Hepatitis B virus (HBV) is a common viral pathogen that currently infects an estimated 4 million people worldwide, including 400 million who have chronic infection. Persons with chronic HBV infection are at a lifelong risk of developing hepatocellular carcinoma (HCC) or cirrhosis, or both. Many persons with HBV are unaware that they carry the infection, and, of those who are chronically infected, only a minority receives routine, scheduled follow-up to monitor their disease status. Persons from high-risk populations, especially immigrants from nations where hepatitis B is highly endemic, should be tested for HBV seromarkers and should be vaccinated if they are found to be negative. The natural history of chronic HBV is a dynamic one: patients can fluctuate between periods of active liver inflammation and periods of inactive disease. Disease progression is influenced by various factors, including viral genotype and specific mutations, demographic features, concurrent viral infections, and social and environmental factors. Recent data suggest that antiviral therapy can decrease the risk of liver decompensation and liver-related death and reduce the risk of HCC in selected individuals with active liver disease and severe fibrosis. Persons identified with chronic HBV infection need lifelong, regular monitoring for the development of active liver disease and HCC.
"Chronic hepatitis B (CHB) is a global health problem with an estimated 400 billion people worldwide being chronically infected with the virus (HBV) . Chronic infection with HBV can significantly impair the quality of life and life expectancy of patients. "
[Show abstract][Hide abstract] ABSTRACT: Objective
. To evaluate the efficacy and safety of Kushenin (KS) combined with nucleoside analogues (NAs) for chronic hepatitis B (CHB).
. Randomized controlled trials (RCTs) of KS combined with NAs for CHB were identified through 7 databases. Frequencies of loss of serum HBeAg, HBeAg seroconversion, undetectable serum HBV-DNA, ALT normalization, and adverse events at 48 weeks were abstracted by two reviewers. The Cochrane software was performed to assess the risk of bias in the included trials. Data were analyzed with Review Manager 5.3 software.
. 18 RCTs involving 1684 subjects with CHB were included in the analysis. KS combined with NAs including lamivudine (LAM), entecavir (ETV), adefovir dipivoxil (ADV), and telbivudine (TLV) showed different degree of improvement in CHB indices. KS combined with NAs increased the frequency of loss of serum HBeAg, HBeAg seroconversion, undetectable HBV-DNA levels, and ALT normalization compared with single agents. It also decreased serum ALT and AST level after one-year treatment. However, KS combined with TLV did not show a significant difference in CHB indices. The side-effects of KS combined with NAs were light and of low frequency.
. KS combined with NAs improves the efficacy of NAs in CHB.
Evidence-based Complementary and Alternative Medicine 09/2015; 2015(3):529636. DOI:10.1155/2015/529636 · 1.88 Impact Factor
"Worldwide, over two billion people are infected with HBV at present, and approximately 400 million are chronically infected carriers  . Furthermore, 80% of chronic HBV carriers have varying degrees of liver damage, which could progress to liver cirrhosis and hepatocellular carcinoma . "
"Chronic HBV infection is currently a major public health burden, affecting approximately 240 million individuals worldwide . These patients have an elevated risk of chronic active hepatitis, cirrhosis or primary hepatocellular carcinoma   . "
[Show abstract][Hide abstract] ABSTRACT: Hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) plays a central role in chronic HBV infection. However, analysis of the molecular mechanism of cccDNA formation is difficult because of the low efficiency in tissue cultured cells. In this study, we developed a more efficient cccDNA expression cell, Hep38.7-Tet, by subcloning from a tetracycline inducible HBV expression cell, HepAD38. Higher levels of cccDNA were produced in Hep38.7-Tet cells compared to HepAD38 cells. In Hep38.7-Tet cells, the cccDNA was detectable at six days after HBV induction. HBV e antigen (HBeAg) secretion was dependent upon cccDNA production. We screened chemical compounds using Hep38.7-Tet cells and HBeAg secretion as a marker. Most of the hit compounds have already been reported as anti-HBV compounds. These data suggested that Hep38.7-Tet cells will be powerful tools for analysis of the molecular mechanism of cccDNA formation/maintenance and development of novel therapeutic agents to control HBV infection.
Biochemical and Biophysical Research Communications 09/2014; 452(3). DOI:10.1016/j.bbrc.2014.08.029 · 2.30 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.