Tenofovir (Viread), one of the leading
antiviral drugs for
hepatitis B treatment, produced no drug resistance in 585 patients
years of treatment.
The report, published in the August issue of
followed 347 hepatitis B "e" antigen-negative patients and 238
"e" antigen-positive patients who had been treated with the daily
antiviral pill for six years.
They examined the molecular make-up of the
hepatitis B virus
of 52 patients who still had detectable HBV DNA after nearly six
years of treatment to see if any of them had
developed viral mutations that could "resist" tenofovir's ability
block viral replication.
The researchers reported that failure to take
as prescribed and natural viral mutations were behind the
persistance of detectable viral
load in these patients. Those patients were either switched to a
tenofovir and emtricitabine
taking tenofovir as prescribed. To date, all patients have
undetecatable viral load.
resistance to tenofovir disoproxil fumarate after 6 years of
patients with chronic hepatitis B.
MD. Gilead Sciences, Inc., Foster City, CA, USA.
in the treatment of chronic hepatitis B
maintain long-term viral suppression without promoting the
We analyzed data from 347 hepatitis
B e antigen-negative and 238 hepatitis
antigen-positive patients receiving tenofovir disoproxil
fumarate (TDF) in an
open-label, long-term extension of two phase 3 studies. To date,
analyses have been completed for patients receiving up to 288
weeks (6 years)
Population sequencing of hepatitis
(HBV) polymerase/reverse transcriptase (pol/RT) was attempted
for all patients
at baseline, and any patient who remained viremic (HBV DNA ≥400
IU/mL]) at week 288 or at the end of treatment with TDF (n = 52)
emtricitabine (FTC)/TDF (n = 7). Phenotypic analyses were
performed in HepG2
cells using recombinant HBV containing patient pol/RT sequences.
half of the patients on open-label treatment who qualified for
pol/RT sequence changes compared to baseline (23/52 [44%] on
TDF, 4/7 [57%] on
FTC/TDF). Most changes were at polymorphic sites and none were
TDF resistance. Virologic breakthrough occurred infrequently and
with nonadherence to study medication in the majority of cases
Per protocol, 57 patients (10%) were eligible to switch to
majority had HBV DNA <400 copies/mL at their last study visit
whether they switched to FTC/TDF (n = 34) or maintained TDF
monotherapy (n =
17). No patient exhibited persistent viremia (HBV DNA never
after week 240.
Conclusion: TDF monotherapy maintains effective
HBV DNA through 288 weeks of treatment with no evidence of TDF