TY - JOUR. T1 - Bone marrow-derived stem cells and hepatocarcinogenesis in hepatitis B virus transgenic mice. AU - Barone, Michele. AU - Scavo, Maria Principia. AU - Maiorano, Eugenio. AU - Di Leo, Alfredo. AU - Francavilla, Antonio. PY - 2014/3. Y1 - 2014/3. N2 - Background: Several studies have demonstrated that cancer can develop with the contribution of bone marrow-derived cancer stem cells. We evaluated the possible involvement of bone marrow-derived stem cells in hepatocarcinogenesis in a hepatitis B virus (HBV) transgenic mouse model. Methods: Bone marrow cells from wild type male mice were transplanted into sublethally irradiated, female, HBV transgenic mice with hepatocarcinoma nodules. Four months later, liver tissue was examined to localize neoplastic nodules/foci and characterize cells by evaluating the Y-chromosome and the hepatocyte lineage marker hepatocyte nuclear factor-1 (HNF1), as well as the HBsAg encoding gene (HBs-Eg) and HBsAg protein (HBs-Pr) (present only in cells of ...
Objectives: A number of studies have shown that chronic hepatitis B virus infection is implicated insusceptibility to pancreatic cancer. However, the results are still controversial. This meta-analysis aimed toquantitatively assess the relationship between chronic hepatitis B virus infection and incidence of pancreaticcancer of cohort and case-control studies. Methods: A literature search was performed for entries from 1990 to2012 using PUBMED and EMBASE. Studies were included if they reported odds ratios (ORs) and corresponding95% CIs of pancreatic cancer with respect to the infection of hepatitis B virus. Results: Eight studies met theinclusion criteria, which included five case-control studies and three cohort studies. Compared with individualswho have not infection of hepatitis B virus, the pooled OR of pancreatic cancer was 1.403 (95%CI: 1.139-1.729,P=0.001) for patients with hepatitis B virus infection. Sub-group analysis by study design showed that thesummary OR was 1.43 (95%CI: 1.06-1.94, P=0
Hepatocyte expression of pre-S1 and pre-S2 in relation to hepatitis B virus replication (hepatitis B virus-DNA in serum and HBcAg in the liver), histological activity and hepatitis delta virus superinfection was studied by indirect immunofluorescence on frozen sections of liver specimens from 68 patients with chronic hepatitis B virus infection. All 44 patients with chronic type B hepatitis had pre-S1 and pre-S2 display in the liver. The distribution of pre-S1 in the liver was membranous in one, mixed membranous and cytoplasmic in 12, and cytoplasmic in 31. The distribution of pre-S2 was membranous in one, mixed membranous and cytoplasmic in 26, and cytoplasmic in 17. Membranous expression of pre-S1 was significantly more prevalent in patients with active hepatitis B virus replication than in those without (13/28 v 0/16, p , 0.001), regardless of the histological activity, as was membranous expression of pre-S2 (27/28 v 0/16, p , 0.001). In contrast, a significantly higher extent of cytoplasmic ...
Get the inner blade of the sample report @ https://researchvector.com/2018/10/05/global-hepatitis-b-virus-core-antibody-diagnostic-kits-market-professional-survey-report-2018/. Data records on the hepatitis B virus core antibody diagnostic kit market. Current Development Status and Future Market Trends: This report will be a valuable appraisal for newcomers who want to enter the market for Hepatitis B Virus Core Antibody Diagnostic Kits as they predict not only current market trends but also future trends. This will help them carefully select their genres to be equal to compete with the global giants who have to end the development studios with huge production capabilities that have years of experience.. Forecast Market by 2025: This comprehensive research is valuable to everyone who is part of the Hepatitis B virus lifting antibody diagnostic kit market. This will help you understand the full view of the entire Hepatitis B Virus Core Antibody Diagnostic Kits market.. Global Hepatitis B Virus ...
1. Hepatitis B: World Health Organization Fact Sheet 204. 2000 : World Health Organization. http://www.who.int/mediacentre/factsheets/fs204/en/ 2. Gust ID. Epidemiology of hepatitis B infection in the Western Pacific and South East Asia. Gut. 1996 ;38(suppl 2):S18-S23 3. Lok AS. Chronic hepatitis B. N Engl J Med. 2002 ;346:1682-1683 4. Mahoney FJ. Update on diagnosis, management, and prevention of hepatitis B virus infection. Clin Microbiol Rev. 1999 ;12:351-366 5. Lee WM. Hepatitis B infection. N Engl J Med. 1997 ;337:1733-1745 6. Margolis HS, Alter MJ, Hadler SC. Hepatitis B: evolving epidemiology and implications for control. Semin Liver Dis. 1991 ;11:84-92 7. Alter M. Epidemiology of hepatitis B in Europe and worldwide. J Hepatol. 2003 ;39:S64-S69 8. Toukan A. Strategy for the control of hepatitis B virus infection in the Middle East and North Africa. Vaccine. 1990 ;8(suppl):S117-S121 9. McQuillan GM, Townsend TR, Fields HA, Carroll M, Leahy M, Polk BF. Seroepidemiology of hepatitis B virus ...
Since its widespread introduction, the hepatitis B vaccine has become an essential part of infant immunization programmes globally. The vaccine has been particularly important for countries where the incidence of hepatitis B virus-related hepatocellular carcinoma is high. Effective treatment options for individuals with chronic hepatitis B infection were limited until 1998 when lamivudine, the first nucleoside analogue drug, was introduced. As a single treatment agent, however, lamivudine has a significant drawback: it induces lamivudine-resistant hepatitis B virus strains that may pose a risk to the global hepatitis B immunization programme. Mutations associated with drug treatment can cause changes to the surface antigen protein, the precise part of the virus that the hepatitis B vaccine mimics. However, the emergence of antiviral drug-associated potential vaccine escape mutants (ADAP-VEMs) in treated patients does not necessarily pose a significant, imminent threat to the global hepatitis B ...
1. Kao JH, Chen DS. Global control of hepatitis B virus infection. The Lancet Infectious diseases. 2002;2:395-403 2. Liaw YF, Chu CM. Hepatitis B virus infection. Lancet. 2009;373:582-92 3. Ren JJ, Liu Y, Ren W, Qiu Y, Wang B, Chen P. et al. Role of general practitioners in prevention and treatment of hepatitis B in China. Hepatobiliary & pancreatic diseases international: HBPD INT. 2014;13:495-500 4. Dandri M, Burda MR, Will H, Petersen J. Increased hepatocyte turnover and inhibition of woodchuck hepatitis B virus replication by adefovir in vitro do not lead to reduction of the closed circular DNA. Hepatology. 2000;32:139-46 5. Moraleda G, Saputelli J, Aldrich CE, Averett D, Condreay L, Mason WS. Lack of effect of antiviral therapy in nondividing hepatocyte cultures on the closed circular DNA of woodchuck hepatitis virus. Journal of virology. 1997;71:9392-9 6. Yuen MF, Lai CL. Treatment of chronic hepatitis B: Evolution over two decades. Journal of gastroenterology and hepatology. 2011;26(Suppl ...
A precore mutant is a variety of hepatitis B virus that does not produce hepatitis B virus e antigen (HBeAg). These mutants are important because infections caused by these viruses are difficult to treat, and can cause infections of prolonged duration and with a higher risk of liver cirrhosis. The mutations are changes in DNA bases from guanine to adenine at base position 1896 (G1896A), and from cytosine to thymine at position 1858 (C1858T) in the precore region of the viral genome. The HBV has four genes: S, P, C, and X. The S gene codes for the major envelope protein (HBsAg). The largest gene is P. It codes for DNA polymerase. The C gene codes for HBeAg and HBcAg. The C gene has a precore and a core region. If translation is initiated at the precore region, the protein product is HBeAg. If translation begins with the core region, HBcAg is the protein product. HBeAg is a marker of HBV replication and infectivity. The precore region is not necessary for viral replication. Precore mutants can ...
The role of hepatitis B virus (HBV) X protein (HBx) in the regulation of HBV replication remains controversial. In the present study, the role of HBx in regulating HBV replication was initially investigated in both HepG2 and Huh7 in vitro cell lines with a transient transfection system. Next, the regions of HBx responsible for transcriptional transactivation and promotion of HBV replication were mapped in an HBV replication mouse model by in vivo transfection of a series of HBx expression plasmids. In an in vitro setting, HBx deficiency had little effect on HBV replication in Huh7 cells, but impaired HBV replication in HepG2 cells. In an in vivo setting, HBx had a strong enhancing effect on HBV transcription and replication. For the C-terminal two-thirds of the protein (amino acids [aa] 51 to 154) was required for this function of HBx, and the regions spanning aa 52 to 72 and 88 to 154 were found to be important for the stimulatory function of HBx on HBV replication. In conclusion, the role of HBx in
The role of hepatitis B virus (HBV) X protein (HBx) in the regulation of HBV replication remains controversial. In the present study, the role of HBx in regulating HBV replication was initially investigated in both HepG2 and Huh7 in vitro cell lines with a transient transfection system. Next, the regions of HBx responsible for transcriptional transactivation and promotion of HBV replication were mapped in an HBV replication mouse model by in vivo transfection of a series of HBx expression plasmids. In an in vitro setting, HBx deficiency had little effect on HBV replication in Huh7 cells, but impaired HBV replication in HepG2 cells. In an in vivo setting, HBx had a strong enhancing effect on HBV transcription and replication. For the C-terminal two-thirds of the protein (amino acids [aa] 51 to 154) was required for this function of HBx, and the regions spanning aa 52 to 72 and 88 to 154 were found to be important for the stimulatory function of HBx on HBV replication. In conclusion, the role of HBx in
The proliferative response of PBMC to hepatitis B virus (HBV) envelope, core, and e Ag was analyzed prospectively in 21 patients with acute self-limited HBV infection and compared with the response of patients with chronic HBV infection and different levels of HBV replication (i.e., hepatitis e Ag (HBeAg)- or anti-HBe-positive) and liver damage (i.e., chronic active hepatitis or chronic asymptomatic carriers). Our results indicate that: 1) HBV-infected subjects who develop a self-limited acute hepatitis show a vigorous PBMC response to hepatitis B core Ag and HBeAg, as expression of T cell activation; 2) appearance of a detectable lymphocyte response to HBV nucleocapsid Ag is temporally associated with the clearance of HBV envelope Ag; 3) in patients with chronic HBV infection the level of T cell responsiveness to hepatitis B core Ag and to HBeAg is significantly lower than that observed during acute infection; 4) T cell sensitization to HBV envelope Ag in acute and chronic HBV infection is ...
BACKGROUND & AIMS: Histologic analyses of liver fibrosis have been limited by small sample sizes and the predominance of samples from patients with active hepatitis. METHODS: We performed a prospective study of transient elastography in treatment-naive patients with chronic hepatitis B, to investigate the relationship between hepatitis B virus (HBV) genotype and liver fibrosis. A validated liver stiffness measurement algorithm was used to define insignificant fibrosis and advanced fibrosis. RESULTS: Of 1106 patients, 711 (64%) were older than age 40, 370 (34%) had positive test results for hepatitis B e antigen (HBeAg), and 386 (35%) had increased serum levels of alanine aminotransferase. Of the patients, 524 (49%) had genotype B and 582 (51%) had genotype C HBV infection. Patients with genotype C infection had insignificant fibrosis less often (42% vs 55%; P ...
Quantitation of low hepatitis B virus (HBV) DNA levels in patients with chronic hepatitis B is important for monitoring natural history of disease and treatment efficacy. This study aimed to compare the quantitation range and analytical sensitivity of the newly developed COBAS TaqMan™ HBV test (TaqMan test) with the COBAS Amplicor™ HBV Monitor Test (Amplicor test), using the Eurohep HBV reference plasma and serum samples from patients. Serial dilutions (2.7 × 101-2.7 × 108 copies/ml) of the Eurohep HBV reference plasma and 50 serum samples from chronic hepatitis B patients were tested by both assays. The TaqMan test could detect seven (2.7 × 102-2.7 × 108 copies/ml) of eight dilutions of the reference plasma, while the Amplicor test could only detect three of them (2.7 × 103-2.7 × 105 copies/ml). The HBV DNA values measured by the TaqMan test correlated very well with the theoretical Eurohep standard values (r = 0.998, P , 0.001). There were good correlations between the HBV DNA levels ...
TY - JOUR. T1 - Hepatitis B virus X protein represses LKB1 expression to promote tumor progression and poor postoperative outcome in hepatocellular carcinoma. AU - Wu, Cheng Chung. AU - Wu, De Wei. AU - Lin, Ying Yu. AU - Lin, Po Lin. AU - Lee, Huei. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Background: Hepatitis B virus X (HBx) protein plays critical roles in hepatitis B virus (HBV)-associated hepatocellular tumorigenesis through different molecular mechanisms, including inactivation of p53, a key transcription factor of liver kinase B1 (LKB1). We hypothesized that p53 inactivation by HBx protein could decrease LKB1 expression, thereby promoting tumor progression and poor outcomes in patients with HBV-associated hepatocellular carcinoma. Methods: Manipulation strategies for HBx protein and/or p53 were used to verify that loss of LKB1 could promote colony formation and invasiveness in HepG2 and Hep3B cells. The expressions of HBx protein and LKB1 in 93 hepatocellular carcinomas (HCC) were also ...
Tong, S.P.; Brotman, B.; Li, J.S.; Vitvitski, L.; Pascal, D.; Prince, A.M.; Trépo, C., 1991: In vitro and in vivo replication capacity of the precore region defective hepatitis B virus variants
PubMed journal article: Occult hepatitis B virus infection in HBs antigen-negative hepatocellular carcinoma in a Japanese population: involvement of HBx and p53. Download Prime PubMed App to iPhone, iPad, or Android
TY - JOUR. T1 - Two core promotor mutations identified in a hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication. AU - Baumert, Thomas F.. AU - Rogers, Steven A.. AU - Hasegawa, Kiyoshi. AU - Liang, T. Jake. PY - 1996/11/15. Y1 - 1996/11/15. N2 - Viral mutations have been implicated in alteration of the biological phenotype of hepatitis B virus (HBV). We recently cloned and sequenced the viral genome of an HBV strain associated with an outbreak of fulminant hepatitis (FH strain). The FH strain contained numerous mutations in all genomic regions and was functionally characterized by a more efficient encapsidation of pregenomic RNA leading to highly enhanced replication. To define the responsible mutation(s) for the enhanced replication, we introduced individual mutations of the FH strain into a wild-type construct by oligonucleotide-directed mutagenesis. Analysis of viral replication showed that two adjacent mutations in the HBV core promotor (C to T ...
1] 中華醫學會肝病學分會、感染病學分會. 慢性乙型肝炎防治指南. 中華肝臟病雜志, 2005,13(12):881-891.. [2] Seeger C, Mason WS. Hepatitis B virus biology. Microbiol Mol Biol Rev, 2000,64(1):51-68.. [3] Scaglioni PP, Melegari M, Wands JR. Biologic properties of hepatitis B viral genomes with mutations in the precore promoter and precore open reading frame. Virology, 1997,233(2):374-81.. [4] Tran TT, Trinh TN, Abe K. New complex recombinant genotype of hepatitis B virus identified in Vietnam. J Virol, 2008,82(11):5657-63.. [5] Olinger CM, Jutavijittum P, Hubschen JM, et al. Possible new hepatitis B virus genotype, southeast Asia. Emerg Infect Dis, 2008,14(11):1777-80.. [6] Chu CJ, Hussain M, Lok AS. Hepatitis B virus genotype B is associated with earlier HBeAg seroconversion compared with hepatitis B virus genotype C. Gastroenterology, 2002,122(7):1756-62.. [7] Chu CM, Liaw YF. Genotype C hepatitis B virus infection is associated with a higher risk of reactivation of ...
Co-infection with HIV and hepatitis B virus (HBV) has become an important factor of co-morbidity and mortality. The aim of this study was to determine the seroprevalence of HIV/HBV co-infection and its effect on the disease progression in people living with HIV/AIDS identified in Yaoundé Central Hospital. Blood samples from 75 HIV positive patients were collected in Yaoundé Central Hospital from November 2015 to February 2016, for the determination of hepatitis B virus surface antigen (HBsAg) using immunoassays. Cluster of differentiation 4 (CD4) T-cells count and biochemical markers of liver function were also collected and analyzed. The socio-demographic data were also collected. The effect sizes were confirmed using G*Power version 3.1.9.2 software. The data were entered and analyzed using the SPSS Version 22.1 software.  The statistical tests performed were x2, and Pearson correlation, with significant difference at the threshold p ≤ 0.05. Hepatitis B virus surface antigen
Blood and blood products are the main routes through which Hepatitis B virus is transmitted. In fact, only 0.00004 ml of blood is sufficient for transmission. Any technique that allows the transfer of blood or serum from one individual to another is potentially likely to transmit Hepatitis B virus. Hepatitis B infection is especially common amongst IV drug abusers, Many cases occured following blood transfusion before the advent of screening. It is also particularly common amongst homosexuals where the practice of anal intercourse is particularly traumatic and frequently results in bleeding. Acupuncture, tatooing and ear piercing have also led to many reported cases of Hepatitis B infection. Hepatitis B is a known occupational hazard and the risk to health workers following accidental innoculation is 6-20%. Health personnel in renal dialysis units are particularly vulnerable. It has become clear that Hepatitis B virus is not spread exclusively by blood and blood products. The virus is infective ...
Hepatitis B, caused by infection with the hepatitis B virus, is a contagious liver disease that ranges in severity from a mild illness lasting a few weeks to a serious, lifelong illness. Acute hepatitis B is a short-term illness that occurs within the first 6 months after someone is exposed to the virus. Acute infection may lead to chronic infection. Chronic hepatitis B virus infection is a long-term illness that occurs when the hepatitis B virus remains in a persons body. This can eventually lead to serious health problems, including liver damage, liver cancer, and even death.. Not all people with acute hepatitis B have symptoms. However, if they appear, symptoms can include fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, clay-colored bowel movements, joint pain, and jaundice (yellow color in the skin or the eyes).. Hepatitis B is spread when blood, semen, or other body fluid infected with the hepatitis B virus enters the body of a person who is not infected. ...
Background: Serial monitoring of hepatitis B virus (HBV) DNA and serum alanine transaminase (ALT) for at least one year is recommended to define an inactive carrier state. Recent studies proposed HBsAg levels as a marker for monitoring HBV infected patients. The aim of our study is to evaluate spontaneous HBV DNA fluctuations among Tunisian HBV infected patients and to assess the role of HBsAg quantification in the determination of viral disease activity. Methods: Seventy three untreated HBeAg negative asymptomatic HBV infected patients were followed up prospectively during a one year period (2014). Patients with persistently serum HBV DNA levels , 2000 IU/ml and persistently normal ALT for at least one year,were considered as inactive carrier of HBsAg. Patients with HBV DNA level fluctuation ≥2000 IU/ml and/or ALT elevation were classified as chronic hepatitis B (CHB) patients.Serum samples for HBV DNA and ALT quantification were obtained at three times with an interval of 6 months (M0, M6 ...
Hepatitis B virus (HBV) genotype influences chronic hepatitis B disease profile but its relevance in liver transplantation (LTx) is not known. HBV genotype was identified by direct sequencing from pre-transplant sera of 119 patients who underwent LTx using lamivudine prophylaxis (genotype A,1; B,43; C,74; D,1). The baseline characteristics and outcome of 43 genotype B and 74 genotype C patients were compared. Genotype B patients had significantly more pre-transplant acute flare, worse liver functions and higher model for end-stage liver disease score. Fewer genotype B patients had HBeAg (13% vs. 32%; p = 0.017), but HBV DNA seropositivity (by bDNA assay) was comparable (26% vs. 23%; p = 0.727). The 3-year graft survival was 83% for genotype B and 89% for genotype C (p = 0.2). The rate of HBsAg clearance or seroreversion was the same. The cumulative rate of viral breakthrough due to lamivudine-resistant mutants at 3 years was 4% for genotype B and 21% for genotype C (p = 0.017). Liver biopsy ...
Hepatitis B virus (HBV) infection is a global public health challenge. Prevalence of current hepatitis B virus infection in the general population in Uganda is about 10%. Health care workers (HCW) have an extra risk of getting infected from their workplace and yet they are not routinely vaccinated against HBV infection. This study aimed at estimating prevalence of hepatitis B virus infection and associated risk factors among health care workers in a tertiary hospital in Uganda. Data were obtained from a cross sectional survey conducted in Mulago, a national referral and teaching hospital in Uganda among health care workers in 2003. A proportionate to size random sample was drawn per health care worker category. A structured questionnaire was used to collect data on socio-demographic characteristics and risk factors. ELISA was used to test sera for HBsAg, anti-HBs and total anti-HBc. Descriptive and logistic regression models were used for analysis. Among the 370 participants, the sero-prevalence of
Hepatitis B vaccination is the most effective measure to prevent hepatitis B virus (HBV) infection and its consequences, including cirrhosis of the liver, liver cancer, liver failure, and death. In adults, ongoing HBV transmission occurs primarily among unvaccinated persons with behavioral risks for HBV transmission (e.g., heterosexuals with multiple sex partners, injection-drug users [IDUs], and men who have sex with men [MSM]) and among household contacts and sex partners of persons with chronic HBV infection. This report, the second of a two-part statement from the Advisory Committee on Immunization Practices (ACIP), provides updated recommendations to increase hepatitis B vaccination of adults at risk for HBV infection. The first part of the ACIP statement, which provided recommendations for immunization of infants, children, and adolescents, was published previously (CDC. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States:
Tanaka, Y., Esumi, M. and Shikata, T. (1990), Persistence of hepatitis B virus DNA after serological clearance of hepatitis B virus. Liver, 10: 6-10. doi: 10.1111/j.1600-0676.1990.tb00429.x ...
Chronic hepatitis B virus infection is a leading cause of morbidity and mortality due to end stage liver disease and liver cancer. Although significant progress has been made in hepatitis B therapy, current knowledge about how to manage the infection is limited. To improve current knowledge on the disease and long-term disease progression, the Hepatitis B Research Network is collecting health and disease information from individuals who have been diagnosed with hepatitis B.. The objectives of this study are to study individuals with acute and chronic hepatitis B to identify factors that affect disease progression. Individuals at least 18 years of age who have been diagnosed with hepatitis B will be eligible to participate. Participants will be screened with a physical examination and medical history. Health information will be collected through questionnaires and surveys on health behaviors and family history of liver disease. Participants will also provide blood samples, and those who have had ...
As a leading supplier of antigens, Creative Diagnostics is proud to launch the new Hepatitis B Virus Antigens for research community all over the world. Along with extensive research, development, and validation, the newly released products are able to help scientists accelerate more scientific discoveries with highest standards of product performance.. Hepatitis B virus, abbreviated HBV, is a species of the genus Orthohepadnavirus, which is likewise a part of the Hepadnaviridae family of viruses. HBV causes the disease hepatitis B. As far as known, HBV is only susceptible to infect human beings and primates, causing hepatitis B disease. Hepatitis B virus has been found by Dana in 1965. The diameter of this virus is 42 nm and viral particle contains two parts, named shell and core.. HBV belongs to the family of hepadnaviridae, and the genome of this species consists of a double-stranded circular DNA possessing 3.2 Kb. HBVs have wide tolerance to various stress conditions, such as boiling in 65 ...
As a leading supplier of antigens, Creative Diagnostics is proud to launch the new Hepatitis B Virus Antigens for research community all over the world. Along with extensive research, development, and validation, the newly released products are able to help scientists accelerate more scientific discoveries with highest standards of product performance.. Hepatitis B virus, abbreviated HBV, is a species of the genus Orthohepadnavirus, which is likewise a part of the Hepadnaviridae family of viruses. HBV causes the disease hepatitis B. As far as known, HBV is only susceptible to infect human beings and primates, causing hepatitis B disease. Hepatitis B virus has been found by Dana in 1965. The diameter of this virus is 42 nm and viral particle contains two parts, named shell and core.. HBV belongs to the family of hepadnaviridae, and the genome of this species consists of a double-stranded circular DNA possessing 3.2 Kb. HBVs have wide tolerance to various stress conditions, such as boiling in 65 ...
TY - JOUR. T1 - The acceptable duration between occupational exposure to hepatitis B virus and hepatitis B immunoglobulin injection. T2 - Results from a Korean nationwide, multicenter study. AU - Chang, Hyun Ha. AU - Lee, Won Kee. AU - Moon, Chisook. AU - Choi, Wonseok. AU - Yoon, Hee Jung. AU - Kim, Jieun. AU - Ryu, Seong Yeol. AU - Kim, Hyun Ah. AU - Jo, Yu Mi. AU - Kwon, Ki Tae. AU - Kim, Hye In. AU - Sohn, Jang Wook. AU - Yoon, Young Kyung. AU - Jung, Sook In. AU - Park, Kyung Hwa. AU - Kwon, Hyun Hee. AU - Lee, Mi Suk. AU - Kim, Young Keun. AU - Kim, Yeon Sook. AU - Hur, Jian. AU - Kim, Shin Woo. PY - 2016/2/1. Y1 - 2016/2/1. N2 - Background Postexposure prophylaxis for occupational exposure to hepatitis B virus (HBV) plays an important role in the prevention of HBV infections in health care workers (HCWs). We examined data concerning the acceptable duration between occupational exposure and administration of a hepatitis B immunoglobulin (HBIG) injection in an occupational clinical setting. ...
Hepatitis B virus (HBV) DNA in serum of chronically infected patients declines by 3-4 log10 units at loss of HBe antigen (HBeAg) from serum. The mechanisms behind this decline, and the much smaller decline of surface antigen (HBsAg) levels, are still not well known. The aim of this study was to get a better understanding of this process by analysing both serum and intrahepatic markers of HBV replication. Levels of HBV DNA and HBsAg in serum, and covalently closed circular DNA (cccDNA), pregenomic RNA (pgRNA) and S-RNA and total intrahepatic HBV DNA (ihDNA) in liver biopsies from 84 chronically infected patients (16 positive and 68 negative for HBeAg) were analysed. Lower HBV DNA levels within HBeAg-positive stage reflected lower levels of cccDNA and pgRNA with strong correlation. In HBeAg-negative patients, ihDNA levels were greater and HBV DNA levels in serum lower than expected from pgRNA levels. A lower HBV DNA/HBsAg ratio corresponded with lower pgRNA/cccDNA (p | 0.01) and higher S-RNA/cccDNA (p | 0
Hepatitis B is the most probable life-threatening liver infection that is caused by the hepatitis B virus. This is a major universal health problem. This can cause chronic infection and put people at high risk of death from liver cancer and cirrhosis.. Hepatitis B is a virus that affects the liver. Most people have it for a short time and then get better. It is called acute hepatitis B.. Sometimes this virus causes a long-term infection, named chronic hepatitis B. Over time this could damage your liver. Infants and young kids infected with the virus are more prone to get chronic hepatitis B.. Most of the people with hepatitis B do not know that they have it, because they do not have any indications. If you do have symptoms, you may only experience it like you have the flue.. Symptoms consist of:. ...
The Global Hepatitis B Virus Core Antibody Diagnostic Kits Market report offers a summary of a substantial number of statistics in the Global Hepatitis B Virus Core Antibody Diagnostic Kits Market . Data collected in the report highlights the current market trends. Also, it provides the users with the detailed statistics of the Global Hepatitis…. ...
TY - JOUR. T1 - Lack of susceptibility of baboons to infection with hepatitis B virus. AU - Michaels, Marian G.. AU - Lanford, Robert. AU - Demetris, Anthony J.. AU - Chavez, Deborah. AU - Brasky, Kathleen. AU - Fung, John. AU - Starzl, Thomas E.. PY - 1996/2/15. Y1 - 1996/2/15. N2 - Historically, hepatitis B virus (HBV) has been considered species specific and unable to infect baboons. Based on this premise, two patients with HBV end-stage liver disease underwent baboon liver xenotransplantation. To study whether baboons are susceptible to HBV infection, four baboons (two receiving immunosuppressive therapy) were inoculated with HBV. Animals were followed for 6 months: clinical examinations and biochemical studies were normal, hepatitis B surface antigen and hepatitis B core antigen staining of biopsies was negative, and HBV serology remained negative. HBV polymerase chain reaction was transiently positive in one animal, which most likely reflects the initial inoculation. This pilot study ...
The nucleic acid polymers REP 2139 and REP 2165 led to hepatitis B surface antigen (HBsAg) reduction or clearance when combined with tenofovir and pegylated interferon, according to early results from a small study presented as a late-breaker at the 2016 AASLD Liver Meeting this month in Boston. This combination may potentially enable functional control of hepatitis B if confirmed in larger studies.. Over years or decades chronic hepatitis B virus (HBV) infection can lead to advanced liver disease including cirrhosis and liver cancer. Antiviral therapy using nucleoside/nucleotide analogues such as entecavir (Baraclude) or tenofovir disoproxil fumarate (Viread) is the mainstay of treatment for chronic hepatitis B. While these drugs can suppress HBV replication during therapy, and can thereby reduce the risk of liver disease progression, they usually do not lead to a cure - as indicated by HBsAg loss and anti-HBs antibody seroconversion - and long-term treatment is generally needed. Researchers ...
|p|Timely public health follow-up is required for acute cases of hepatitis B, including immunoprophylaxis of susceptible contacts. Passive public health follow-up is provided for chronic cases. The majority of cases of hepatitis B virus in VCH are chronic. Positive hepatitis B virus surface antigen (HBSAg) results are reported once only - subsequent positive results do not get reported.   Public Health also works in conjuction with external providers to ensure delivery of prenatal, antenatal, and 7-mos follow-up for infants at high risk of hepatitis B infection.|/p|
Hepatitis B virus (HBV) core protein (HBc) can shuttle between nucleus and cytoplasm. Cytoplasm-predominant HBc is clinically associated with severe liver inflammation. Previously, we found that HBc arginine-rich domain (ARD) can associate with a host factor NXF1 (TAP) by coimmunoprecipitation. It is well known that NXF1-p15 heterodimer can serve as a major export receptor of nuclear mRNA as a ribonucleoprotein complex (RNP). In the NXF1-p15 pathway, TREX (transcription/export) complex plays an important role in coupling nuclear pre-mRNA processing with mRNA export in mammalian cells. Here, we tested the hypothesis whether HBc and HBV specific RNA can be exported via the TREX and NXF1-p15 mediated pathway. We demonstrated here that HBc can physically and specifically associate with TREX components, and the NXF1-p15 export receptor by coimmunoprecipitation. Accumulation of HBc protein in the nucleus can be induced by the interference with TREX and NXF1-p15 mediated RNA export machinery. HBV transcripts
Summary The entire nucleotide sequence of genomic DNA was determined for hepatitis B virus (HBV) of subtype ayr, which had been derived from the blood of a Japanese asymptomatic carrier. The genome was 3215 nucleotides long, and differed in DNA sequence by 10% from that of subtypes adw or ayw, but by only 2% from that of subtype adr. Amino acid sequences coded for by the S, C, P and X genes, as well as by the pre-S region, closely resembled those of subtype adr, indicating that the evolution of HBV/ayr from HBV/adr was more recent than the differentiation of the other three subtypes. In the product of the S gene, the mutually exclusive subtypic determinants of the surface antigen, d and y, were associated with variation of amino acid residues at only the 68th and 122nd positions from the N terminus, in contrast to the variation at as many as seven positions for the other set of subtypic determinants, w and r. Sequences representing high local hydrophilicity in the product of the S gene were involved in
During that investigation several cats, that had previously died as a result of FIV, also seemed infected with a virus. The virus itself was elusive and it showed only 73-94% amino acid identity with known Hepatitis B viruses. This suggested the presence of a novel virus that was divergent from currently known Hepatitis B viruses. Such a large genetic distance merits assignment of a new species within the genus Orthohepadnavirus, which was tentatively named Domestic Cat Hepadnavirus or Domestic Cat Hepatitis B Virus ...
World Health Organization. World Health Organization Hepatitis B Factsheet. Geneva: World Health Organization, 2017. S. Baig, A. A. Siddiqui, W. Ahmed, H. Qureshi and A. Arif. The association of complex liver disorders with HBV genotypes prevalent in Pakistan. Virology Journal, vol. 4, no. 1, p. 128, 2007. G. Fattovich. Natural history of hepatitis B. Journal of Hepatology, vol. 39, pp. 50-58, 2003. I. Pita, A. M. Horta-Vale, H. Cardoso and G. Macedo. Hepatitis B inactive carriers: An overlooked population? GE Portuguese Journal of Gastroenterology, vol. 21, no. 6, pp. 241-249, 2014. L. M. Villar, H. M. Cruz, J. R. Barbosa, C. S. Bezerra, M. M. Portilho and L. de Paula Scalioni. Update on hepatitis B and C virus diagnosis. World Journal of Virology, vol. 4, no. 4, p. 323, 2015. I. J. Radii and A. M. Saud. Comparative assessment between serological and molecular diagnosis for patients groups with hepatitis b virus. International Journal of Current Microbiology and Applied Science, ...
Hepatitis B virus strains of subgenotype A2 with an identical sequence spreading rapidly from the capital region to all over Japan in patients with acute hepatitis B ...
The authors followed 147 children from 113 families who were susceptible to hepatitis B virus infection for a total of 275 person-years. Among these children, 19 became infected with the hepatitis B virus and thus became new subclinical cases. In this cohort study, parents played a minor role in hepatitis B virus horizontal transmission. On the...
There is currently no universally accepted numbering convention for the antiviral drug-related resistance mutations in the reverse transcriptase (rt) domain of the human hepatitis B virus (HBV) polymerase. The published inconsistencies have resulted from different HBV genotypes. A standardized numbering system for HBV polymerase is proposed. The new system is based on functional observations of HBV surface gene proteins (preS1, preS2, and HBsAg) and on the current convention used for human immunodeficiency virus type 1 (HIV-1) polymerase proteins (protease, rt, and integrase), in which the amino acid numbering restarts at the first codon position of each domain. The HBV polymerase protein can be divided into 4 domains (terminal protein, spacer, rt, ribonuclease H) and each of these can be numbered separately. In this proposal, the HBV rt domain starts with the highly conserved EDWGPCDEHG motif, contains 344 amino acids, and the lamivudine-related resistance mutations are found at amino acid ...
Corresponding author. Mailing address: Department of Medical and Molecular Science, Division of Frontier Medical Science, Programs for Biomedical Research, Graduate School of Biomedical Science, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. Phone: 81-82-257-5190. Fax: 81-82-255-6220. E-mail: chayama{at}hiroshima-u.ac.jp ...
Rapid Quantification of Hepatitis B Virus DNA by Automated Sample Preparation and Real-Time PCR: Monitoring of hepatitis B virus (HBV) DNA in serum by molecular
Background/Purpose: The prevalence of chronic hepatitis B virus (HBV) infection is high in China. 4% patients with HBV infection can present with polyarthritis and positive rheumatic factor similar to RA, which implied similar pathogenic mechanism.We aimed to investigate the association between HBV infection and serological, radiological or histological disease status in RA. Methods: 223 continuous hospitalized Chinese patients with RA were enrolled retrospectively. Clinical and laboratory data including HBV detection, and hand X ray were collected. Among 133 active RA patients, synovium was obtained by closed-needle biopsy from inflamed knee joint. Serial tissue sections were stained immunohistochemically for HBV surface antigen (HBsAg), CD79a, CD20, CD38, CD68, CD3, and CD34. Densities of positive-staining cells and synovitis score were determined. Results: According to HBV infection status, 25/223 had chronic HBV infection (including 4 chronic hepatitis B and 21 HBV carriers), 72/223 had past ...
Omata, M.; Ehata, T.; Yokosuka, O.; Hosoda, K.; Ohto, M., 1991: Mutations in the precore region of hepatitis B virus DNA in patients with fulminant and severe hepatitis
Shop a large selection of products and learn more about Hepatitis B Virus X antigen Mouse anti-Virus, Alexa Fluor 594, Clone: X36C, Hepatitis B Virus X antigen Antibody; Alexa
Hepatitis B virus (HBV) X gene encodes a multifunctional protein that can regulate cellular signaling pathways, interact with cellular transcription factors, and induce hepatocellular oncogenesis. In spite of its diverse activities, the precise role of the X protein in the viral life cycle of HBV remains unclear. To investigate this question, we have produced transgenic mice that carry either the wild-type HBV genome or a mutated HBV genome incapable of expressing the 16.5-kDa X protein. Our results indicate that while the X protein is not absolutely essential for HBV replication or its maturation in transgenic mice, it can enhance viral replication, apparently by activating viral gene expression. These results demonstrate a transactivation role of the X protein in HBV replication in transgenic mice. ...
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1. European Association For The Study Of The L. EASL clinical practice guidelines: Management of chronic hepatitis B virus infection. Journal of hepatology. 2012;57:167-85 2. Wang J, Shen T, Huang X, Kumar GR, Chen X, Zeng Z. et al. Serum hepatitis B virus RNA is encapsidated pregenome RNA that may be associated with persistence of viral infection and rebound. Journal of hepatology. 2016;65:700-10 3. Bertoletti A, Ferrari C. Innate and adaptive immune responses in chronic hepatitis B virus infections: towards restoration of immune control of viral infection. Gut. 2012;61:1754-64 4. Seetharam A, Perrillo R, Gish R. Immunosuppression in Patients with Chronic Hepatitis B. Current hepatology reports. 2014;13:235-44 5. Pang J, Zhang G, Lin Y, Xie Z, Liu H, Tang L. et al. Transforming growth factor beta-activated kinase 1 transcriptionally suppresses hepatitis B virus replication. Scientific reports. 2017;7:39901 6. Matsumoto T, Takahashi K, Inuzuka T, Kim SK, Kurosaki T, Kawakami S. et al. Activation ...
Mouse monoclonal antibody raised against recombinant hepatitis B virus core antigen Recombinant protein corresponding to hepatitis B virus core antigen core. (MAB5402) - Products - Abnova
Mouse monoclonal antibody raised against recombinant hepatitis B virus core antigen Recombinant protein corresponding to hepatitis B virus core antigen core. (MAB5403) - Products - Abnova
For additional information on hepatitis B virus (HBV) and HIV, see HIV/Hepatitis B (HBV) Coinfection in the Adult and Adolescent Guidelines1 and Hepatitis B Virus Infection in the Adult and Adolescent OI Guidelines.2 The management of HIV/HBV coinfection in pregnancy is complex and consultation with an expert in HIV and HBV infection is strongly recommended.. Screening and Vaccination All women living with HIV should be screened for HBV and hepatitis C virus (HCV) at entry into general HIV care. All pregnant women living with HIV should be screened during each pregnancy for HBV unless they are known to have HIV/HBV coinfection and for HCV unless they are known to have HIV/HCV coinfection. Screening for HBV should include hepatitis B surface antigen [HBsAg], hepatitis B core antibody [anti-HBc], and hepatitis B surface antibody [anti-HBs]. Women who test positive for HBsAg should have follow-up testing that includes liver function tests, prothrombin time, HB e antigen, HB e antibody, and HBV DNA ...
Buy our Recombinant Hepatitis B Virus E Antigen protein. Ab91273 is an active full length protein produced in Escherichia coli and has been validated in WB…
During previous studies of susceptibility to hepatitis B virus (HBV) infection, HBV DNA was detected in 2/6 wildcaught baboons. In the present study, HBV DNA was amplified from 15/69 wild-caught baboons. All animals were negative for HBV surface antigen and antibody against HBV core antigen. Liver tissue from 1 baboon was immunohistochemically negative for HBV surface antigen but positive for HBV core antigen. The complete HBV genome of an isolate from this liver clustered with subgenotype A2. Reverse transcription PCR of liver RNA amplified virus precore and surface protein genes, indicating replication of virus in baboon liver tissue. Four experimentally naive baboons were injected with serum from HBV DNA-positive baboons. These 4 baboons showed transient seroconversion, and HBV DNA was amplified from serum at various times after infection. The presence of HBV DNA at relatively low levels and in the absence of serologic markers in the baboon, a nonhuman primate, indicates an occult infection ...
BioAssay record AID 378283 submitted by ChEMBL: Inhibition of Hepatitis B virus E antigen activity in human MS-G2 cells at 10 ug/mL.
Background: Hepatitis B virus (HBV) infection is a major global health burden with distinct geographic public health significance. Oman is a country with intermediate HBV carrier prevalence; however, little is known about the incidence of HBV variants in circulation. We investigated the HBV genotype distribution, the occurrence of antiviral resistance, and HBV surface antigen (HBsAg) escape mutations in HBsAg-positive patients in Oman. Methods: Serum samples were collected from 179 chronically HBV-infected patients enrolled in various gastroenterology clinics in Oman. HBV genotypes were determined by sequencing and phylogenetic analysis. Mutations in the HBV polymerase and the HBsAg gene were characterized by mutational analysis. Results: HBV genotypes D (130/170; 76.47%) and A (32/170; 18.28%) are predominant in Oman. The HBV genotypes C and E were less frequent (each 1.18%), while the HBV genotypes B, G, F, and H were not detected. Four patients revealed HBV genotype mixtures (HBV-A/D and ...
Yum, J. S., B. C. Ahn, H. J. Jo, D. Y. Kim, K. H. Kim, H. S. Kim, Y. C. Sung, J. Yoon, J. Morrey, and H. M. Moon. 2012. Use of pre-s protein-containing hepatitis B virus surface antigens and a powerful adjuvant to develop an immune therapy for chronic hepatitis B virus infection. Clin Vaccine Immunol 19:120-127. PMID22155769. ...
The underlying mechanisms for earlier hepatitis B e antigen (HBeAg) seroconversion in patients with chronic hepatitis B virus (HBV) genotype B when compared with genotype C are unknown. We aimed to determine whether there were any differences in the T helper (Th) responses during hepatitis flares in HBeAg-positive patients with genotypes B and C. Proliferative response measured by 3H-thymidine uptake and Th responses measured by Enzyme-Linked Immunosorbent Spot assays for interleukin (IL)-2, interferon-gamma (IFN-γ), IL-4, IL-5 and IL-10 were performed in 10 patients with genotype B and 10 with genotype C with hepatitis flares. HBV genotypes, core promoter, precore mutations, sequence of HBV core region and HBV DNA levels were determined. There was no difference in the HBV DNA levels during hepatitis flares between patients with genotypes B and C. Patients with genotype B had a significantly higher number of IFN-γ producing cells [with hepatitis B core antigen (HBcAg) stimulation] and lower ...
References for Abcams Recombinant Hepatitis B Virus Core Antigen protein (ab119471). Please let us know if you have used this product in your publication
Hepatitis B virus (HBV) is one of the major causes of chronic hepatitis, cirrhosis and liver cancer. In combating HBV infections, HBV diagnosis and vaccination are therefore critical. The hepatitis B virus surface antigen (HBsAg) is a key target molecule in developing vaccines and diagnostic systems. To date, although HBsAg has been expressed in bacteria, yeasts and mammalian cells, there are still limitations in the existing ones, which leave the necessity for searching new HBsAg production methods. In this study, a simple phage display-based method was developed to produce the purified full-length HBsAg molecules for further immunization studies. For this purpose, the HBsAg coding gene was cloned into a pCANTAB5E phagemid vector and expressed on the surface of M13 filamentous phages. The HBsAg-expressing phage nanosystem was then used as immunization agent in BALB/cJ mice. The ELISA results for sera obtained from mice immunized with HBsAg-displaying phage particles revealed an immune response ...
The purpose of this study is to identify the effect of prophylactic entecavir in HBsAg Negative/HBcAb Positive/hepatitis B virus DNA Negative patients with lymphoma are randomized into entecavir prophylaxis group or observation group. In entecavir prophylaxis group, entecavir 0.5 mg/day orally is initiate on day 1 of the first course of antitumor therapy, and will be continued until at least 6 months after completion of antitumor therapy. In observation group, entecavir 0.5mg daily will be prescribed for patients with hepatitis B virus reactivation ...
Chronic hepatitis B virus (HBV) infection in endemic areas usually starts since infancy and early childhood and persists lifelong. The clinical course varies among different chronic infected subjects. Majority of chronic HBV infected children present with immune-tolerant status initially, experience the immune clearance phase with various degree of liver injury during or beyond puberty, and then enter the inactive phase after hepatitis B e antigen (HBeAg) seroconversion. Part of them may have HBV DNA titers elevation with hepatitis flare after HBeAg seroconversion, the so call HBeAg-negative hepatitis flare. Liver cirrhosis, and even hepatocellular carcinoma may develop afterward. The complex course of chronic HBV infection is associated with the age/route of viral acquisition, host factors such as immune and endocrine factors, viral factors, and host-viral interactions. The adrenarche and puberty onset modulate the start of immune clearance and the severity of liver inflammation in chronic HBV infected
Hepatitis B Virus Core Antigen antibody [H6F5] for ELISA, WB. Anti-Hepatitis B Virus Core Antigen mAb (GTX22045) is tested in Hepatitis B virus samples. 100% Ab-Assurance.
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SPEARMAN, C W N et al. South African guideline for the management of chronic hepatitis B: 2013. SAMJ, S. Afr. med. j. [online]. 2013, vol.103, n.5, pp.335-349. ISSN 2078-5135.. Hepatitis B remains a significant yet preventable health issue in South Africa. The introduction of the hepatitis B vaccine into the country some 18 years ago has demonstrated benefit, but the exposure to, and prevalence of chronic HBsAg positivity remain unacceptably high. Those with chronic hepatitis B virus infection have an elevated risk of developing cirrhosis with end-stage liver disease and a markedly elevated risk of hepatocellular carcinoma, independent of the presence of cirrhosis. The challenge in South Africa remains prevention through the universal vaccination coverage of all children and the identification of those with chronic hepatitis B virus infection. Over the last decade our understanding of hepatitis B and its behaviour and natural history in those with chronic infection has significantly improved. ...
Results: Of the 1000 samples 55 (5.5%) were found to be reactive, of which 87.3% (48/55) were positive for hepatitis B surface antibody, indicating immunity as a result of previous infection however, that does not exclude active infection with escaped mutant HBV. Nested PCR results showed the presence of hepatitis B viral DNA in all the 55 samples that were positive for core protein, which is in agreement with the hepatitis B surface antibody result ...
Occult Hepatitis B infection is characterized by the presence of HBV DNA without detectable HBsAg, with or without the presence of HBV antibodies outside the acute phase window period [8]. A number of possible mechanisms have been suggested for the pathogenesis of occult Hepatitis B infection, although it is most likely multifactorial, depending upon both host and viral factors. The majority of cases are secondary to overt HBV infection and represent a residual low level viraemia suppressed by a robust immune response, together with abnormal histological findings on liver biopsy which developed either during the acute or chronic phase of HBV infection [9,10].. In our study, a sensitive real time quantitative PCR assay was used to determine the presence of occult Hepatitis B infection in a large cohort of inner city adult patients receiving maintenance haemodialysis. We did find occult HBV, although the prevalence and levels of detectable circulating HBV were low.. Some studies have observed a ...
OBJECTIVES: Chronic hepatitis B virus (HBV) infection is associated with a higher risk of liver diseases. Substantial uncertainty remains, however, about the associations of HBV infection with mortality from extrahepatic causes, especially from subtypes of cardiovascular diseases. We prospectively examined the association of chronic HBV infection with total and cause-specific mortality. DESIGN: Population-based prospective cohort study. SETTING: China Kadoorie Biobank in which participants from 10 geographically diverse areas across China were enrolled between 2004 and 2008. PARTICIPANTS: 475 801 participants 30-79 years of age without reporting major chronic diseases at baseline were enrolled. Hepatitis B surface antigen (HBsAg) was tested using an on-site rapid test strip at baseline. PRIMARY AND SECONDARY OUTCOME MEASURES: Total and cause-specific mortality. RESULTS: A total of 35 822 deaths were recorded during ~10 years of follow-up. In multivariable-adjusted analyses, compared with HBsAg-negative
Hepatitis B is a serious liver infection caused by Hepatitis B virus. Chronic Hepatitis B infection leads to increased risk for liver cirrhosis, liver cancer and consequent death due to these conditions. The major modes of transmission include mother to child during birth, blood exposure and during sexual contact. The Hepatitis B infection can be prevented through three doses of Hepatitis B vaccination given over a period of six months and the control of Hepatitis B infections includes costly antiviral medications. As per World Health Organization (WHO), the regions of the world with hepatitis B prevalence rate less than 2% have low endemicity, those having prevalence rate of 2-7% are of medium endemicity and regions with prevalence rate greater than 7% are categorized as highly endemic. India falls in medium endemic region with Hepatitis B prevalence rate ranging from 2-7%.. In the context of the exile Tibetan population, Department of Health, CTA recognizes Hepatitis B as a major public health ...
Lamivudine is an oral nucleoside analogue widely used for the treatment of chronic hepatitis B. The main limitation of lamivudine use is the selection of resistant mutations that increases with time of utilization. Hepatitis B virus (HBV) isolates have been classified into eight genotypes (A to H) with distinct geographical distributions. HBV genotypes may also influence pathogenic properties and therapeutic features. Here, we analyzed the HBV genotype distribution and the nature and frequency of lamivudine resistant mutations among 36 patients submitted to lamivudine treatment for 12 to 84 months. Half of the patients were homosexual men. Only 4/36 (11%) patients were HBV DNA negative. As expected for a Brazilian group, genotypes A (24/32 positive individuals, 75%), D (3/32, 9.3%) and F (1/32, 3%) were present. One sample was from genotype C, which is a genotype rarely found in Brazil. Three samples were from genotype G, which had not been previously detected in Brazil. Lamivudine resistance mutations
Screening and identification of interacting proteins with hepatitis B virus core protein in leukocytes and cloning of new gene C1
The mechanisms of hepatitis B virus (HBV) persistent infection are not completely understood. Interleukin (IL)-35, which is a newly identified cytokine belongs to IL-12 family, has been demonstrated to induce immunotolerance. Thus, the aim of current study was to investigate the role of IL-35 during chronic HBV infection. A total of 61 patients with chronic HBV infection (37 chronic hepatitis B [CHB] and 24 asymptomatic HBV carriers [ASC]) and 20 healthy individuals were enrolled. IL-35 concentration as well as the modulatory function of IL-35 on CD4+CD25+CD127dim/- regulatory T cells (Tregs) and on HBV antigen-specific CD8+ T cells was investigated. IL-35 expression was significantly increased in both CHB and ASC, and was positively correlated with the levels of HBV DNA. Inhibition of viral replication induced the reduction in serum levels of IL-35. IL-35 stimulation led to inhibition of proinflammatory cytokine productions and elevation of apoptosis in peripheral blood mononuclear cells, but not in
Hepatitis B The disease known as Hepatitis B is caused by the infectuous Hepatitis B virus (HBV). HBV alone has infected about 400 million people in the world, which makes HBV one of the most common pathogens. Almost 700 million U.S. Dollars are spent every year for treating Hepatitis patients. Structure: HBV is a 42 nm doubleshelled deoxyribonucleic acid (DNA) virus of the class Hepadnaviridae. The outer surface membrane contains Hepatitis B surface antigen (HBsAg), which also circulates in blood as 22 nm spherical and tubular particles. The inner core of the virus contains Hepatitis B core antigen (HBcAG), Hepatitis B e antigen (HBeAg), a single molecule of partially doublestranded DNA, and DNA dependent DNA polymerase.. How it is transmitted? Hepatitis B is transmitted by sexual contact or by blood. People who are at risk by being infected by HBV are drug users, homosexuals, active heterosexuals, infants born from infected mothers and children of immigrants from disease-endemic areas. ...
The objective of the practice guideline is to update the natural history of hepatitis B virus infection and to give recommendations for optimal management of chronic hepatitis B.. The guideline is based on the best available evidence. The goal of treatment of chronic hepatitis B is to improve quality of life and survival by preventing progression of hepatitis to cirrhosis and hepatocellular carcinoma.. The progression of liver disease is associated with HBV DNA level in the blood. In HBeAgpositive and HBeAg-negative patients, the ideal end-point of treatment is sustained HBsAg loss. Maintained undetectable HBV DNA under long-term antiviral treatment in HBeAg-positive patients who do not achieve antiHBe seroconversion and in HBeAg-negative patients is the next most desirable end point.. Indication for treatment is identical for HBeAg-positive and HBeAg-negative patients and is based on a combination of serum HBV DNA level, ALAT elevation, and liver histology.. Treatment should be considered in ...
1) Most positive HBsAg results picked up on ante-natal screening represent chronic infection? T/F. True, probably more than 95% of such results represent chronic infection, most of whom have probably had the infection for years or even since birth.. 2) IgM Anti-HBc can be used to differentiate acute from chronic Hepatitis B infection? T/F. True, but in my opinion only occasionally needed to confirm acute infection in someone who is either symptomatic or has had a recent contact with Hepatitis B. For the majority of cases, chronic infection can be assumed.. 3) A patient with negative HBeAg will always have a low HBV viral load? T/F. False. Hepatitis B viruses containing pre-core mutants may be HBeAg -ve but still have high HBV DNA levels.. 4) Anti-HBc (total) is usually negative in chronic Hepatitis B infection? T/F. False: Anti-HBc should always be positive in chronic Hepatitis B infection. If it is negative, it should prompt you to look at the validity of your HBsAg result.. 5) A patient who ...
Co-infections of hepatitis B and C viruses are frequent with HIV due to shared routes of transmission. In most of the tertiary care health settings, HIV reactive patients are routinely tested for HBsAg and anti-HCV antibodies to rule out these co-infections. However, using the routine serological markers one can only detect active HBV infection while the occult HBV infection may be missed. There is insufficient data from India on HIV-HBV co-infection and even scarce on occult HBV infection in this group. We estimated the burden of HBV infection in patients who were tested positive for HIV at a tertiary care centre in north India. We also attempted to determine the prevalence and clinical characteristics of occult HBV infection among these treatment-naïve patients and compare their demographic features with other HIV patients. During a period of 6 years between January 2002 to December 2007, 837 HIV positive patients (631 males and 206 females (M: F :: 3.06:1) were tested for serological markers of HBV
Abstract Current estimates put the prevalence of hepatitis B virus (HBV) infection in Kenya at 5-8%. We determined the HBV infection prevalence in the human immunodeficiency virus (HIV)-negative Kenyan adult and adolescent population based on samples collected from a national survey. We analyzed data from HIV-negative participants in the 2007 Kenya AIDS Indicator Survey to estimate the HBV infection prevalence. We defined past or present HBV infection as presence of total hepatitis B core antibody (HBcAb), and chronic HBV infection (CHBI) as presence of both total HBcAb and hepatitis B surface antigen (HBsAg). We calculated crude and adjusted odds of HBV infection by demographic characteristics and risk factors using logistic regression analyses. Of 1,091 participants aged 15-64 years, approximately 31.5% (95% confidence interval [CI] = 28.0-35.3%) had exposure to HBV, corresponding to approximately 6.1 million (CI = 5.4-6.8 million) with past or present HBV infection. The estimated prevalence of CHBI
Hepatitis B virus (HBV) is a major global health problem especially in sub-Saharan Africa and in East Asia. Ten hepatitis B virus genotypes have been described that differ by geographic distribution, disease progression, and response to treatment. Escape mutations within the surface open reading frame (ORF) affect HBV antigenicity leading to failures in diagnosis, vaccine and hepatitis B immunoglobulin therapy. However, the molecular characteristics of HBV in Botswana, a highly endemic country, are unknown. We describe the molecular characteristics of HBV and prevalence of escape mutants among HIV/HBV coinfected individuals Botswana. DNA was extracted from archived plasma samples from 81 HIV/HBV co-infected participants from various clinical studies at the Botswana Harvard AIDS Institute Partnership. A 415 base pair (bp) fragment of the polymerase gene was amplified by semi-nested PCR. In a subset of samples, a 2100 bp fragment was amplified. The PCR product was genotyped using Big Dye sequencing
TY - JOUR. T1 - The mannose receptor acts as hepatitis B virus surface antigen receptor mediating interaction with intrahepatic dendritic cells. AU - den Brouw, M.L.O.. AU - Binda, R.S.. AU - Geijtenbeek, T.B.H.. AU - Janssen, H.-G.. AU - Woltman, A.M.. PY - 2009. Y1 - 2009. U2 - 10.1016/j.virol.2009.07.015. DO - 10.1016/j.virol.2009.07.015. M3 - Article. VL - 393. SP - 84. EP - 90. JO - Virology. JF - Virology. SN - 0042-6822. IS - 1. ER - ...
TY - JOUR. T1 - Serological subtype (serotype) of hepatitis B virus surface antigen. AU - Iwasaki, Yoshiaki. AU - Tsuji, T.. PY - 1995/10. Y1 - 1995/10. UR - http://www.scopus.com/inward/record.url?scp=0029380199&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0029380199&partnerID=8YFLogxK. M3 - Article. VL - 53 Suppl. SP - 293. EP - 298. JO - Nippon rinsho. Japanese journal of clinical medicine. JF - Nippon rinsho. Japanese journal of clinical medicine. SN - 0047-1852. IS - Pt 2. ER - ...
TY - JOUR. T1 - Retroviral-mediated transfer and expression of hepatitis B e antigen in human primary skin fibroblasts and Esptein-Barr virus-transformed B lymphocytes. AU - Raney, A. K.. AU - Milich, D. R.. AU - Hughes, J. L.. AU - Sorge, J.. AU - Chisari, F. V.. AU - Mondelli, M. U.. AU - McLachlan, A.. PY - 1989. Y1 - 1989. N2 - Previously, an amphotropic retroviral expression system coding for the neomycin resistance gene was developed and used to synthesize hepatitis B e antigen (HBeAg) and hepatitis B core/e antigen (HBc/eAg) in transfected mouse NIH 3T3 fibroblasts (A. McLachlan et al., 1987, J. Virol. 61, 683-692). In the present study, these transfected cell lines were infected with a helper amphotropic murine leukemia virus resulting in the production of infectious recombinant retrovirus. The recombinant retrovirus was examined for its capacity to transmit resistance to the antibiotic, G418, and to express hepatitis B virus antigens in mouse NIH 3T3 fibroblasts, human primary skin ...
The hepatitis B virus core (HBc) virus-like particle (VLP) is known as one of the most immunogenic antigens and carrier vehicles in different immunization strategies. Recent findings are suggesting the potential of the HBc VLPs as an oral immunogen. Here, we focus on the induction of serum humoral responses by oral administration of HBc VLPs in preparations substantially free of lipopolysaccharide and immunomodulating encapsidated RNA. The full-length HBc antigen was used, because the C-terminal arginine-rich tail may contribute to the immunogenicity of the antigen as the region is involved in cell surface heparan sulfate binding and internalization of the protein. Serum antibody levels and isotypes were determined following oral administration of the HBc VLPs with the perspective of using the HBc VLP as an immunostimulatory and carrier molecule for epitopes of blood-borne diseases in oral immunization vaccination strategies. Following oral administration of the HBc VLP preparations to mice, a strong
Hepatitis B is NOT spread through sneezing, coughing, hugging or breastfeeding. Even though the virus can be found in saliva, you cant get it from kissing or sharing forks, spoons, or knives with someone whos infected.. If you dont have hepatitis B, get vaccinated and ask your partner to get vaccinated, too. Vaccination is the best way to prevent hepatitis B.. Hepatitis B and pregnancy. If you have hepatitis B during pregnancy and its not treated, you can pass it to your baby. This can happen during a vaginal delivery or a c-section. About 9 out of 10 babies (90 percent) infected at birth develop chronic hepatitis B infection. This infection can cause life-long liver problems for your baby.. Getting tested for hepatitis B is a routine part of prenatal care. Your health care provider will test for hepatitis B and other infections at your first prenatal care checkup.. If you do test positive for hepatitis B, your health care provider may prescribe you an antiviral medication during your ...
May is Hepatitis Awareness Month and Saturday, May 19this National Hepatitis Testing Day in the United States. This day is an opportunity to increase awareness and testing for both hepatitis B and C. It is also a reminder for health care providers and the public of the importance of testing for viral hepatitis.. Why is hepatitis B testing necessary? Hepatitis B is largely asymptomatic, which means that symptoms dont always occur or are not obvious. Some people will not know that they have hepatitis B until it is too late, or they may learn of their infection from a blood donation screening or lab work. There are groups of people who have a greater risk of hepatitis B compared to others, so it doesnt hurt to be sure. here are some places around the world that have an extremely high hepatitis B prevalence (where many people are infected). It is important that people who are at high risk for a hepatitis B infection see a doctor to get tested, to find out if they have a hepatitis B infection. ...