Chronic infection with hepatitis B /C virus (HBV /HCV)is a widespread epidemic in China.The single nucleotide polymorphisms (SNPs)in interleukin 28B (IL28B)gene have been associated with chronic HBV /HCV infection and response to interferon therapy.The biological functions and characteristics of IL28B are elaborated on,the associations between HCV infection and IL28B SNPs are commented on,and current reports of associations between HBV infection and IL28B SNPs are reviewed.The results support the associations between IL28B SNPs and disease progression of HCV infection or the curative effect of interferon therapy.However,contradictive results have been obtained in studies of associations between IL28B SNPs and disease progression of HBV infection,the incidence of liver cirrhosis and primary liver cancer after HBV infection,or the curative effect of interferon therapy,so further investigation is needed.

Objective To investigate the effect of HBV on the expression of fibrosis-related factors in hepatic stellate cells(HSC)and its relation with liver fibrosis.Methods HSCs were co-cultured with HepG2 or HepG2.2.15 in vitro and HSCs cultured alone served as the control.The mRNA expression of matrix metalloproteinase(MMP)-2 and tissue inhibitor of metalloproteinase(TIMP)-1 was detected by realtime PCR.The protein expression of MMP-2 and TIMp-1 was detected by Western-blot.Results Compared with the control and the HSCs co-cultured with HepG2,the expression of MMP-2 and TIMP-1 mRNA in HSCs co-cultured with HepG2.2.15 was increased remarkably and the most significant difference was found at 72 h(F=11.91,23.13;P=0.008,0.001);the expression of MMP-2 and TIMP-1 protein in HSCs co-cuhured with HepG2.2.15 was also increased remarkably and the most significant difference was found at 72 h(F=20.70,6.54;P=0.002,0.003)too.Conclusion The expression of fibrosis-related factors in HSCs increased significantly after co-cultured with HepG2.2.15,which suggests that HBV could promote liver fibrosis.

3' Untranslated Regions ; genetics ; Base Sequence ; China ; DNA, Complementary ; chemistry ; genetics ; Genetic Variation ; Hepacivirus ; genetics ; Humans ; Molecular Sequence Data ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Alignment ; Sequence Analysis, DNA ; Sequence Homology, Nucleic Acid

OBJECTIVETo obtain very end full-length cDNA of hepatitis C virus (HCV) 5' untranslated region (5' UTR), and analyse its primary and secondary structure.

METHODSBy reverse transcription-nested polymerase chain reaction (RT-PCR) and restriction fragment length polymorphism (RFLP), a patient infected with genotype 2a HCV was found. Total RNA isolated from the serum as template, the cDNA of 5' noncoding region was amplified using rapid amplification of cDNA ends methods (RACE), the fragments were recombined by A-T clone strategy, the recombinants were confirmed by RFLP and PCR then sequenced. Secondary structures were analysed by RNA draw.

RESULTSVery end full-length cDNA of 2a genotype HCV 5' UTR was obtained by RACE. In five clones obtained, three contained full-length 5' UTR cDNA, and A21G, G170A, T222C, T247C, C339T substitutions were found compared with HC-J6. he homologies with HCV-1,HC-J6,HC-C2, HC-J8 were 93.6%-94.4%, 92.1%-93.0%, 98.8%-99.7%, 96.2%-96.5%, respectively; however, the substitutions did not alter the secondary structure. Two out of five clones were deleted to have 53 and 144 bases at 5' terminus of HCV 5' UTR, respectively.

CONCLUSIONSRACE is rapid and effective, works well to obtain very end of virus genome. With that, Authors obtained full-length cDNA of genotype 2a of HCV 5' UTR. There are genes deleted at 5' terminus circulated in hepatitis C patients.

5' Untranslated Regions ; genetics ; Base Sequence ; DNA, Complementary ; genetics ; DNA, Viral ; genetics ; Hepacivirus ; classification ; genetics ; isolation & purification ; Hepatitis C ; virology ; Humans ; Molecular Sequence Data ; Nucleic Acid Amplification Techniques ; methods ; Polymorphism, Restriction Fragment Length ; Reverse Transcriptase Polymerase Chain Reaction ; Sequence Analysis, DNA

The incidence rate of nonalcoholic fatty liver disease (NAFLD) is gradually increasing, and NAFLD has become the most important chronic liver disease in China. At present, the pathogenesis of NAFLD has not been fully elucidated and there are still no effective drugs. From the perspectives of pathogenesis, noninvasive diagnosis, and drug action and efficacy, this article introduces the research advances in metabolomics regarding endogenous small molecule metabolites in NAFLD, so as to provide new ideas and methods for further exploration of NAFLD.