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Introduction: Infection due to hepatitis B virus (HBV) could be due to wild or mutant viruses. The HBeAg negative chronic hepatitis B (HbeAg-CHB) is unable to produce hepatitis B, e antigen (HbeAg), so that patients with this varient do not present with HBV characterized by HbcAg in the serum. HbeAg-CHB usually proceeds to serious liver disease. The prevalence of different viral forms in patients with chronic liver disease in Iran has not been established.
Materials and Methods: Seventy-six Hamadanian patients with over 6 months HBSAg positivity were enrolled. Patients with co-infection of HIV, HCV, past history of alcoholism, fatty liver, using of hepatotoxic drugs, autoimmune hepatitis and other metabolic liver disease were excluded. All patients were screened for Hhe Ag. HbeAb. HBV DNA by PCR, AST, ALT, ALK. pH and bilirubin.
Results: Eleven (14.5%) patients had HheAg-CHB (HbsAg +ve, HbeAg-ve / ve/anti HbeAb + ve, HBV DNA + ve and elevated AST, ALT) and 6 (8%) had normal transminases (AST and ALT) accompanied by the remaining criteria of HbeAg-CHB. 59 patients (77.5%) were infected with wild type HBV, ie: HBSAg + ve, HbeAg-ve, HbeAb + ve, HBV DNA- ve, and normal AST, ALT.
Conclusion: Frequency of HbeAg.CHB in Hamadan is 14.5% knowing of this varient of chronic hepatitis B is important since the HbeAg-CHB have worse prognosis than wild type and more better response to lamivudine than interferon.

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Background: Nucleos(t)ide analogues, such as lamivudine and adefovir, are effective drugs for treatment of hepatitis B patients. However, long-term treatment with these drugs leads to the emergence of the nucleos(t)ide analogue resistant strains. The impact of nucleos(t)ide analogues on the emergence of HBsAg escape mutations is not clarified. Hence, the aim of this study was to determine HBsAg escape mutations in chronic hepatitis B patients treated with nucleos(t)ide analogues. Materials and Methods:A cross-sectional study was performed on 50 patients with chronic hepatitis B under treatment with nucleos(t)ide analogues (lamivudine and/or adefovir) and 50 naive chronic hepatitis B patients. HBV DNA was extracted from plasma and S gene of virus was amplified by Nested-PCR followed by direct sequencing. HBsAg gene sequence of the samples was evaluated for detection of HBsAg escape mutations. Results: Among the 100 patients, the following HBsAg escape mutations were identified: sQ101H, sG119R, sP120S, sP127S, sA128V, sG130N, sG130R, sT131I, sM133I, and sY134N. The frequency of HBsAg escape mutations in patients under treatment of nucleos(t)ide analogues was 16% and in naïve patients was 6% (p=0.2, OR=2.98). Conclusion:According to the obtained results, there seems to be no association between using nucleos(t)ide analogues and emergence of HBsAg escape mutations.