The Mouse Anti-HBsAg IgG ELISA Kit detects and quantifies HBsAg specific IgG in mouse serum or plasma of vaccinated, immunized and/or infected animals. This immunoassay is suitable for: 1. Determining immune status relative to non-immune controls; 2. Assessing efficacy of vaccines, including dosage, adjuvantcy, route of immunization and timing; 3. Qualifying and/or standardizing vaccine batches and protocols. The kit contains no virus (live or killed) or viral proteins to avoid infection. This kit is for research use only (RUO) and not for diagnosis cure or prevention of the disease.
Contents of Kit
1. Wash Solution Concentrate(100×), 10ml. Dilute the entire volume 10ml + 990ml with distilled or deionized water into a clean stock bottle. Label as Wash Solution and store at ambient temperature until kit is used entirely. 2. Sample Diluent Concentrate (20×), 10ml. Dilute the entire volume, 10ml + 190ml with distilled or deionized water into a clean stock bottle. Label as Working Sample/Conjugate Diluent and store at 2~8°C until the kit lot expires or is used up. 3. Anti-Mouse lgG-HRP Conjugate Concentrate(100×), 0.15ml. Peroxidase conjugated anti-mouse lgG in buffer with protein, detergents and antimicrobial as stabilizers. Dilute fresh as needed; 10μl of concentrate to 1ml of Working Sample/Conjugate Diluent is sufficient for 1 8-well strip. Use within the working day and discard. Returm 100× to 2~8°C storage. 4. HBsAg Microwell Strip Plate, 8-well strips(12). Coated with recombinant HBsAg and post-coated with stabilizers. 5. Anti-HBsAg Calibrators, 0.65 mL. Four (4) vials, each containing anti-HBsAg in arbitrary activity Units; diluted in buffer with protein, detergents and antimicrobial as stabilizers. 10 U/ml, 25 U/ml, 50 U/ml, 100 U/ml 6. Anti-HbsAg Positive Control, 0.65 mL. Anti-HbsAg antibody, diluted in buffer with protein detergents and antimicrobial as stabilizers. [Value range on label]. 7. Low NSB Sample Diluent, 30 mL. Buffer with protein, detergents and antimicrobial as stabilizers. Use as is for sample dilution. 8. TMB Substrate, 12 mL. Chromogenic substrate for HRP containing TMB and peroxide. 9. Stop Solution, 12 mL. Dilute sulfuric acid.
Storage
The microtiter well plate and all other reagents, if unopened, are stable at 2-8°C until the expiration date Stabilities of the working printed on the box label.
Sensitivity
Assay Sensitivity The HBsAg -coated plated, the anti- mouse lgG HRP concentration, and the Low NSB Sample Diluent are optimized to differentiate anti-HBsAg IgG from background (non-antibody) signal with mouse serum samples diluted 1:50
General Description
Hepatitis B is an infectious disease caused by hepatitis B virus (HBV). Hepatitis, the acute illness, inflames the liver, causing jaundice, vomiting and (rarely) death. Chronic hepatitis B, however, can cause cirrhosis and liver cancer—a fatal disease. Although viral replication occurs in the liver, HBV spreads to the blood where virus-specific antigens and antibodies may be found in the infected host. Blood tests for these antigens and antibodies are used to diagnose the infection. Acute and chronic hepatitis B can be prevented by vaccination.HBV is divided into four major serotypes (adr, adw, ayr, ayw) based on antigenic epitopes presented on its envelope proteins, and into eight genotypes (A-H) according to overall nucleotide sequence variation of the genome. Genotypes differ by at least 8% of their sequences, differences which affect severity of disease and response to treatment and possibly vaccination. The hepatitis B surface antigen (HBsAg) is the first detectable viral antigen to appear during infection, and is most frequently used to screen for the presence of infection. HBsAg is also the basis for several recent vaccines, which use synthetic recombinant HBsAg and contain no blood products. Therefore, they cannot cause HBV infection, a problem with the original vaccine prepared from plasma from patients with long-term HBV infection. Following vaccination, HBsAg may be detected in serum for several days. These vaccines have provided protection for 85-90% of individuals. HBV Vaccine common brands available are: Engerix-B (GSK), Elovac B (Human Biologicals Institute, A division of Indian Immunologicals Limited), Genevac B (Serum Institute), Shanvac B etc. These vaccines are given intramuscularly.
Citations
Publication ()
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Background
Hepatitis B virus (HBV) has an outer envelope, which consists of a lipid bilayer and three sizes of glycoproteins i.e. L, M and S-HBs. Hepatitis B Surface Antigen (HBsAg) is not only a structural component but also acts as an immunomodulator responsible for the establishment of chronic infection. HBsAg can lead to dysregulation of the innate and adaptive immune response by interacting with immune and non-immune cells, which in turn leads to the ability of HBV to evade and control the host's immune system and to cause liver injury.
Figure 1. LHBs contains preS1, preS2 and S domains (Source: Inoue J, et al. 2021)
When the HBV virus infects human cells and begins to replicate, HBsAg is produced in large quantities and released into the bloodstream, making the detection of HBsAg one of the most important tools for the diagnosis of hepatitis B. The HBsAg test is used for the diagnosis of hepatitis B infection. In clinical practice, HBsAg testing is primarily used to screen for and diagnose acute and chronic hepatitis B infections, with HBsAg positivity lasting longer than 6 months usually considered chronic infection (CHB). Because hepatitis B is highly contagious, appropriate precautions need to be taken in HBsAg-positive populations to avoid further transmission of the virus, including HBsAg screening of specific populations, such as pregnant women's populations, as HBV can be vertically transmitted to newborns during labor and delivery. In addition, HBsAg positivity is also associated with an increased risk of long-term liver disease, including cirrhosis and hepatocellular carcinoma. Therefore, long-term HBsAg-positive patients usually require regular medical follow-up and monitoring in order to detect and manage possible complications in a timely manner.
There are two common treatment strategies for HBV infection, a limited 48-week PEG-IFN-α therapy and long-term treatment with nucleoside analogs (NAs).PEG-IFN-α therapy clears HBsAg and reduces ccDNA, leading to a functional cure of CHB, but it is limited in efficacy, requires subcutaneous injections, and can lead to numerous adverse effects. And although NAs therapy has better efficacy and safety, it does not achieve HBsAg clearance, does not completely cure HBV infection, and is a lifelong therapy accompanied by increased costs, poor treatment adherence, and potential toxicity.
Alternative Names
Anti-Hepatitis B Surface Antigen IgG ELISA
References
1. Inoue J, et al. Envelope Proteins of Hepatitis B Virus: Molecular Biology and Involvement in Carcinogenesis. Viruses. 2021 Jun 11;13(6):1124.
2. Lazarevic I, et al. Hepatitis B Surface Antigen Isoforms: Their Clinical Implications, Utilisation in Diagnosis, Prevention and New Antiviral Strategies. Pathogens. 2024 Jan 3;13(1):46.
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References
Hepatocellular carcinoma reduced, HBsAg loss increased, and survival improved after finite therapy in hepatitis B patients with cirrhosis
Hepatology
Authors: Jeng WJ, Chien RN, Chen YC, Lin CL, Wu CY, Liu YC, Peng CW, Su CW, Hsu CE, Liaw YF.
Background and aims: Long-term nucleos(t)ide analog (Nuc) treatment can reduce HCC in patients with HBV-related liver cirrhosis (HBV-LC). Earlier small cohort studies showed a comparable 5-year incidence of HCC in HBeAg-negative patients with HBV-LC who stopped and those continued Nuc therapy. This study aimed to validate these findings using a large cohort with 10-year follow-up.
Approach and results: From 2 centers, 494 HBeAg-negative patients with HBV-LC who stopped (finite group) and 593 who continued (continuous group) Nuc therapy were recruited. HCC, HBsAg loss, liver-related mortality/transplantation, and overall survival rates were compared between 2 groups with 1:1 propensity score matching of sex, treatment history, types of Nuc, age, transaminases, platelet count, and HBsAg levels at end of therapy in finite group or 3-year on-therapy in continuous groups. During a median follow-up of 6.2 (3.4-8.9) years, the annual and 10-year HCC incidence were lower in finite group (1.6 vs. 3.3%/y and 10-y 15.7% vs. 26.8%, respectively; log-rank test, p <0.0001). The finite group showed greater HBsAg decline/year (-0.116 vs. -0.095 log 10 IU/mL, p =0.0026) and 7.6 times higher 10-year incidence of HBsAg loss (22.7% vs. 3%, p <0.0001). Multivariate Cox regression showed finite therapy an independent factor for HBsAg loss (adjusted HR: 11.79) but protective against HCC (adjusted HR: 0.593), liver-related mortality/transplantation (adjusted HR: 0.312), and overall mortality (adjusted HR: 0.382).
Conclusions: Finite Nuc therapy in HBeAg-negative HBV-LC may reduce HCC incidence, increase HBsAg loss, and improve survival. Greater HBsAg decline/loss may reflect enhanced immunity and contribute to the reduction of hepatic carcinogenesis.
Spatial transcriptomics reveals a low extent of transcriptionally active hepatitis B virus integration in patients with HBsAg loss
Gut
Authors: Yu X, Gong Q, Yu D, Chen Y, Jing Y, Zoulim F, Zhang X.
Objective: Hepatitis B virus (HBV) can integrate into the chromosomes of infected hepatocytes, contributing to the production of hepatitis B surface antigen (HBsAg) and to hepatocarcinogenesis. In this study, we aimed to explore whether transcriptionally active HBV integration events spread throughout the liver tissue in different phases of chronic HBV infection, especially in patients with HBsAg loss.
Design: We constructed high-resolution spatial transcriptomes of liver biopsies containing 13 059 tissue spots from 18 patients with chronic HBV infection to analyse the occurrence and relative distribution of transcriptionally active viral integration events. Immunohistochemistry was performed to evaluate the expression of HBsAg and HBV core antigen. Intrahepatic covalently closed circular DNA (cccDNA) levels were quantified by real-time qPCR.
Results: Spatial transcriptome sequencing identified the presence of 13 154 virus-host chimeric reads in 7.86% (1026 of 13 059) of liver tissue spots in all patients, including three patients with HBsAg loss. These HBV integration sites were randomly distributed on chromosomes and can localise in host genes involved in hepatocarcinogenesis, such as ALB, CLU and APOB. Patients who were receiving or had received antiviral treatment had a significantly lower percentage of viral integration-containing spots and significantly fewer chimeric reads than treatment-na?ve patients. Intrahepatic cccDNA levels correlated well with viral integration events.
Conclusion: Transcriptionally active HBV integration occurred in chronically HBV-infected patients at different phases, including in patients with HBsAg loss. Antiviral treatment was associated with a decreased number and extent of transcriptionally active viral integrations, implying that early treatment intervention may further reduce the number of viral integration events.
COA
Publication 
Figure 1. LHBs contains preS1, preS2 and S domains
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