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PURPOSE OF THE STUDY:The monitoring of cccDNA levels can provide a direct indication of HBV activity in the liver of HBV infected patients. The aim of this study was to quantify the cccDNA levels in sera and intrahepatic levels of HBV DNA and cccDNA in liver biopsies of treatment na€ ıve patients with chronic hepatitis B. METHOD: Eighty one chronic HBV treatment na€ ıve patients were enrolled from January 2009 to June 2011. The levels of intrahepatic HBV DNA and cccDNA were quantified using real time PCR method. SUMMARY OF RESULTS: The mean age of recruited patients was 34 AE 11.5 years. A total of 54 patients (66.7%) were HBeAg negative. Liver biopsy was done in 23 patients (21 HBeAg negative and 2 HBeAg positive). The levels of total intrahepatic HBV DNA ranged from 0.09 to 1508.92 copies/cell. The median intrahepatic HBV cccDNA were 0.31 copies/cell (range 0.14-0.49 copies/cell) and 0.20 copies/cell (range 0.01-1.63 copies/cell) in HBeAg positive and HBeAg negative cases, respectively. The rate of serum HBV cccDNA detection was 85.2% and 48.1% in HBeAg positive and negative patients, respectively. The median level of serum HBV cccDNA was 46,000 copies/ mL in HBeAg positive cases, while it was 26,350 copies/ mL in HBeAg negative disease. The levels of intrahepatic HBV total DNA had a positive correlation with intrahepatic HBV cccDNA (r = 0.533, p = 0.009). A positive correlation was observed between serum cccDNA levels and serum HBV DNA levels (r = 0.871, p < 0.001). CONCLUSION: It was concluded that serum HBV DNA and serum cccDNA levels were significantly higher in HBeAg positive patients than HBeAg negative patients. P38The effect of 're-cycling' genome DNA of HBV for the intracellular replication dynamics J Nakabayashi Yokohama City University, Yokohama, Japan Hepatitis B virus (HBV) is a major causative agent of the acute and chronic hepatitis. The viral load observed in the peripheral blood is quite different between the acute and chronic hepatitis. The replication dynamics of HBV plays a critical role determining the clinical course of the hepatitis. We constructed a mathematical model for the replication process of HBV in infected cell to investigate the intracellular replication dynamics of HBV. The amount of newly produced virion is drastically changed by the slight alteration of the expression rate of viral genes, 3.5 kb RNA that contributes to the replication of the core particle and 2.1 kb RNA that is translated into HBs antigen. This model is based on the single cycle of HBV replication because the re-cycling of the genome in the newly replicated core particle is not taken into consideration. A part of the newly replicated HBV genome in the core particle should participate in further replication of HBV. On the other hand, a part of the core particle is packaged by the envelope to produce new virions those are released through the exocytosis of the host to expand the infection. Here we present the expanded model including the 're-cycling' process of the genome DNA of HBV. The model reveals that the...

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