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HBV Sequences (hbv + sequence)
Selected AbstractsPrevalence, whole genome characterization and phylogenetic analysis of hepatitis B virus in captive orangutan and gibbonJOURNAL OF MEDICAL PRIMATOLOGY, Issue 6 2008Pattaratida Sa-nguanmoo Abstract Background, Hepatitis B virus (HBV) is a public health problem worldwide and apart from infecting humans, HBV has been found in non-human primates. Methods, We subjected 93 non-human primates comprising 12 species to ELISA screening for the serological markers HBsAg, antiHBs and antiHBc. Subsequently, we detected HBV DNA, sequenced the whole HBV genome and performed phylogenetic analysis. Results, HBV infection was detected in gibbon (4/15) and orangutan (7/53). HBV DNA isolates from two gibbons and seven orangutans were chosen for complete genome amplification. We aligned the Pre-S/S, Pre-C/C and entire genomes with HBV sequences and performed phylogenetic analysis. The gibbon and orangutan viruses clustered within their respective groups. Conclusions, Both geographic location and host species influence which HBV variants are found in gibbons and orangutans. Hence, HBV transmission between humans and non-human primates might be a distinct possibility and additional studies will be required to further investigate this potential risk. [source] Can the serological status of "anti-HBc alone" be considered a sentinel marker for detection of "occult" HBV infection?JOURNAL OF MEDICAL VIROLOGY, Issue 4 2008Francesco Vitale Abstract Some individuals have "occult" infection with hepatitis B virus (HBV), defined as presence of HBV genome in the serum or liver tissue without HBV surface antigen (HBsAg) in the serum. The aim of this study was to investigate whether serum antibodies against HBV core antigen in isolation ("anti-HBc alone") are a useful marker of "occult" HBV in patients with or without hepatitis C virus (HCV) infection. "Anti-HBc alone" was detected in the sera of 119/6,544 (1.8%) asymptomatic outpatients referred to the diagnostic laboratory for routine testing for viral hepatitis, 62/607 (10.2%) drug users, and 42/195 (21.5%) patients with hepatocellular carcinoma. Using three in-house nested-PCR amplification assays to detect HBV preS-S (S), precore-core (C), and Pol viral regions, respectively, "occult" HBV sequences were found in 9 of the 223 sera (4.0%) with "anti-HBc alone." The highest prevalence of "occult" HBV sequences (5.9%) was detected in "anti-HBV alone" sera of individuals referred to the diagnostic laboratory without HCV antibodies. Direct sequencing of all PCR products confirmed the specificity of the PCR reactions and revealed the predominance of HBV genotype D. The data presented in this study suggest that detection of "anti-HBc alone" could reflect unrecognized "occult" HBV infection and that physicians should consider investigating such patients with HBV molecular tests. J. Med. Virol. 80:577,582, 2008. © 2008 Wiley-Liss, Inc. [source] Comparison of full length sequences of hepatitis B virus isolates in hepatocellular carcinoma patients and asymptomatic carriers of Korea,JOURNAL OF MEDICAL VIROLOGY, Issue 1 2005Byung-Cheol Song Abstract Relatively few genomic sequences of Korean hepatitis B virus (HBV) isolates are available. Moreover, no comparative study has been made between the full-length genomes of Korean HBV isolates and clinical status. To evaluate mutations in HBV isolates obtained from chronically infected HBV patients in terms of clinical significance, we determined the genomic sequences of HBV isolates obtained from three hepatocellular carcinoma (HCC) patients (He52, He53, and He82) and from three asymptomatic carriers (He74, He100, and He127). A comparison of sequence variations showed that the HBV isolates from the three HCC patients showed higher frequencies of mutation than the isolates from the three asymptomatic carriers. Three characteristic mutation patterns were identified in the HBV isolates from the HCC patients, which distinguished the HBV isolates from the asymptomatic carriers. First, HBV isolates from the three HCC patients both had double mutations in a core promoter (T1762/A1764) and a precore mutation (A1896). Second, although these isolates belonged to genotype C, 11 amino acids deletions in the preS1 region, specific for HBV genotype D, were detected in the isolates of two HCC patients (He52 and He82). Third, mutations (I127T/N, K130M, and V131I) at three codons in the carboxy functional region of X protein were observed in isolates from all three HCC patients. Additionally, phylogenetic analysis based on the entire HBV sequences showed that all six isolates belonged to genotype C2, as do other Korean strains. J. Med. Virol. 75:13,19, 2005. © 2005 Wiley-Liss, Inc. [source] Long-term ethanol exposure causes human liver cancer cells to become resistant to mitomycin C treatment through the inactivation of bad-mediated apoptosis,MOLECULAR CARCINOGENESIS, Issue 8 2010Ching-Shui Huang Abstract The aim of this study was to test whether long-term ethanol consumption confers therapeutic resistance to human liver cancer patients infected with hepatitis B virus (HBV). Chronic ethanol-treated cells were established by consecutively culturing a human hepatocellular carcinoma cell line, Hep 3B, which contains integrated HBV sequences, for 20,40 passages with or without 10,mM ethanol (designated as E20,E40 and C20,C40, respectively). Flow cytometry analysis demonstrated that a growth promoting effect of long-term ethanol treatment was induced in the E40 cells through preferential acceleration of S-phase in these cells. Lower protein expression levels of p16, p21/Cip1, and p27/Kip1 were detected in the ethanol-treated E40 cells. We further demonstrated that long-term ethanol-treated E40 cells develop drug resistance in response to mitomycin C (MMC) treatment (>8,µM). Immunoblot analysis revealed that caspase-8-mediated mitochondrial apoptotic signals (such as Bad) were inactivated in the MMC-resistant E40 cells. Immunoprecipitation experiments demonstrated that the sequestration of phosphorylated Bad (Ser-112) through its binding with 14-3-3 was detected more profoundly in the MMC-resistant E40 cells. Next, we examined the therapeutic efficacy of MMC (10,mg MMC/kg body weight, three times per week) in severe combined immunodeficient (SCID) mice bearing E40- and C40-xenografted tumors. Significant reductions (>3-fold) in tumor growth were detected in MMC-treated C40-xenografted mice. In vivo and in vitro studies demonstrated that AKT- and extracellular signal-regulated kinase (ERK)-mediated survival factors inhibited the Bad-induced mitochondrial apoptotic signals that were involved in E40 tumor cells and that conferred resistance to MMC. © 2010 Wiley-Liss, Inc. [source] | ||||||||||