Skip Navigation LinksHome > September 10, 2013 - Volume 27 - Issue 14 > Influence of HIV infection on response to tenofovir in patie...
doi: 10.1097/QAD.0b013e328362fe42
Clinical Science

Influence of HIV infection on response to tenofovir in patients with chronic hepatitis B

Plaza, Zulemaa; Aguilera, Antoniob; Mena, Álvaroc; Vispo, Eugeniaa; Sierra-Enguita, Rocíoa; Tomé, Santiagob; Pedreira, Joséc; Rodriguez, Carmend; Barreiro, Pabloa; del Romero, Jorged; Soriano, Vicentea; Poveda, Evaa,c

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HIV worsens the natural history of chronic hepatitis B virus (HBV) infection. Suppression of HBV replication slows progression of liver damage. Information about the influence of HIV on response to tenofovir in HIV/HBV-coinfected patients is scarce.


All individuals with persistent HBsAg+ at four clinics in Spain were identified. Information from the subset that initiated tenofovir therapy was examined.


A total of 176 patients with chronic hepatitis B were evaluated, of whom 138 (78.4%) were coinfected with HIV. Prior lamivudine exposure was extensive in both groups, and nearly half of HBV viremic patients harboured drug resistance mutations. Most patients took tenofovir coformulated along with emtricitabine (Truvada). Of 101 HBV viremic patients at the time of beginning tenofovir (78 with HIV coinfection and 33 with HBV alone), a similar proportion achieved undetectable HBV-DNA at weeks 24, 48 and 96 of tenofovir therapy. Interestingly, HIV/HBV-coinfected patients with positive HBeAg showed a lower response than HBeAg-negatives. In multivariate analysis, however, baseline serum HBV-DNA was the only predictor of virological response to tenofovir.


The antiviral efficacy of tenofovir is similar in HIV/HBV-coinfected and HBV-monoinfected patients, achieving undetectable HBV-DNA nearly 90% of patients at week 96 of therapy. Baseline serum HBV-DNA is the major determinant of time-trends in virological response, with no significant influence of HBeAg, drug resistance mutations nor coinfection with hepatitis C or delta viruses.

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins


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