This anti-HBs ELISA kit is an enzyme linked immunosorbent assay for quantitative detection of antibodies to hepatitis B virus surface antigen (anti-HBs) in human serum or plasma and assessing antibody response levels to HBsAg-vaccine.
Contents of Kit
MICROWELL PLATE, 1plate. Blank microwell strips fixed on a white strip holder. The plate is sealed in aluminium pouch with desiccant. 8×12/12×8-well strips per plate. Each well contains recombinant HBsAg. The microwell strips can be broken to be used separately. Place unused wells or strips in the plastic sealable storage bag together with the desiccant and return to 2~8°C. CALIBRATION CURVE STANDARDS, 6vials. Yellowish liquids filled in a vial with green screw cap. The kit contains the following standards: 0 mIU, 10 mIU, 20 mIU, 40 mIU, 80mIU, 160mIU/ml, 500μl each. anti-HBs diluted in protein-stabilized buffer. Preservative: ProClin 300. HRP-CONJUGATE REAGENT, 1vial. Red-colored liquid filled in a white vial with red screw cap. 6.5ml per vial. Horseradish peroxidase-conjugated HBsAg. Ready to use as supplied. Once open, stable for one month at 2-8°C. STOCK WASH BUFFER, 1bottle. DILUTE BEFORE USE. Colorless liquid filled in a clear bottle with white screw cap. 30ml per bottle. PH 7.4 20 × PBS (Contains Tween-20 as detergent). The concentration must be diluted 1 to 20 with distilled/deionized water before use. Once diluted, stable for one week at room temperature, or for two weeks when stored at 2-8°C. CHROMOGEN SOLUTION A, 1vial. Colorless liquid filled in a white vial with green screw cap. 7ml per vial. Urea peroxide solution. Ready to use as supplied. Once open, stable for one month at 2-8°C. CHROMOGEN SOLUTION B, 1vial. Colorless liquid filled in a black vial with black screw cap. TMB solution( Tetramethyl benzidine dissolved in citric acid). 7ml per vial. Ready to use as supplied. Once open, stable for one month at 2-8°C. STOP SOLUTION, 1vial. Colorless liquid filled in a white vial with white screw cap. 7 ml per vial. Diluted sulfuric acid solution (2.0M H2SO4). Ready to use as supplied. PLASTIC SEALABLE BAG, 1unit. For enclosing the strips not in use. CARDBOARD PLATE COVER, 1sheet. To cover the plates during incubation and prevent evaporation or contamination of the wells. PACKAGE INSERTS, 1copy
Storage
The components of the kit will remain stable through the expiration date indicated on the label and package when stored between 2-8 °C; do not freeze. To assure maximum performance of this anti-HBs quantitative ELISA kit, during storage protect the reagents from contamination with microorganism or chemicals.
Detection Limit
Analytical Sensitivity (lower detection limit): In the follow-up of vaccinated individuals the value of 10 WHO mIU/ml is the minimum concentration at which the recipient is considered protected. This kit shows sensitivity of 5 mIU/ml.
Sensitivity
The performance characteristics of this assay were evaluated by a panel of samples obtained from 600 individuals receiving HBV vaccines in which the titers of anti-HBs were evaluated in a direct comparison with another commercially available anti-HBs ELISA kit. From this group, 594 individuals showed antibody titer higher than 10 mIU/ml, which was confirmed with the reference anti-HBs ELISA kit. In another group of 220 individuals with confirmed hepatitis B vaccination history, 220 of the tested samples showed antibody titer higher than 10 mIU/ml. From this study, overall agreement of 100% was obtained between this kit and the reference test in linear regression analysis.
General Description
Hepatitis B virus (HBV) is an enveloped, double-stranded DNA virus belonging to the Hepadnaviridae family and is recognized as the major cause of blood transmitted hepatitis together with hepatitis C virus (HCV). Infection with HBV induces a spectrum of clinical manifestations ranging from mild, inapparent disease to fulminant hepatitis, severe chronic liver diseases, which in some cases can lead to cirrhosis and carcinoma of the liver. Classification of a hepatitis B infection requires the identification of several serological markers expressed during three phases (incubation, acute and convalescent) of the infection. Now several diagnostic tests are used for screening, clinical diagnosis and management of the disease. Hepatitis B surface antigen (HBsAg) is an important viral envelope protein, which appears shortly after infection and is a key serological marker for detection and diagnosis of HBV. Clearance during treatment shows recovery and development of neutralizing antibodies (anti-HBs) occurs in 90% of the patients. Due to the introduction of hepatitis B vaccination programs, the detection of anti-HBs has become important method for monitoring of recipients upon vaccination with synthetic and natural HBsAg. The absence of anti-HBs indicates susceptibility to HBV infection. For this, screening for anti-HBs in high-risk populations is recommended for identifying individuals who may benefit from vaccination.
Standard Curve
For illustration purpose only- the average values are given only: (*0mIU/ml=Negative Samples or Negative Control).
Citations
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Hepatitis B virus genotypes A1 and A2 have distinct replication phenotypes due to polymorphisms in the HBx gene
Zhang M, Mouzannar K, Zhang Z, Teraoka Y, Piotrowski J, Ishida Y, Tateno-Mukaidani C, Saito T, Abe-Chayama H, Chayama K, Liang TJ
PLoS Pathog2025 Jan 9PubMed ID:39787208Read Article
Applications: ELISA Reactive species: HBV
"Abstract: HBV genotype A has two major subtypes, A1 (commonly in Africa) and A2 (commonly in Europe) with only 4% nucleotide differences. Individuals infected with these two subtypes appear to have different clinical manifestations and virologic features. Whether such a difference results from the virus or host has not been established. Using HBV generated from molecule clones of subtypes A1 and A2 in cell culture (HBVcc), we demonstrate that HBVcc of subtypes A1 and A2 can be passaged in vitro and in vivo and respond equally well to human IFN-α treatment. HBVcc passaged in human liver chimeric mice (HBVmp) infected human hepatocytes more efficiently than that of the original HBVcc. Subtype A2 showed a much higher viral replication level than that of subtype A1. Mechanistic investigations using constructs with chimeric A1/A2 sequences and specific mutations indicated that subtype A2 has an inherently higher replication phenotype due to specific polymorphisms in the HBx gene resulting in amino acid variations. Studies of HBx expression demonstrated that A1 HBx is expressed at a much lower level than that of A2 HBx. Mutagenesis studies identified two HBx amino acid variations responsible for the observed phenotypic difference. Using AlphaFold2, we generated structural models of HBx proteins of A1 and A2. Superposition of the two models reveal that the overall structural motifs are similarly aligned, except for the C-terminal peptides diverging between the A1 and A2 models, possibly explaining their functional difference. In conclusion, using various in vitro and in vivo models, here we show that subtype A2 has an inherently higher replication phenotype due to polymorphisms in HBx that result in possible differences in structure and expression level of the two subtype HBx proteins. This genotypic difference potentially explains the reported clinical differences between the two subtypes as well as providing a previously unrecognized association between viral sequence variations and clinical manifestations of HBV infection in humans." Article snippet: HBeAg and HBsAg in cell culture supernatants was measured by ELISA kits (Creative-Diagnostics, NY, USA) according to the protocol. Samples outside the assay linear range were
diluted and re-assayed.
Figure 1. Infection of PXB-cells and human liver chimeric mice with HBVcc subtypes A1 and A2.
Background
Hepatitis B surface antigen (HBsAg) was found in hepatitis B virus subviral particles (SVP) in 1965 and was originally called "Australia Antigen". Since then, much has been learned about HBV infection. Hepatitis B virus infection can lead to hepatitis, while in the case of chronic hepatitis B (CHB), persistent liver inflammation may lead to fibrosis, cirrhosis, liver decompensation, and even associated with the incidence of hepatocellular carcinoma (HCC).
Figure 1. Hepatitis B virions and subviral particles under electron microscopy (Source: Yuen MF, et al. 2018)
These multiple complications of chronic hepatitis B are the causes of major death. The data from the source WHO show that 254 million people were living with chronic hepatitis B infection in 2022, with 1.2 million new infections each year. In 2022, hepatitis B resulted in an estimated 1.1 million deaths, mostly from cirrhosis and hepatocellular carcinoma (primary liver cancer).
Figure 2. Estimated HBsAg epidemic in 2024 (Source: CDA Foundation Polaris Observatory.)
During infection, antibody response plays an important role in the clearance of hepatitis B virus particles and infected hepatocytes. In infected people, patients may naturally clear HBsAg and produce hepatitis B surface antibodies (anti-HBs), while other patients may develop from chronic hepatitis to cirrhosis and hepatocellular carcinoma (HCC). Hepatitis B surface antigen is the most important marker for the diagnosis of hepatitis B virus infection. Anti-HBs is a specific protective antibody produced under the stimulation of exposed epitopes, which can neutralize hepatitis B surface antigen in serum. The marker for establishing immune control of hepatitis B virus infection is the removal of hepatitis B surface antigen from the blood. In the absence of treatment, if HBsAg is continuously cleared without detection of the virus and normal liver function, patients are thought to have established a "functional cure" similar to those who have successfully resolved their acute hepatitis B virus infection. Therefore, we need timely and continuous monitoring of HBsAg to assess the degree of infection in patients and adjust treatment decisions.
Alternative Names
hepatitis B virus surface antigen ELISA Kit
References
1. Yuen MF, et al. Hepatitis B virus infection. Nat Rev Dis Primers. 2018 Jun 7;4:18035.
2. Vaillant A. HBsAg, Subviral Particles, and Their Clearance in Establishing a Functional Cure of Chronic Hepatitis B Virus Infection. ACS Infect Dis. 2021 Jun 11;7(6):1351-1368.
Q: Is this ELISA kit for both antigen and antibody?
A: This kit can detect antibodies to hepatitis B virus surface antigen (anti-HBs) in human serum or plasma.
Q: What's the volume of the sample needed per well?
A: 50ul samples will be added to sample wells.
Q: Are the standards used in this kit traceable to the WHO International Standard Second International Standard for anti-hepatitis B surface antigen (anti-HBs) immunoglobulin, human NIBSC code: 07/164?
A: Yes
Q: How long is the shelf life of the kit?
A: 13 months.
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References
HBsAg, Subviral Particles, and Their Clearance in Establishing a Functional Cure of Chronic Hepatitis B Virus Infection
In diverse viral infections, the production of excess viral particles containing only viral glycoproteins (subviral particles or SVP) is commonly observed and is a commonly evolved mechanism for immune evasion. In hepatitis B virus (HBV) infection, spherical particles contain the hepatitis B surface antigen, outnumber infectious virus 10 000-100 000 to 1, and have diverse inhibitory effects on the innate and adaptive immune response, playing a major role in the chronic nature of HBV infection. The current goal of therapies in development for HBV infection is a clinical outcome called functional cure, which signals a persistent and effective immune control of the infection. Although removal of spherical SVP (and the HBsAg they carry) is an important milestone in achieving functional cure, this outcome is rarely achieved with current therapies due to distinct mechanisms for assembly, secretion, and persistence of SVP, which are poorly targeted by direct acting antivirals or immunotherapies. In this Review, the current understanding of the distinct mechanisms involved in the production and persistence of spherical SVP in chronic HBV infection and their immunoinhibitory activity will be reviewed as well as current therapies in development with the goal of clearing spherical SVP and achieving functional cure.
Hepatitis B virus infection
Nat Rev Dis Primers
Authors: Yuen MF, Chen DS, Dusheiko GM, Janssen HLA, Lau DTY, Locarnini SA, Peters MG, Lai CL.
Hepatitis B virus (HBV) is a hepatotropic virus that can establish a persistent and chronic infection in humans through immune anergy. Currently, 3.5% of the global population is chronically infected with HBV, although the incidence of HBV infections is decreasing owing to vaccination and, to a lesser extent, the use of antiviral therapy to reduce the viral load of chronically infected individuals. The course of chronic HBV infection typically comprises different clinical phases, each of which potentially lasts for decades. Well-defined and verified serum and liver biopsy diagnostic markers enable the assessment of disease severity, viral replication status, patient risk stratification and treatment decisions. Current therapy includes antiviral agents that directly act on viral replication and immunomodulators, such as interferon therapy. Antiviral agents for HBV include reverse transcriptase inhibitors, which are nucleoside or nucleotide analogues that can profoundly suppress HBV replication but require long-term maintenance therapy. Novel compounds are being actively investigated to achieve the goal of HBV surface antigen seroclearance (functional cure), a serological state that is associated with a higher remission rate (thus, no viral rebound) after treatment cessation and a lower rate of cirrhosis and hepatocellular carcinoma. This Primer addresses several aspects of HBV infection, including epidemiology, immune pathophysiology, diagnosis, prevention and management.
COA
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Publication ()
Figure 1. Infection of PXB-cells and human liver chimeric mice with HBVcc subtypes A1 and A2. 
Figure 1. Hepatitis B virions and subviral particles under electron microscopy
Figure 2. Estimated HBsAg epidemic in 2024
