacyclovir helped reduce HIV levels and worked by decreasing the immune activation caused by HSV-2.
With fewer immune cells to attack, the theory went, HIV-1 could not spread as widely.
After conducting laboratory studies with Acyclovir, an earlier sibling drug of Valacyclovir, Leonid Margolis, of the National Institutes of Health (NIH), saw that the medication clearly blocked HIV-1 reproduction, even when HSV-2 was absent.
Those results helped spur clinical trials of Valacyclovir in people.
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Beginning in June, 2009, patients from University Hospitals Case Medical Centre and from IMPACTA, the Civic Association for Health and Education in Lima, Peru, started participating in the trials, which lasted until July, 2012.
Under its protocols, half the patients took Valacyclovir twice daily for 12 weeks, while the other half took a placebo for the same period of time.
After a two-week break from any medications, the two groups switched: those previously on placebo got 12 weeks of the Valacyclovir, and those who already had taken the medication now received placebos.
When study participants took Valacyclovir, their HIV viral loads went down, and when they took the placebo, their HIV viral loads went up. Ultimately, a total of 18 patients participated.
"Our most recent clinical study demonstrates that acyclovir blocks HIV replication directly. The anti-HIV activity of valacyclovir does not depend on blocking the inflammation caused by herpes simplex virus 2," said Michael M Lederman, also a senior author.
The study was published in the journal Clinical Infectious Diseases.
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