title: Influence of HIV infection on response to tenofovir in patients with chronic hepatitis B.
abstract: BACKGROUND
  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.
  
  
  METHODS
  All individuals with persistent HBsAg+ at four clinics in Spain were identified. Information from the subset that initiated tenofovir therapy was examined.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: aDepartment of Infectious Diseases, Hospital Carlos III bHospital Conxo-CHUS, Santiago de Compostela cInibic-Complexo Hospitalario Universitario, A Coruña dCentro Sanitario Sandoval, Madrid, Spain.
authors.forename: Zulema
authors.initials: Z
authors.lastname: Plaza
authors.forename: Antonio
authors.initials: A
authors.lastname: Aguilera
authors.forename: Alvaro
authors.initials: A
authors.lastname: Mena
authors.forename: Eugenia
authors.initials: E
authors.lastname: Vispo
authors.forename: Rocío
authors.initials: R
authors.lastname: Sierra-Enguita
authors.forename: Santiago
authors.initials: S
authors.lastname: Tomé
authors.forename: José
authors.initials: J
authors.lastname: Pedreira
authors.forename: Carmen
authors.initials: C
authors.lastname: Rodriguez
authors.forename: Pablo
authors.initials: P
authors.lastname: Barreiro
authors.forename: Jorge
authors.initials: J
authors.lastname: del Romero
authors.forename: Vicente
authors.initials: V
authors.lastname: Soriano
authors.forename: Eva
authors.initials: E
authors.lastname: Poveda
mesh_terms: D000225:Adenine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use*; D004279:DNA, Viral / Q000097:blood; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006514:Hepatitis B Surface Antigens / Q000097:blood; D006515:Hepatitis B virus / Q000302:isolation & purification*; D019694:Hepatitis B, Chronic / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D063065:Organophosphonates / Q000627:therapeutic use*; D013030:Spain; D000068698:Tenofovir; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D006514:Hepatitis B Surface Antigens; D063065:Organophosphonates; D000068698:Tenofovir; D000225:Adenine