| The life cycle of hepatitis B virus can be divided into several steps: attachment of the virus to the hospital cells; penetration into the cell; release of the viral genome; assembly of virions; release of the virus. In contrast to most other virus, HBV comprises a further pathway, allowing the entry of viral DNA from cytosol into the nucleus. The mechanism of HBV nucleus translocation contains two aspects, one is from cytosol into the nucleus, and another is from the nucleus into cytosol. There still exist contradiction, although many study in this area have been done over past two decade. The focus is whether exists nucleus translocation of core particles. Kamimura T , Me Caul TF ,Yamaguchi et al .found core particles migrated from the nucleus into the cytoplasm through the nuclear pores by electron microscopic observations. Core particles existed in nucleus in most cells. Nucleus translocation site is the mid of nucleus pore. Recent study showed that the maximal diameter of nucleus pore of 25 nm is exceeded by the exprementally-determined size of the core particles of 36 nm by far. The core particles cannot cross the nuclear membrane in ether direction. HBV nucleo-capsids were exclusively in nuclear, but they were released to cytoplasm when nuclear membrane disintegrated during mitosis. The entry of HBV genome to nuclear is an important step of HBV replication in hepatocytes. In the first part of our study, we inspect the core particle protein and genome location and migration during the nucleus translocation by cytobiological technique and isotopes traced method. Inaddition, we clarify the suspicion that nucleo-capsids be dispersed before HBV genome entry to nucleus.Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA), the generator of offspring virus particles, is a continuous double chain ring, while other DNA forms contain a gap on each chain at the position of direct repeat 1 sequence (DRl) and direct repeat 2 sequence (DR2) respectively. Once HBV enters cytoplasm, it releases the nucleocapid from the surface antigen envelope; subsequently, the circular genome is translocated to the nucleus. HBV RNA transcription can only occur only after modifications of infecting viral genome. The single strand DNA region of the HBV genome is then converted to double-stranded DNA. Both legations of the nicks that occur in the double strand DNA generate HBV cccDNA. In a sense, cccDNA is the real template of the next generation virus. A 3.5 KB terminally redundant transcript was produced to serve as the pregenomic RNA templates for next generation DNA synthesis through host cellular RNA polymerase II. The minus strand of HBV genome is synthesized by the viral reverse transcriptase. HBV cccDNA appears to be the major viral replicate DNA species; and is resistant to conventional antiviral agents. Lamivudine and interferon are two agents used commonly for treatment of chronic hepatitis B. Lamivudine in particular, is reported to have greatest clinical significance in China. Other studies showed that it could inhibit viral polymerase reverse transcriptase activity, and then repress the production of HBV. It was reported that most patients that continued intaking lamivudine for a period of time, had rapidly falling serum HBV DNA level. However, the decrease of the HBsAg and HBeAg is not as obvious as HBV DNA. The patients' cccDNA, which synthesizes directly HBV, remaining stable in the hepatocyte nucleus, may account for the resistance of the virus. If the treatment in which lamivudine is discontinued, HBV particles will reappear rapidly so it is difficult to decide how long patients' treatment with lamivudine should continue. Quantitative analysis of cccDNA is of importance; however, there is still shortage of good methods to detect the HBV cccDNA. Southen blot is a classical method to analyze HBV cccDNA; but, the process is too complex; and the sensitivity is not high developed a quantitativecompetitive PCR assay for DHBV cccDNA. However, in such an assay,electrophoresis and Sou...
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