November 23, 2017 |
New Evidence That Genetic Differences May Help Explain Inconsistent Effectiveness Of Anti-Hiv Drug
July 22, 2015  | 

Baltimore, MD - Research with human tissue and cells suggests that genetic variations, in addition to failure to comply with treatment regimens, may account for some failures of an anti-HIV drug to treat and prevent HIV infection.

In a report described online in the journal EBioMedicine, investigators at Johns Hopkins found that tenofovir, marketed as Viread, is processed differently according to cell location, so that if the drug is eventually marketed as a topical gel, it could work differently depending on whether it is applied to the vagina or the rectum. Tenofovir has been approved since 2001 by the U.S. Food and Drug Administration to treat HIV. It is also a component of Truvada, a drug that was approved in 2012 as an oral prophylactic for use in preventing HIV infection. 

“If confirmed by further studies, our results suggest that in the future, before prescribing tenofovir to a patient, a doctor could order genetic testing and know in advance if it works, and prescribe a different drug if it won’t,” says Namandje Bumpus, Ph.D., associate professor of medicine at the Johns Hopkins University School of Medicine. 

Bumpus and her colleagues focused their research on a search for the human enzymes that convert tenofovir from its original form to an activated one that combats HIV. Previous studies had revealed that the key to such activation is the addition of two molecules known as phosphate groups, she says. Working with blood and tissue from healthy research subjects, her team “knocked out” genes for phosphate-adding enzymes one by one, then exposed the tissues’ cells to tenofovir to test whether they were able to activate the drug.  Continue>

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