Background: Despite widespread use in HIV and hepatitis B virus (HBV) infection, the effectiveness of tenofovir (TDF) has not been studied extensively outside of small cohorts of coinfected patients with HBV-HIV. We examined the effect of prior lamivudine (3TC) treatment and other factors on HBV DNA suppression with TDF in a multisite clinical cohort of coinfected patients.
Methods: We studied all patients enrolled in the Centers for AIDS Research Network of Integrated Clinical Systems cohort from 1996 to 2011 who had chronic HBV and HIV infection, initiated a TDF-based regimen continued for ≥3 months and had on-treatment HBV DNA measurements. We used Kaplan–Meier curves and Cox-proportional hazards to estimate time to suppression (HBV DNA level <200 IU/mL or <1000 copies/mL) by selected covariates.
Results: Among 397 coinfected patients on TDF, 91% were also on emtricitabine or 3TC concurrently, 92% of those tested were hepatitis B e antigen positive, 196 (49%) had prior 3TC exposure; 192 (48%) achieved HBV DNA suppression over a median of 28 months (interquartile range: 13–71). Median time to HBV DNA suppression was 17 months for those who were 3TC-naive and 50 months for those who were 3TC exposed. After controlling for other factors, prior 3TC exposure, baseline HBV DNA level >10,000 IU/mL, and lower nadir CD4 count were independently associated with decreased likelihood of HBV DNA suppression on TDF.
Conclusions: These results emphasize the role of prior 3TC exposure and immune response on delayed HBV suppression on TDF.
*Department of Medicine, University of Washington, Seattle, WA;
†Departments of Medicine, Epidemiology, University of North Carolina, Chapel Hill, NC;
‡Department of Medicine, Johns Hopkins University, Baltimore, MD;
§Department of Medicine, University of Alabama, Birmingham, AL;
‖University of California, San Francisco, San Francisco, CA;
¶Department of Medicine, Case Western Reserve University, Cleveland, OH;
#Department of Medicine, University of California, San Diego, La Jolla, CA; and
**Department of Medicine, Harvard University and Fenway Community Health, Boston, MA.
Correspondence to: H. Nina Kim, MD, MSc, University of Washington, 325 Ninth Avenue, Box 359930, Seattle, WA 98104 (e-mail: firstname.lastname@example.org).
Supported by the Centers for AIDS Research Network of Integrated Clinical Systems CNICS (5R24AI067039) funding from the National Institutes of Allergy and Infectious Diseases and National Heart, Lung, and Blood Institute. This research was also made possible by National Institutes of Health–funded programs for the Centers for AIDS Research (P30 AI027757 and P30 AI027763).
Presented in part at the 20th Conference on Retroviruses and Opportunistic Infections 2013, March 4, 2013, Atlanta, GA (abstract 667).
J.J.E. is a consultant to Gilead and Glaxo-Smith Klein. E.T.O. is a consultant for Gilead and receives research funding from Gilead. M.M. has been a consultant for Gilead and Bristol-Myers Squibb (BMS) and has received research funding from BMS. The remaining authors have no conflicts of interest to disclose.
Received January 17, 2014
Accepted January 17, 2014