Ronald E. Rose

TL;DR: Long‐term monitoring showed low rates of resistance in nucleoside‐naïve patients during 5 years of ETV therapy, corresponding with potent viral suppression and a high genetic barrier to resistance, support ETV as a primary therapy that enables prolonged treatment with potentiral suppression and minimal resistance.

TL;DR: Infrequent ETV resistance can emerge during prolonged therapy, with selection of additional RT substitutions within a 3TCr HBV background, leading to reduced ETV susceptibility and treatment failure.

TL;DR: Mechanism of action studies demonstrated that BMS-378806 binds to gp120 and inhibits the interactions of the HIV-1 envelope protein to cellular CD4 receptors, and displays many favorable pharmacological traits, such as low protein binding, minimal human serum effect on anti-HIV-1 potency, good oral bioavailability in animal species, and a clean safety profile in initial animal toxicology studies.

TL;DR: It is suggested that the rapid, sustained suppression of HBV replication, combined with a requirement for multiple substitutions, creates a high genetic barrier to ETVr in nucleoside naïve patients.

TL;DR: In HBeAg-positive and H beAg-negative lamivudine-refractory patients, treatment with entecavir 1.0 and 0.5 mg daily was well tolerated and resulted in significant reductions in HBV DNA levels and normalization of alanine aminotransferase levels.