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Chronic hepatitis B (CHB) infection is actually a leading cause of improvement of liver cirrhosis and/or hepatocellular carcinoma (HCC).1 Due to the fact the higher serum HBV DNA level indicating active virus replication has been identified as an independent threat element for improvement of cirrhosis and HCC in two large-scale research,2,three the remedy of goal inside the current era of antiviral therapy is sustained suppression of viral replication via antiviral therapy.four For this purpose, current antiviral agents with very good potency and security, tolerability, and convenience to raise adherence was continuously developed. Since lamivudine (LAM), a first-generation oral nucleoside analogue (NA) have been accessible in 1998, the paradigm of CHB treatment has been changed substantially. Actually, the usage of LAM had substantially reduced the incidence of hepatic events in sufferers with advanced fibrosis or compensated cirrhosis.5 Having said that, such a clinical benefit may be substantially offset by a high rate of resistance of as much as 80 .six,7 The incidence rates of telbivudine resistance had been four.4 at year 1 and 21.6 at year two in HBeAg positive CHB sufferers, and 2.7 at 1 year and 8.6 at year 2 in HBeAg damaging CHB individuals.8,9 Virological breakthrough with rtM204V/I mutations occurred in four at year 1 and 20 at year two in CHB sufferers with clevudine.ten For those who created resistance to NAs which includes LAM, telbivudine or clevudine, the adverse effects of HBV drug resistance mutations may possibly be overcome by the addition of adefovir dipivoxil (ADV).11 Having said that, in accordance with the study carried out in Korea, comprehensive virological response (CVR) was accomplished only in 32.4 throughout ADV and LAM combination (referred as ADV+NA) therapy in LAM-resistant patients.12 In an additional study, cumulative rates of CVR had been 29.9 at 1 year and 86.9 at five ye.