HBV Active Surface Antigen (subtype adw ) (DAG-P2446)

HBV Active Surface Antigen (aa 1 - 227) (subtype adw ), recombinant protein from Yeast

Product Overview
Active Hepatitis B Surface Antigen (Adw) full length protein
Molecular Weight
24 kDa
Cellular Localization
Membrane Virion
The activity of this antigen was identified in a functional ELISA assay with anti-Hepatitis B Surface Antigen (Adw) antibodies (capture and conjugate).
> 97 % by SDS-PAGE.This antigen is lyophilized from 0.22 μm filtered solution.
pH: 7.20Constituents: 93% Phosphate Buffer, 5% Trehalose, 1.17% Sodium chloride
Store at +4°C. Aliquot and store at -20°C or -80°C when reconstituted. Avoid repeated freeze/thaw cycles.
It is recommended to reconstitute the lyophilized protein in sterile deionized water. Solubilize for 30 to 60 minutes at room temperature with occasional gentle mixing. Carrier protein (0.1% HSA or BSA) is strongly recommended for further dilution and lon
Hepatitis B virus, abbreviated HBV, is a species of the genus Orthohepadnavirus, which is likewise a part of the Hepadnaviridae family of viruses. This virus causes the disease hepatitis B.
Antigen Description
HBV belongs to the Hepadnaviridae family of viruses. Its genome consists of partially double stranded circular DNA. The DNA is enclosed in a nucleocapsid, or core antigen (HBcAg), which is surrounded by a spherical envelope (surface antigen or HBsAg). The core antigen shares its sequences with the e antigen (HBeAg) but no cross reactivity between the two proteins has been observed. The HBV genome also encodes a DNA polymerase that also acts as a reverse transcriptase. Hepatitis B infection is normally diagnosed from serological tests that detect HBsAg but as the disease progresses this antigen may no longer be present in the blood and tests for HBcAg are used. If HBsAg can be detected in the blood for longer than six months, chronic hepatitis B is diagnosed. The antigenic determinant of the protein moiety of the HBsAg determines specific characteristics of different serotypes and provides the basis of immunodetection. HBsAg has antigenic heterogeneity, specifically, two pairs of sub specific determinants, d/y and w/r allow the following combinations: adw, ayw, adr, ayr.
HBsAg; S gene subtype adw2; sAg; ssAg


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First molecular epidemiological study of hepatitis B and D in individuals infected with human T-lymphotropic virus 1/2 from Argentina


Authors: Pataccini, Gabriela; Andrea Berini, Carolina; Rene Pedrozo, Williams; Marcela Biglione, Mirna; Maria Delfino, Cecilia

Human T-lymphotropic virus 1/2 (HTLV-1/2), hepatitis B virus (HBV), and hepatitis D virus (HDV) share transmission routes. Argentina shows low prevalence of HTLV-1/2, HBV, and HDV infections; however, this situation may vary according to the geographic region and group studied. The aim of this study was to estimate the prevalence of HBV and HDV infections and detect both viral genotypes in HTLV-1/2 individuals from Argentina. A total of 202 HTLV-1/2 confirmed samples (blood donors [BD] and individuals with risk factors for HTLV-1/2 [RF]) were tested for HBsAg and total anti-HBc by enzyme-linked immunosorbent assay. All reactive samples for some HBV markers were analyzed for HBV DNA characterization and HDV serological and molecular analysis. Total prevalence was 1.5% for HBsAg and 6.4% for anti-HBc. Prevalence was 23.1% for anti-HDV in all HBV-reactive samples. No significant difference was observed for HBV and HDV prevalence within HTLV subtypes. The population study showed that prevalence of anti-HBc was higher in the RF than in the BD population, with no significant differences between them. The HBsAg marker and anti-HDV were only found in RF, showing significant differences when compared to BD. Regarding molecular detection, one sample amplified for HBV DNA and none for HDV RNA. HBV sequence was classified as subgenotype F1b. New and updated background on serological markers of HBV and HDV infection in patients with HTLV-1/2 was provided.

A large real-world cohort study examining the effects of long-term entecavir on hepatocellular carcinoma and HBsAg seroclearance


Authors: Ko, Kwan-Lung; To, Wai-Pan; Mak, Lung-Yi; Seto, Wai-Kay; Ning, Qin; Fung, James; Lai, Ching-Lung; Yuen, Man-Fung

Real-world studies examining reduction in risk of hepatocellular carcinoma (HCC) in patients receiving antivirals are limited by the small size of the studies, or by data insufficiency and heterogeneity with short follow-up duration. We aimed to examine the real-world long-term outcome of patients receiving entecavir treatment on HCC incidence and HBsAg seroclearance. The incidence of HCC in 1225 entecavir-treated patients between 2002 and 2015 was compared with the HCC incidence estimated using the REACH-B, GAG-HCC and CU-HCC scores. Standardized incidence ratios (SIR) were calculated. The impact of entecavir treatment on HBsAg seroclearance was also explored. The median follow-up of the cohort was 6.6 years, with 66 cases of HCC development. Using the REACH-B model, the reduction of HCC risk was significant from year 6 onwards with SIR of 0.68 (95% CI 0.535-0.866) at year 10. In subgroup patients without cirrhosis, consistent risk reduction was observed from the fifth year and the SIR reached 0.51 (95% CI 0.271-0.704) by year 10. Benefit in cirrhotic patients was demonstrated when using the GAG-HCC and CU-HCC score, with the SIR at year 10 being 0.38 (95% CI 0.259-0.544) and 0.46 (95% CI 0.314-0.659), respectively. The cumulative rate of HBsAg seroclearance was 5.2%. HBsAg level at third year of treatment and baseline-to-3-year percentage reduction was predictive of subsequent HBsAg seroclearance. In conclusion, long-term entecavir therapy was associated with significant reduction in the risk of HCC in the real world. However, HBsAg seroclearance rate remained low. Additional therapy may be considered in patients with adverse predictive factors for subsequent HBsAg seroclearance.

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