The HBV Drug Entecavir — Effects on HIV-1 Replication and Resistance

Moira A. McMahon(Johns Hopkins University), Benjamin L. Jilek(Johns Hopkins Medicine), Timothy Brennan(Johns Hopkins University), Lin Shen(Johns Hopkins University), Yan Zhou(Johns Hopkins University), Megan Wind‐Rotolo(Johns Hopkins Medicine), Sifei Xing(Johns Hopkins Medicine), Shridhar Bhat(Johns Hopkins Medicine), Braden Hale(Naval Medical Center San Diego), Robert W. Hegarty(Johns Hopkins Medicine), Curtis R. Chong(Johns Hopkins University), Jun O. Liu(Johns Hopkins University), Robert F. Siliciano(Howard Hughes Medical Institute), Chloe L. Thio(Johns Hopkins Medicine)
New England Journal of Medicine
June 20, 2007
10.1056/nejmoa067710
Cited by 286Open Access
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Abstract

Entecavir, a drug approved by the Food and Drug Administration for the treatment of chronic hepatitis B virus (HBV) infection, is not believed to inhibit replication of human immunodeficiency virus type 1 (HIV-1) at clinically relevant doses. We observed that entecavir led to a consistent 1-log(10) decrease in HIV-1 RNA in three persons with HIV-1 and HBV coinfection, and we obtained supportive in vitro evidence that entecavir is a potent partial inhibitor of HIV-1 replication. Detailed analysis showed that in one of these patients, entecavir monotherapy led to an accumulation of HIV-1 variants with the lamivudine-resistant mutation, M184V. In vitro experiments showed that M184V confers resistance to entecavir. Until more is known about HIV-1-resistance patterns and their selection by entecavir, caution is needed with the use of entecavir in persons with HIV-1 and HBV coinfection who are not receiving fully suppressive antiretroviral regimens.

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