Hepatitis B ; virology ; Hepatitis B virus ; physiology ; Humans ; Virus Replication

Binding Sites ; Hepatitis B virus ; physiology ; Virus Attachment

Hepatitis B virus (HBV) infection is an important public health concern, as approximately 3.5% of the world's population is currently chronically infected. Chronic HBV infection is the primary cause of cirrhosis, hepatocellular carcinoma, and deaths related to liver disease globally. Studies have found that in HBV infection, viruses can directly or indirectly regulate mitochondrial energy metabolism, oxidative stress, respiratory chain metabolites, and autophagy, thereby altering macrophage activation status, differentiation types, and related cytokine secretion type and quantity regulations. Therefore, mitochondria have become an important signal source for macrophages to participate in the body's immune system during HBV infection, providing a basis for mitochondria to be considered as a potential therapeutic target for chronic hepatitis B.
Humans ; Hepatitis B virus/physiology* ; Hepatitis B/complications* ; Hepatitis B, Chronic/complications* ; Mitochondria ; Liver Neoplasms ; Macrophages

Critical Illness ; Hepatitis B virus ; genetics ; physiology ; Hepatitis B, Chronic ; virology ; Humans ; Transcription, Genetic ; Virus Replication

Hepatitis B ; immunology ; virology ; Hepatitis B Antibodies ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; immunology ; physiology ; Humans ; Immunologic Tests ; methods ; Virus Replication

Background: Hepatitis B is an infectious illness caused by hepatitis B virus (HBV) which infects the liver of hominoidea, including humans, and causes an inflammation called hepatitis. Objectives: The aim of study is to clarify clinical features and molecular characteristics of HBV in chronic HBV-infected patients with A 1899 mutation. Subjects and method: HBV genotype, HBV-ONA level, HBeAg and anti-HBe in 29 chronic HBV-infected patients were determined by PCR-RFLP, Real-time PCR and ELISA, respectively. Mutations were analyzed by direct sequencing. Results: Mutations in core-promoter/precore regions of HBV genome can suppress HBeAg secretion and stimulate HBV-ONA replication. The prevalence of hepatocel- lular carcinoma (HCc): 10/29, liver cirrhosis (LC) : 15/29 are significantly higher than that in chronic hepatitis (CH) : 4/29 (P < 0.001). HbeAg seroconversion rate in CH (75%) is higher than that in HCC \r\n', u'(40%) and in LC (53.3%), but not significant (P > 0.05). ALT level is the highest in CH and the lowest in HCC \r\n', u'(P = 0.02), 8/10 (80%) HCC patients have normal range of ALT. HBV-ONA level in HCC and in LC is significantly higher than that in CH (P = 0.024). The emerging of A 1899 is often accompanied by C/G1753 mutation (37.9%) and dual core-promoter mutation T1762A1764 (79.3%). Conclusion: A1899 mutation can play a role in the pathogenesis of liver diseases in chronic HBV-infected Vietnamese.\r\n', u'
Hepatitis B virus/ growth & ; development ; physiology ; Hepatitis B ; Chronic/ pathology ; transmission

Animals ; Disease Models, Animal ; Hepatitis B ; physiopathology ; Hepatitis B virus ; physiology

<b>OBJECTIVEb>To clarify the relationship between fatal severe form hepatitis occurred during chronic hepatitis B and superinfections of hepatitis A, C, D or E virus as well as hepatitis B e system status and to adopt corresponding measures to reduce the mortality of chronic hepatitis B.

<b>METHODSb>This study detected the superinfections with hepatitis A, C, D or E virus and hepatitis B e system status in 219 patients with fatal severe form hepatitis occurred during chronic hepatitis B by enzyme linked immunosorbent assay.

<b>RESULTSb>The superinfections with hepatitis A, C, D or E virus were found in 1.4% (3/219), 9.6% (21/219), 1.8% (4/219) and 30.1% (66/219) of the patients, respectively, altogether 42.9% (94/219); hepatitis E was prominent and steady in superinfection rate in recent ten years. The causes of 57.1% (125/219) patients were not clear. The positive rate of HBeAg and anti-HBe were 17.0% (16/94) and 54.2% (51/94) in the group of superinfections with hepatitis A, C, D or E virus; and were 27.2% (34/125) and 47.2% (59/125) in the group with unknown causes, respectively.

<b>CONCLUSIONb>These results suggested that the patients with superinfections reached 42.9% (94/219), and the superinfections may be a part of causes of fatal severe form hepatitis, and the mortality of chronic hepatitis B may be decreased by strict food sanitation and use of safe blood products. There were no significant relation between hepatitis B e antigen seroconversion and the fatal severe form hepatitis occurred during chronic hepatitis B.

Adult ; DNA, Viral ; blood ; genetics ; Female ; Hepacivirus ; genetics ; physiology ; Hepatitis A virus ; genetics ; physiology ; Hepatitis B Core Antigens ; blood ; Hepatitis B Surface Antigens ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; genetics ; immunology ; physiology ; Hepatitis B, Chronic ; blood ; mortality ; virology ; Hepatitis Delta Virus ; genetics ; physiology ; Hepatitis E virus ; genetics ; physiology ; Host-Pathogen Interactions ; Humans ; Male ; Middle Aged ; Superinfection ; virology ; Survival Rate

<b>OBJECTIVEb>To evaluate the replication and encapsidation of HBV mutants with the truncated C gene.

<b>METHODSb>The HBV mutants with the truncated C gene were constructed by molecular cloning and PCR-based deletion in vitro. The replication and encapsidation of HBV mutants were investigated by Southern blotting, PCR and real-time fluorescence PCR respectively after transfecting the HBV mutants plasmid into HepG2 cells by using liposome.

<b>RESULTSb>The C-truncated HBV mutant vectors were constructed successfully and confirmed exactly by clone sequencing and enzymes digestion. The C-truncated HBV mutants were replication defective, however, all types of HBV DNA could be detected positive in the cytoplasm and supernatant after co-transfecting the C-truncated HBV mutants plasmid and the helper constructs into HepG2 cells. The C-truncated HBV mutants were proved to produce 3-40 folds more progeny DNA than that of the wild-type HBV by DNA quantitative assay.

<b>CONCLUSIONb>The C-truncated HBV mutants are replication-deficient and could not replicate and encapsulate in the hepatocytes when transfected solely, however, the progeny HBV-variant viruses are encapsidated more effectively to secrete into supernatant when co-transfected with the helper construct which lacks part of 5 prime-proximal HBV RNA packaging signal Epsilon.

Cell Line, Tumor ; Hepatitis B Core Antigens ; genetics ; Hepatitis B virus ; genetics ; physiology ; Humans ; Mutation ; Plasmids ; genetics ; Transfection ; Virus Replication

Genotype ; Hepacivirus ; genetics ; physiology ; Hepatitis B ; complications ; Hepatitis B virus ; Hepatitis C ; complications ; Humans ; RNA, Viral ; analysis