Moira McMahon and colleagues at Johns Hopkins used a sensitive infection assay of white blood cells, and observed that acyclovir could directly inhibit HIV replication.
The researchers said that the drug particularly targeted the reverse transcriptase (RT) enzyme, which converts HIV's RNA into DNA to enable it to replicate.
However, as early as five days after initial infection, a mutant version of HIV (V75I) appeared in the cells, and spread to comprise over 90 per cent of the viral population within 94 days.
The V75I strain is part of the resistance pathway to many drugs, including the commonly used RT inhibitors.
Based on their observations, the researchers came to the conclusion that acyclovir could be a great model for designing future HIV treatments, but also could be a risky drug if given to HSV patients co-infected with HIV by potentially promoting cross-resistance to current treatments.
An article on the study has been published in JBC online.