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1.乙型肝炎病毒（HBV）属嗜肝DNA病毒科，其基因组结构为长约3.2kb的不完全环状双链DNA分子。HBV共有4个开放阅读框，分别为S、C、P和X。4个阅读框之间有部分重叠。HBV基因组还有4个启动子和2个增强子，启动子和开放阅读框之间也有部分重叠。牛磺胆酸钠共转运多肽（sodium taurocholate co-transporting polypeptide, NTCP）可与乙型肝炎病毒包膜蛋白前S1的关键受体结合域发生特异性相互作用，被认为是HBV的受体。LHBs的PreS1区域与NTCP结合以及HBV进入细胞的过程需要细胞表面的硫酸肝素蛋白多糖与表皮生长因子受体共同作用。
2.HBV DNA在细胞核内转化为共价闭合环状DNA（cccDNA），作为转录模板合成不同大小的mRNA，进入细胞质翻译为病毒的各种蛋白质，另有一部分3.5kb的mRNA作为病毒前基因组，是病毒复制的模板。cccDNA与细胞的组蛋白结合，以微染色体的形式在细胞核中稳定存在，这也是HBV难以被彻底清除的原因。外周血中的HBV RNA病毒颗粒的含量与肝组织中cccDNA的水平和活性有关。
3.重型肝炎的发生和发展受病毒、宿主等多个方面因素的影响。HBV复制活性的增加、基因组变异及机体免疫状态的变化等均可诱发乙型重型肝炎。HBV的B基因型以及前C基因区的G1896A变异和C基因启动子区的A1762T/G1764A变异可能与慢加急性肝衰竭的发生相关。HBV基因突变可能导致病毒复制水平的改变，从而导致乙型肝炎重症化，不同区域的变异可能影响病毒生活周期的不同环节。
4.病毒蛋白对参与炎性损伤的某些宿主基因具有转录调控作用，导致相关基因的高度表达及炎症反应的暴发，参与重型肝炎的病理生理过程。
1.HBV belongs to thehepadnaviridae family.The HBV virion genome consists of an incomplete annular double-stranded DNA molecule approximately 3.2kb in size.HBVhas four overlapping open reading frames（ORFs），which encode the S，C，X and polymerase（P）genes.The HBV genome alsohas four promoters and two enhancers, and there are some overlaps between promoters and open reading frames.The receptor binding region of preS1has been reported to interact specifically with sodium taurocholate co-transporting polypeptide（NTCP）,a multiple transmembrane transporter predominantly expressed in the liver and shown to be a functional receptor for HBV.The bind of preS1 region of LHBs and sodium taurocholate co-transporting polypeptide（NTCP）and HBV entry into cells require the interaction ofheparan sulfate proteoglycans （HSPGs）and epidermal growth factor receptor（EGFR）on the cell surface.
2.Upon entry into the nucleus ofhost cells，HBV DNA forms a covalently closed circular form called cccDNA.The strand of cccDNA is the template for transcription of mRNAs of different length.The 3.5kb mRNA is called the pregenome；shorter subgenomic transcripts are translated into virus proteins. HBV cccDNA binds tohistones of the cell and they exist stably in the nucleus as microchromosomes. The HBV RNA virus particles in peripheral blood can be used to reflect the level and activity of cccDNA in liver tissue.
3.The “start point or control point” of the occurrence and development of severehepatitis is affected by both virus andhost factors. The increase of HBV replication activity, genomic variation and the change of immune state can induce the occurrence of severehepatitis B.HBV genotype B and the G1896A mutation in the preC gene may be associated with the development of acute-on-chronic liver failure.Mutations in HBV genes may lead to changes in viral replication levels that lead to severehepatitis B.
4.Viral proteinshave some functions like transcriptional regulation on somehost genes involved in inflammatory injury, leading tohigh expression of related genes and the outbreak of inflammatory response, participating in the pathophysiological process of severehepatitis.