September 8, 2015
"The incidence of herpes simplex viruses resistant to acyclovir is going up and up," said Toby Maurer, MD, professor of clinical dermatology at the University of California, San Francisco, at a recent HIV grand rounds presentation at San Francisco General Hospital.
Acyclovir is an antiviral medication commonly used to reduce pain and hasten healing of herpes simplex (HSV) sores. But when HSV develops a resistance to acyclovir, infected people can develop skin lesions -- hypertrophic masses near or on the genitals that can be painful and unsightly. These occur more frequently in people who are living with HIV or have compromised immune systems, may be difficult to treat and can recur even after treatment.
Maurer cited a retrospective study of immunocompromised people that showed an incidence increase in acyclovir-resistant herpes simplex from 3% to 14% over ten years. She also pointed to examples from recent cases she's seen as a dermatologist in the U.S. and Africa.
She said that acyclovir-resistant herpes simplex can develop even in people with healthy CD4 counts. "We saw resistance in the [past] when CD4 counts were under 50. But these folks have a range of CD4 counts. They're not particularly immunosuppressed."
It's possible, said Maurer, that long courses of acyclovir taken to prevent herpes simplex outbreaks can lead to development of drug-resistant forms of the virus -- although there's no definitive evidence yet.
In one long-term follow-up study that included 13 people who were diagnosed with acyclovir-resistant HSV infection, all had been previously treated with long courses of acyclovir before their first hypertrophic herpes simplex breakout. "Are those patients who have acyclovir resistant herpes selecting out for these particular mutations, because we're putting them on long-term suppressant doses? This is the only study that has implied this. I don't know the answer, but it's something we need to look at," said Maurer.
This excerpt was cross-posted with the permission of BETAblog.org. Read the full article.
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