HBV Surface Antigen (hbv + surface_antigen)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Hepatitis B or hepatitis C coinfection in HIV-infected pregnant women in Europe

HIV MEDICINE, Issue 7 2008
M Landes
Objectives The aim of the study was to investigate the prevalence of and risk factors for hepatitis C or B virus (HCV or HBV) coinfection among HIV-infected pregnant women, and to investigate their immunological and virological characteristics and antiretroviral therapy use. Methods Information on HBV surface antigen (HBsAg) positivity and HCV antibody (anti-HCV) was collected retrospectively from the antenatal records of HIV-infected women enrolled in the European Collaborative Study and linked to prospectively collected data. Results Of 1050 women, 4.9% [95% confidence interval (CI) 3.6,6.3] were HBsAg positive and 12.3% (95% CI 10.4,14.4) had anti-HCV antibody. Women with an injecting drug use(r) (IDU) history had the highest HCV-seropositivity prevalence (28%; 95% CI 22.8,35.7). Risk factors for HCV seropositivity included IDU history [adjusted odds ratio (AOR) 2.92; 95% CI 1.86,4.58], age (for ,35 years vs. <25 years, AOR 3.45; 95% CI 1.66,7.20) and HBsAg carriage (AOR 5.80; 95% CI 2.78,12.1). HBsAg positivity was associated with African origin (AOR 2.74; 95% CI 1.20,6.26) and HCV seropositivity (AOR 6.44; 95% CI 3.08,13.5). Highly active antiretroviral therapy (HAART) use was less likely in HIV/HCV-seropositive than in HIV-monoinfected women (AOR 0.34; 95% CI 0.20,0.58). HCV seropositivity was associated with a higher adjusted HIV RNA level (+0.28log10 HIV-1 RNA copies/mL vs. HIV-monoinfected women; P=0.03). HIV/HCV-seropositive women were twice as likely to have detectable HIV in the third trimester/delivery as HIV-monoinfected women (AOR 1.95; P=0.049). Conclusions Although HCV serostatus impacted on HAART use, the association between HCV seropositivity and uncontrolled HIV viraemia in late pregnancy was independent of HAART. [source]


Occult hepatitis B virus infection in Southern African blacks with hepatocellular carcinoma

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2008
Michael C Kew
Abstract Background and Aim:, To ascertain the prevalence of occult hepatitis B virus (HBV) infection in southern African blacks with hepatocellular carcinoma. Methods:, Sera from 118 patients negative for HBV surface antigen but positive for HBV antibodies were studied. HBV-DNA was detected using a nested polymerase chain reaction (PCR) assay and confirmed by nucleotide sequencing of the surface and precore/core genes. Results:, Surface gene HBV-DNA was detected in a single PCR assay in 48.4% of the patients. Positive results increased to 57.7% after two PCR assays (not significant) and 75.7% after four assays (P < 0.001). No false positive results were obtained in these assays or in the 15 control samples for which PCR assays were performed four times. Significant differences in positivity rates were not observed between patients positive for HBV core antibody alone and those positive for core and surface antibodies. The sensitivity of the PCR amplification of the precore/core gene was significantly less than that of the surface open reading frame: the yield of positive results was 23.7% after one assay, 32.2% after two assays (not significant), and 52% after four assays (P < 0.001). Combining the results of the assays of the two genes increased the yield of positive results for the first assay (by 11.9%, P = 0.015), but not the second (6.1%) or fourth assays (4.6%). Conclusion:, Occult HBV infection is present in the serum of the majority of hepatocellular carcinomas in southern African blacks whose serum is negative for hepatitis B surface antigen but positive for anti-HBV core antigen. The yield of positive results increases if more than one PCR assay is performed. [source]


Prevalence of hepatitis B virus infections in nonhuman primates

JOURNAL OF MEDICAL PRIMATOLOGY, Issue 1 2001
Jens-Ove Heckel
The aim of this study was to determine the prevalence of hepatitis B virus (HBV) infection in nonhuman primates. Serum samples from Europe, Thailand and Vietnam were analyzed. Sera obtained from 262 apes and 454 monkeys were tested for HBV infection serologically and for HBV DNA using nested PCR (nPCR). A total number of 198 ape sera and all but one (Cercopithecus aethiops) of the 4543 monkey sera had no serological signs of HBV infection. Among the 64 of 262 (24.4%) seropositive ape sera, we found, as in humans, different stages of HBV infection: very early HBV infection, active infection with high level of infectivity, virus carriers with low infectivity, and passed HBV infection. In the cases with passed infection, 47.8% harbored HBV DNA in the presence of protective antibodies to the HBV surface antigen (HBsAb). This indicates HBV persistence in apes despite immune control. In contrast to apes, in monkeys HBV infection is a very rare event. [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 2008
Francesco 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]


Decline of hepatitis B carrier rate in vaccinated and unvaccinated subjects: Sixteen years after newborn vaccination program in Taiwan

JOURNAL OF MEDICAL VIROLOGY, Issue 4 2003
Hans Hsienhong Lin
Abstract Taiwan was an endemic area for hepatitis B virus (HBV) infection, and related liver diseases cause a significant drain of public resources. To control the endemic, a nation-wide newborn vaccination program was started in 1985. We reviewed the results of the annual survey for HBV surface antigen (HBsAg) performed in freshmen class of two high schools in Hualien, eastern Taiwan, from 1991 to 2001. A total of 10,194 students, most of them 15 years old, were tested for serum HBsAg using enzyme immunoassays. There is a significant trend (P,<,0.0001) of decreasing HBsAg carrier rate from 20.3 to 4.4% in males and 14.3% to 2.4% in females, respectively, over 11 years. The HBsAg carrier rate was 16.0,20.3% in students surveyed during 1991,1993 (born more than 6 years before the start of the national vaccination program), which decreased to 7.7,11.9% during 1994,1999 (born 1,6 years before the program). It further declined to 4.7% and 3.4% in 2000 and 2001 (born after the start of the program). The HBsAg carrier rate in male students was significantly higher than that in female students in most of the years. The HBV newborn vaccination program not only successfully prevented most of the perinatal transmission of HBV but also reduced horizontal transmission of HBV to children born up to 6 years before the start of the program. Also, the protection persisted for at least 15 years. J. Med. Virol. 69:471,474, 2003. © 2003 Wiley-Liss, Inc. [source]


Sequencing of human-viral DNA junctions in hepatocellular carcinoma from patients with HCV and occult HBV infection

JOURNAL OF MEDICAL VIROLOGY, Issue 4 2003
Akihiro Tamori
Abstract DNA of free hepatitis B viruses (HBV) has been detected in the liver of patients infected with hepatitis C virus (HCV). It is unknown whether HBV DNA is integrated into such livers; if so, it may affect hepatocarcinogenesis. Hepatocellular carcinomas (HCCs) from 34 patients without HBV surface antigen (HBsAg) and with anti-HCV, and from 7 patients with HBsAg and without anti-HCV as controls, were examined, using the cassette-ligation,mediated polymerase chain reaction and primers based on HBV DNA sequence. In the controls, HBV DNA had been integrated into human DNA of all HCCs. On the basis of HBV DNA in tumor tissue, 23 of the 34 patients with anti-HCV had occult infection. Junctions between human DNA and HBV DNA were detected in 10 of the 34 patients without HBsAg and with anti-HCV. HBV DNA was integrated into chromosome 11q in 4 of the 10 HCCs with junctions. The DNA to either side of the human-viral junctions was sequenced. Clinically, the mean tumor size of these 10 HCCs was 39 mm; that of the 24 HCCs without integrated HBV was 25 mm. The surrounding tissue was cirrhotic in 2 of the 10 former HCCs and in 16 of the latter 24 HCCs. In conclusion, integrated HBV was detected in some patients with HCV infection; in these patients, the integrated DNA was associated with accelerated hepatocarcinogenesis. J. Med. Virol. 69:475,481, 2003. © 2003 Wiley-Liss, Inc. [source]


Targeted destruction of the polymerized human serum albumin binding site within the preS2 region of the HBV surface antigen while retaining full immunogenicity for this epitope

JOURNAL OF VIRAL HEPATITIS, Issue 1 2003
J.-H. Park
summary. The 55-amino acid (a.a.) preS2 region of the hepatitis B virus (HBV) envelope protein is highly immunogenic, and antibodies against this epitope confer seroprotection against HBV infections. Accordingly, various experimental and clinical studies for developing and evaluating HBV vaccines that include this particular epitope have been reported. However, a pitfall in using preS2 epitopes as part of a vaccinating antigen is that polymerized human serum albumin (pHSA), which is a normal constituent of the human serum, binds to and makes complexes with this particular region. Consequently, it is most likely that the antigen epitope is masked by serum pHSA and subsequently not detected by the immune system. To overcome these limitations, a novel single a.a substitute of the preS2 region was designed that corresponds to a tyrosine to serine exchange at position 140 of preS2. Competitive enzyme-linked immunosorbent assay showed that this substitution completely abolishes pHSA-binding activities in the mutated preS2 peptide, and CD spectra analysis revealed that this property might have been induced by slight conformational changes in its secondary structure. Nevertheless, the original B-cell epitope was still preserved in the mutated preS2 as determined by experimental immunization in mice. In this regard, the preS2(120,145/Y140S) sequence may be an HBV vaccine where epitopes, with intrinsic properties have been deleted without affecting the immunogenicity of the epitope itself. It is expected that the inclusion of this point mutated preS2 epitope will improve the efficacy of conventional preS2-containing HBV vaccines. [source]


Quantitative detection of hepatitis B virus DNA in serum by a new rapid real-time fluorescence PCR assay

JOURNAL OF VIRAL HEPATITIS, Issue 6 2001
R. Jardi
A sensitive and accurate HBV DNA quantification assay is essential for monitoring hepatitis B virus (HBV) replication. This study evaluated a real-time PCR method performed in the LightCyclerTM analyser for quantitative HBV DNA assay. HBV DNA results with this method were compared with those obtained using a branched-chain DNA (bDNA) solution hybridization assay. Real-time PCR was performed using two adjacent fluorescently labelled probes and primers corresponding to the HBV core gene. The same standard employed in the bDNA assay was used for calibration. Serum samples came from 193 HBV surface antigen (HBsAg)-positive patients (34 HBV e antigen (HBeAg)-positive and 93 with antibody to HBeAg (anti-HBe)), and 66 asymptomatic HBV carriers. In addition, we analysed serum samples from 8 anti-HBe-positive patients who had been receiving lamivudine treatment for more than three years. A linear standard curve was seen in the range from 103 to 108 copies/mL. In the reproducibility analysis, intra-assay coefficient of variation (CVs) at two known HBV DNA concentrations were 4% and 2% and interassay CVs were 6% and 4%. The median of serum HBV DNA by real-time PCR was 9.2 × 108 copies/mL in HBeAg-positive patients with persistently elevated alanine aminotransferase (ALT) levels, 1.3 × 107 copies/mL in anti-HBe-positive cases with persistently elevated ALT levels, 3.7 × 104 copies/mL in anti-HBe-positive patients with fluctuating ALT levels and 104 copies/mL in asymptomatic HBV carriers. The differences in HBV DNA levels among the various groups studied were statistically significant (P < 0.05). The cut-off between chronic hepatitis patients and asymptomatic carriers was found to be at a serum HBV DNA concentration of 5 × 104 copies/mL. Of the 109 serum samples with a viral load < 7.5 × 105 (negative by bDNA assay) 44 (40%) were positive by real-time PCR: 24 (56%) chronic hepatitis and 20 (33%) asymptomatic carriers. There was a positive association between HBV DNA levels determined by real-time PCR and ALT levels (P < 0.05), which was not observed with the bDNA assay for HBV DNA quantification. At 12 months of lamivudine treatment, 6 patients (75%) showed HBV DNA levels < 5 × 104 copies/mL (range < 103,2 × 103), significantly lower than at baseline. At 36 months, 2 of 8 (25%) showed HBV DNA levels persistently lower than 5 × 104 copies/mL (1.7 × 103, 6 × 103). The LightCycler quantitative real-time PCR is a practical, sensitive, reproducible single-tube assay with a wide dynamic range of detection. The assay is automatic except for DNA extraction and the running time is only 70 min. The LightCycler real-time PCR is useful for identifying different states of HBV infection and for evaluating the efficacy of viral therapy. [source]


Occult hepatitis B virus infection in patients with autoimmune liver diseases

LIVER INTERNATIONAL, Issue 3 2009
Sarah P. Georgiadou
Abstract Background: Occult hepatitis B virus (HBV) infection is characterized by undetectable serum HBV surface antigen (HBsAg) but detectable HBV-DNA in serum or liver. Aims: To determine the prevalence and clinical impact of occult HBV in autoimmune liver diseases as similar data are missing. Methods: One hundred and ninety-six sera samples from HBsAg-negative patients, including 66 autoimmune hepatitis (AIH), 93 primary biliary cirrhosis (PBC) and 37 primary sclerosing cholangitis (PSC), were investigated for HBV-DNA using the polymerase chain reaction (PCR) before treatment initiation. One hundred and three serial samples from 38 AIH patients under immunosuppression and 282 selected blood donors (HBsAg negative; antibodies to HBV-core antigen positive) were also investigated. Fourteen available paraffin-embedded AIH liver samples were also investigated for HBV-DNA by nested-PCR. Results: Hepatitis B virus DNA was detected in the serum of 24/196 patients (12.2%) and 0/282 donors (P=0.0000). Nine patients had AIH (13.6%), eight had PBC (8.6%) and seven had PSC (18.9%) (P=0.0000 vs healthy). HBV-DNA detection in AIH livers was higher than in serum. HBV-DNA was associated neither with HBV markers nor with epidemiological, laboratory and clinical data. Serial testing of AIH patients revealed two HBV-DNA-negative patients before treatment becoming positive during treatment, while all HBV-DNA-positive patients before immunosuppression became negative. Conclusion: Based mainly on serum HBV-DNA, we found a significant proportion of autoimmune liver disease patients with occult HBV compared with donors. However, taking into account our results in a small number of liver tissues, it should be emphasized that occult HBV could be even higher when both serum and liver specimens are investigated. Occult HBV does not seem to affect the clinical and laboratory features of the diseases, while AIH patients with occult HBV under immunosuppression do not deteriorate during follow-up. [source]


Prevalence of human immunodeficiency virus and its association with hepatitis B, C, and D virus infections among incarcerated male substance abusers in Taiwan

JOURNAL OF MEDICAL VIROLOGY, Issue 6 2009
Fang-Yeh Chu
Abstract Taiwan has been facing a rising epidemic of human immunodeficiency virus (HIV) infection since 2004. Injection drug users comprised 38.5% of accumulated HIV cases by 2007. This cross-sectional study investigated the seroprevalence of hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and HIV infection in 753 male substance users who were detained in a detoxification center in Taoyuan, Taiwan. The subjects were enrolled into the study consecutively between February and October, 2005. The seroprevalence rates of HIV antibodies, HCV antibodies, and HBV surface antigens among all subjects, and HDV antibodies among HBV carriers were 6.9% (95% confidence interval [CI]: 5.19,8.95), 30.5% (95% CI: 27.23,33.93), 16.9% (95% CI: 14.24,19.71) and 13.7% (95% CI: 8.19,21.04), respectively. Subjects in the heroin injection group had significantly higher rates of HIV infection, HCV infection and HDV superinfection (25.5%, 89.6%, and 38.7%) than those in the heroin non-injection group (0.9%, 24.5%, and 6.25%), the methamphetamine group (0.3%, 8.1%, and 6.7%), and the club drug group (1%, 3%, and 0%; P,<,0.001). The odds of HCV, HIV, or HDV infection were 74.7, 63.8, and 11.1 higher, respectively, for heroin injection drug users than for non-injection drug users (P,<,0.0001). Compared to HIV-negative individuals, the odds of being a heroin injector and the odds of HCV co-infections were 64-fold and 149-fold higher, respectively, in HIV-positive individuals. The impact of HBV, HCV, and HDV infection on the HIV epidemic in Taiwan should be monitored closely. J. Med. Virol. 81:973,978, 2009. © 2009 Wiley-Liss, Inc. [source]


Hepatitis B virus pre-S mutants, endoplasmic reticulum stress and hepatocarcinogenesis

CANCER SCIENCE, Issue 8 2006
Hui-Ching Wang
Although hepatitis B virus (HBV) has been documented to cause hepatocellular carcinoma (HCC), the exact role of HBV in the development of HCC remains enigmatic. Several hypotheses have been proposed to explain the potential mechanism, including insertional mutagenesis of HBV genomes and transcriptional activators of HBV gene products such as hepatitis B x protein (HBx) and truncated middle S mutants. In the past few years, we have identified two types of large HBV surface antigens (LHBs) with deletions at the pre-S1 (,S1-LHBs) and pre-S2 (,S2-LHBs) regions in ground glass hepatocytes. The pre-S mutant LHBs are retained in the endoplasmic reticulum (ER) and escape from immune attack. The pre-S mutants, particularly ,S2-LHBs, are increasingly prevalent in patients with hepatitis B e antigen (HBeAg)-positive chronic HBV infection, ranging from 6% before the 3rd decade to 35% in the 6th decade. In HCC patients, the two pre-S mutants were detected in 60% of HCC patients, in the serum and in HCC tissues. Pre-S mutant LHBs can initiate ER stress to induce oxidative DNA damage and genomic instability. Furthermore, pre-S mutant LHBs can upregulate cyclooxygenase-2 and cyclin A to induce cell cycle progression and proliferation of hepatocytes. In transgenic mice, the pre-S mutants can induce dysplasia of hepatocytes and development of HCC. In a nested control study, the presence of pre-S mutants carried a high risk of developing HCC in HBV carriers. In summary, the findings we describe in this review suggest a potential role for HBV pre-S mutants in HBV-related hepatocarcinogenesis, providing a model of viral carcinogenesis associated with ER stress. (Cancer Sci 2006; 97: 683,688) [source]