IntroductionHEPATITIS B virus (HBV) infection is a global health problem. Current estimates are that 2 billion people have been infected worldwide, of these, 360 million suffer from chronic HBV infection resulting in over 520 000 deaths from acute HEPATITIS B and 470 000 from cirrhosis or liver cancer(1). The prevalence of HEPATITIS B carriers varies in different parts of the world, ranging from less than 1% to 15%. In the Middle East, the endemicity is intermittent, with a carrier rate of 2% to 7% (2). It is estimated that over 35% of Iranians have been exposed to the HBV and about 3% are chronic carriers, ranging from 1.7% in Fars Province to over 5% in Sistan and Balouchestan(3).

Background and Aims: To initially explore the underlying pathogenesis of the relationship between genotypes of HEPATITIS B virus (HBV) and its clinical manifestations. Methods: The S and C genes of HBV from 60 serum samples, infected by HBV of genotypes B or C were amplified by PCR. The products were recombined with vector pEGFP-C1, which is an internal reference for transfection, to construct the eukaryotic expression recombinant plasmids, followed by cloning and subcloning. Then they were transfected into hepatocarcinoma cell HepG2. The increment rates and apoptosis rates of these transfected cells were determinated by MTT and flow cytometer, respectively. Results: The 120 eukaryotic expression recombinant plasmids were all constructed successfully. As an internal reference for transfection, EGFP confirmed that large S protein and C protein of HBV had been expressed in all HepG2 cells. It was found by flow cytometer that the apoptosis rates of HepG2 cells transfected by pEGFP-C1/HBs or pEGFPC1/HBc from HBV-genotype C samples were all significantly higher than that from HBV-genotype B samples (P=0.009 & P=0.001, respectively).Conclusions: HBV of genotype C can induce more serious cell apoptosis than HBV of genotype B. Difference in apoptosis may be an important reason that HBV of genotype C can induce more severe liver injury than HBV of genotype B.

Autoimmune HEPATITIS (AIH) is one of causes of chronic liver diseases. It is an unresolving inflammation of liver tissue and characterized by elevated transaminases, hypergammaglobulinemia, and circulating autoantibodies. The disorder occurs mostly in females (F:M ratio is 3.6 to 1) and is a relatively uncommon disorder with point prevalence of 8-16.8 per 100 000 population in western countries. Hiostologic hallmarks are interface HEPATITIS (also called piecemeal necrosis), and portallymphoplasmacytic infiltration.Dignostic criteria are based on excluding other etiologies of chronic liver disease,such as viral hepatic (A, B, C), metabolic disorders eg Wilson disese,drug induced HEPATITIS and alcoholic liver disease. Conventional autoantibodies are Antinuclear antibody (ANA), Smooth muscle antibody (SMA) and Anti liver kidney microsomal 1 (Anti LKM1).Some cases have combined clinical, laboratory or histologic features of Primary Biliary Cirrhosis (PBC) or Primary Sclerosing Cholangitis (PSC) with AIH and are known as overlap syndrome. Standard treatments of AIH as the most successful treated form of chronic HEPATITIS are based on immunosuppression with corticosteroids alone or in combination with azathioprine.

Introduction: Chronic HEPATITIS B is a major medical problem, distributing all over the world. Affecting more than 400 million people. In highly prevalence places, childhood transmission is the most common form but in low prevalence areas, injection, drug use and familial transmission are the main routes of acquisation of infection. Hepatocellular carcinoma and cirrhosis are significant problems of chronic HEPATITIS B. Exposure to HBV early in life may progress to hepatocellar carcinoma. The annual number of deaths from HBV infection and related diseases throughout the world is about 1.2 million. The goal of treatment of chronic HEPATITIS B with Lamivudin or INF-Alpha is sustained suppression of virus replication and liver disease remission. INF, Alpha and Lamivudin have similiar efficacy. The adventage of Lamivudin is that it is less expensive and is well tolerated and adventages of INF. Alpha are the short duration of treatment and absence of resistance but it is expensive and has many side effects. The response rate of INF. Alpha is better than Lamivudin but it is associated with a large number of side effects, sometimes we have to stop or decrease the dose of INF. Viral genotypes and other factors such as pretreatment viral load, fatty liver and liver histiology may alter the response rate. The long-term use of Lamivudin may be with the emergence of YMDD mutations. Treatment of YMDD form of chromic HEPATITIS B, with combination of Lamivudin and Adefovir dipivoxil, may improve liver function; and YMDD mutations may be over come. The emergence of YMDD mutations reduces the benefit of Lamivudin but does not negate it.