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  • Author: Jun Cheng x
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Chinese Consensus on Diagnosis and Treatment of Hepatic Encephalopathy
Chinese Expert Committee on Hepatic Encephalopathy
Open access
Consensus. Chinese Consensus on Combination Therapy of Chronic Hepatitis B
Professional Staff Committee of Combination Therapy of Chronic Hepatitis B
Open access
Chinese Expert Consensus for the Diagnosis and Treatment of Cholestatic Liver Disease
Chinese Expert Committee on the Diagnosis and Treatment of Cholestatic Liver Disease
Open access
Editorial. The Role of Autophagy in Hepatitis C Virus Infection

Abstract

Hepatitis C virus (HCV) infects ≈2% of the world’s population. HCV infection not only causes acute and chronic hepatitis, but also leads to liver cirrhosis and hepatocellular carcinoma (HCC). The molecular pathogenesis of HCV infection has been explored and many evidence indicated that autophagy is an important process for its life cycle, although autophagy was thought as a mechanism to eliminate invaded HCV from hepatocyte. Structural and non-structural proteins of HCV are important regulators of autophagy, and HCV uses autophagy as a necessary step in its replication. Down-regulation of innate immune response by HCV through unfolded protein response (UPR) and autophagy induction was used as a pathway to establish chronic HCV infection in the liver. Meanwhile, the infected hepatocyte is also using autophagy mechanism to eradicate HCV virus from liver. The study on relationship between HCV and autophagy will pave the new way to understand HCV life cycle and to find new strategy for prevention and treatment of liver diseases caused by HCV infection.

Open access
Quasispecies of Hepatitis B Virus

Abstract

Hepatitis B virus (HBV) circulates in blood and replicates in the presence of quasispecies. During HBV replication, HBV DNA polymerase lacks fidelity and proofreading function partly because its exonuclease activity is either absent or deficient. Therefore, HBV genome is mutated with unusually high frequency. And these mutations can affect more than one open reading frame due to overlapping genes. Otherwise, natural substitutions, deletions or insertions involving the Cp/EN∥ locus in the X gene can significantly alter the extent of viral replication activity. Particular selection pressures such as host immune system and antiviral therapy readily select out escape mutants from this pre-existing quasispecies pool. Antiviral drug resistance in chronic hepatitis B (CHB) can be caused by the viral mutation frequency, the intrinsic mutability of the antiviral target site, the selective pressure exerted by the drug, the magnitude and rate of virus replication, the overall replication fitness of the mutant, the genetic barrier of the compound and the availability of replication space. Potent inhibition of HBV replication could be able to prevent the development of drug resistance because mutagenesis is replication dependent. Viral load may decline to a point where the continued production of quasispecies with the potential to resist new drug treatments no longer occurs, if viral replication can be suppressed for a sufficient length of time.

Open access
Acute Onset Pancreatitis in the Third Trimester of Pregnancy in HBV Carrier Women Taking Telbivudine for Blocking Mother-to-Infant Transmission

Abstract

Acute pancreatitis in pregnancy (APIP) is rare and the reasons for APIP are biliary disease and congenital or acquired hypertriglyceridemia, which could occur during any trimester but more than 50% cases happened during the third trimester. In this report, one case of a young pregnant woman, a HBV carrier in her 37th week + 5 d of gestation, was admitted to Emergency Department due to acute abdominal pain, vomiting and diarrhea. The patient was in antiretroviral treatment with telbivudine from 28 weeks of gestation to prevent motherto- child transmission of HBV. Laboratory tests demonstrated hypertriglyceridemia, abdominal computed tomography scan revealed peripancreatic edema. Hyperlipidemic pancreatitits was primary diagnosed and the patient was admitted to the intensive care unit. Considering the possible role in the pathogenesis of pancreatitis, telbivudine was interrupted after birth giving. After supportive treatment, her condition gradually improved. Since it is the first description of APIP during treatment with telbivudine, the association between pregnancy, hyperlipidemia, telbivudine and acute pancreatitis has been well investigated.

Open access
Regulation Mechanism of HBV cccDNA

Abstract

Covalently closed circular (ccc) DNA of hepatitis B virus (HBV) existed in the nuclei of HBV infected hepatocytes with a half-life time of 14.3 years in a mathematic model. Viral protein feedback regulation in HBV life cycle to maintain vital viral replication is an important mechanism. Interleukin-6, epithelial growth factor, heme oxygenase-1, histones, and hepatocyte nuclear factors are demonstrated as the key regulators for HBV life cycle. CpG island structure and methylation status are involved in the regulation of HBV DNA replication. Nucleos(t)ide analogues are widely used in the clinical practice for the treatment of chronic hepatitis B patients, although no evidence indicating a direct inhibiton of HBV cccDNA. In the future, along with the study of HBV life cycle, new drugs including RNA interference technique, will pave the way to eliminate the HBV cccDNA from infected hepatocytes resulting final cure of chronic hepatitis B.

Open access
Molecular Pathogenesis of Liver Steatosis Induced by Hepatitis C Virus

Abstract

Liver steatosis is a pathological hallmark in patients with chronic hepatitis C (CHC). Increased lipid uptake, decreased lipid secretion, increased lipid synthesis and decreased lipid degradation are all involved in pathogenesis of steatosis induced by hepatitic C virus (HCV) infection. Level of low density lipoprotein receptor (LDL-R) and activity of peroxisome proliferator-activated receptor (PPAR) α is related to liver uptake of lipid from circulation, and affected by HCV. Secretion via microsomal triglyceride transfer protein (MTTP), and formation of very low density lipoprotein (VLDL) have been hampered by HCV infection. Up-regulation of lipid synthesis related genes, such as sterol regulatory element-binding protein (SREBP)-1, SREBP-2, SREBP-1c, fatty acid synthase (FASN), HMG CoA reductase (HMGCR), liver X receptor (LXR), acetyl-CoA carboxylase 1 (ACC1), hepatic CB (1) receptors, retinoid X receptor (RXR) α, were the main stay of liver steatosis pathogenesis. Degradation of lipid in liver is decreased in patients with CHC. There is strong evidence that heterogeneity of HCV core genes of different genotypes affect their effects of liver steatosis induction. A mechanism in which steatosis is involved in HCV life cycle is emerging.

Open access