“…Other mutations with clinical significance were sY100S, sK122R, sM197T, sW201*, sS204R and sS204N which impair the production and secretion of HBsAg, associated with low HBV viral load and OBI [ 25 , 26 , 27 , 28 , 29 , 34 , 35 , 37 ]. In the polymerase region, the most common mutations were rtS109P, rtM129L and rtV163I found in seven participants each similar to other studies which reported these mutations in genotype A and indeed these mutations were present in genotype A in this study [ 49 , 50 , 51 ]. These three mutations appeared together in six genotype A participants; rtS109P was also found in genotype E. We report no classic drug resistance-associated mutations such as rtL80I/V, rtV173L, rtL180M, rtA181S, rtA194T, rtS202I, rtM204V/I, rtN236T and rtM250L/V associated with resistance against lamivudine, telbivudine, adefovir, entecavir and tenofovir in this study similar to other studies [ 21 , 51 , 52 ].…”