Tenofovir monotherapy is effective in hepatitis B patients with antiviral treatment failure to adefovir in the absence of adefovir-resistant mutations

Profile of Mutations in the Reverse Transcriptase and Overlapping Surface Genes of Hepatitis B Virus (HBV) in Treatment-Naïve Indonesian HBV Carriers

“…It also contributes to compensation for replication defects in multidrug-resistant mutants (6). In contrast, the role of the rtI233V mutation in adefovir dipivoxil resistance is still controversial (36). An in vitro study has revealed that the appearance of rtN248H increases resistance to adefovir dipivoxil 5.71-fold, but the strain is still susceptible to lamivudine, telbivudine, entecavir, and tenofovir (37).…”

Current and future directions for treating hepatitis B virus infection

“…With tenofovir treatment, the serum HBV DNA-negative conversion rate for patients without adefovir-resistance was 100%, but the rate was down to 52% for patients with adefovir-resistance [89] . An important feature of tenofovir is that tenofovir alone or with emtricitabine exerts an anti-viral effect to lamivudine, adefovir or entecavir resistance mutants [85,86,93,95,96] . For example, an article reported that for patients who achieved an insufficient effect by lamivudine, adefovir or the combination of these two drugs, tenofovir resulted in a serum HBV DNA-negative conversion rate of 79%, HBeAg-negative conversion rate of 24% and HBsAg-negative conversion rate of 3% of all patients (the median time from administration to HBsAg-negative conversion was 23 mo) [86] .…”

Tenofovir and its potential in the treatment of hepatitis B virus

“…Of these 9 patients, who were switched to TDF monotherapy, 2 had a suboptimal response while 7 had rapid virological response with undetectable serum HBV DNA within 3 to 15 months. 20,22 Lada et al showed, in vitro, the excellent effi cacy of TDF on LAM-resistant virus independently of the resistance mutation profi le. 22,23 In the study of van Bömmel et al limited to 3 patients with ADV-resistant HBV infection, although TDF monotherapy had signifi cant antiviral effi cacy in patients with ADV resistance, it could not induce complete suppression of HBV DNA in any of the three patients studied or prevent further selection of ADV-associated resistance mutations.…”

“…20,22 Lada et al showed, in vitro, the excellent effi cacy of TDF on LAM-resistant virus independently of the resistance mutation profi le. 22,23 In the study of van Bömmel et al limited to 3 patients with ADV-resistant HBV infection, although TDF monotherapy had signifi cant antiviral effi cacy in patients with ADV resistance, it could not induce complete suppression of HBV DNA in any of the three patients studied or prevent further selection of ADV-associated resistance mutations. 22,24 These in vivo observations confi rm in vitro data that TDF has decreased antiviral activity against ADV-resistant HBV compared to wild type virus, indicating the potential for cross-resistance.…”

“…22,23 In the study of van Bömmel et al limited to 3 patients with ADV-resistant HBV infection, although TDF monotherapy had signifi cant antiviral effi cacy in patients with ADV resistance, it could not induce complete suppression of HBV DNA in any of the three patients studied or prevent further selection of ADV-associated resistance mutations. 22,24 These in vivo observations confi rm in vitro data that TDF has decreased antiviral activity against ADV-resistant HBV compared to wild type virus, indicating the potential for cross-resistance. 11,22 In terms of antiviral activity against multi-drug-resistance mutations, in vitro analysis indicates that TDF is far superior to the combination of LAM and ADV, and has a marginal benefi t over entecavir.…”