RecombinantHepatitis B Surface Antigen (adw Mutant G-145-R)
Nature
Recombinant
Tag/Conjugate
Unconjugated
Molecular Weight
25 kDa (monomer)
Purity
Greater than 85% as determined by SDS-PAGE
Format
Liquid
Buffer
50 mM Tris-HCl, pH8.0, 200 mM NaCl
Preservative
None
Storage
Short term storage 4°C, long term storage -20°C. Prepare aliquots and store at -20°C. Avoid freeze/thaw cycles.
Ship
Dry ice
Introduction
Hepatitis B Virus (HBV) infection inducesa disease state characterised by liver damage, inflammation and viralpersistence. Infection also increases the risk of hepatocellular carcinoma.HBV belongs to the Hepadnaviridae family of viruses. Its genome consists ofpartially double stranded circular DNA. The DNA is enclosed in anucleocapsid, or core antigen (HBcAg), which is surrounded by a sphericalenvelope (surface antigen or HBsAg). The core antigen shares its sequenceswith the e antigen (HBeAg) but no cross reactivity between the two proteinshas been observed. The HBV genome also encodes a DNA polymerase that alsoacts as a reverse transcriptase.
Citations
Publication ()
Have you cited DAG3933 in a publication? Let us know and earn a reward for your research.
Background
Chronic hepatitis B virus (HBV) infection can lead to cirrhosis, hepatocellular carcinoma (HCC) and liver-related death. The current treatment can inhibit virus replication and slow down the progress of the disease, but it cannot be completely cured. Hepatitis B surface antigen (HBsAg) is generally used as a biomarker for judging the treatment of HBV, and its seroclearance and HBsAg conversion are the most important outcomes in chronic hepatitis B trials, predicting the prognostic outcome of patients. Three types of HBsAg make up the viral envelope wrapped around the nucleocapsid and they are L- (large), M- (medium) and S- (small) types of HBsAg.
The HBsAg protein is encoded by the PreS1 and PreS2/S mRNA viral transcripts, which are derived from one of the four overlapping open reading frames (ORFs) in the HBV genome. The presence of a second weak start codon on PreS2/S mRNA leads to S-HBsAg translation. PreS1 and PreS2/S mRNA generate L-HBsAg protein and M-HBsAg protein. The L-HBsAg PreS1 domain interacts with receptors on HBV and plays a crucial role in the attachment of HBV to hepatocytes, leading to hepatocyte infection. The three HBsAg proteins share an S domain with four putative transmembrane domains at the C-terminal. S-HBsAg contains only the S domain and is the smallest HBsAg. The N-terminal of the M-HBsAg protein contains an additional PreS2 domain, and the N-terminal of the L-HBsAg protein has PreS2 and PreS1 domains.
Figure 1. Schematic model of Dane particle and HBsAg proteins (Source: Tout I, et al. 2020)
Circulating HBsAg levels may reflect cccDNA transcription and serve as an assessment of treatment efficacy. Current clinical diagnostics primarily detect epitopes in the HBsAg "a" determining region, a highly conformationally hydrophilic structural domain ranging from positions 124 to 147. Natural HBsAg seroclearance rarely occurs, and accumulation of large amounts of HBsAg in the endoplasmic reticulum after HBV infection activates the unfolded protein response, leading to the formation of hairy glass hepatocytes and sensitizing hepatocytes to apoptosis. Overexpression of L-HBsAg inhibited subviral particles (SVP) morphogenesis and SVP filament accumulation, and suppressed HBsAg secretion. Overexpression of S-HBsAg did not result in any detectable changes in HBsAg secretion or hepatotoxicity. Chronic elevation of HBsAg in vivo is associated with episodes of HCC. Chronic elevation of HBsAg in vivo is associated with the onset of HCC, which may result from chronic endoplasmic reticulum stress-mediated cellular injury or interferon-mediated liver inflammation.
Alternative Names
HBsAg
References
1. Tout I, et al. Hepatitis B surface antigen seroclearance: Immune mechanisms, clinical impact, importance for drug development. J Hepatol. 2020 Aug;73(2):409-422.
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.
My Review for Recombinant HBV Surface Antigen (subtype adw, mutation G-145-R)
Creative Diagnostics products are for RESEARCH USE ONLY, please make sure your review is research based.
Required fields are marked with *
Terms and conditions:
We will select high-quality review customers and offer a $30 coupon for your next purchase.
All product reviews must be submitted in the English language.
Creative Diagnostics will not share any personal information of applicants, and all information will be treated with strict confidentiality and will not be sold or disclosed to a third party.
References
Therapeutic efficacy of hepatitis B virus vaccine in treatment of chronic HBV infections: A systematic review and meta-analysis
REVIEWS IN MEDICAL VIROLOGY
Authors: Ghozy, Sherief; Nam, Nguyen Hai; Radwan, Ibrahim; Karimzadeh, Sedighe; Tieu, Thuan Minh; Hashan, Mohammad Rashidul; Abbas, Alzhraa Salah; Eid, Peter Samuel; Vuong, Nguyen Lam; Khang, Nguyen Vinh; Elgabalawy, Eman; Sayed, Ahmed Kamal; Hoa, Pham Thi Le; Huy, Nguyen Tien
There is a need for improved treatment of patients with chronic hepatitis B (CHB). We reviewed the literature to explore the efficacy of HB vaccines alone or in combination therapy (CT) with antiviral drugs in CHB patients and to meta-analyze data from randomized controlled trials. We conducted a systematic search in ten databases. All studies investigating the efficacy of HBV vaccine in HBV infected patients were included with no restrictions. Among 1359 studies initially identified, 23 studies (n = 1956 patients) were included for the final analysis. CT showed a significant reduction of HBV DNA compared with analogue monotherapy (AM) at the 12-month follow-up period (odds ratio (OR) = 2.835, 95% confidence interval (CI) [1.275, 6.306], p = .011). Additionally, CT also remarkably induce HbsAg loss in comparison with AM (OR = 11.736, 95% CI [1.841, 74.794], p = .009). Our pooled data revealed no difference between treatment and control regarding alanine aminotransferase normalization, HBeAg seroconversion, and HBeAg disappearance. In addition, CT using vaccine and NAs resulted in a statistically significant higher incidence of adverse effects than AM. The therapeutic effects of combination therapy for patients with CHB were encouraging, but future studies need to investigate all possible treatment combinations and assess their cost-effectiveness.
Meta-analysis: Association between hepatitis B virus preS mutation and hepatocellular carcinoma risk
Previous observational studies suggested that hepatitis B virus (HBV) preS mutation plays an important role in the existence of HBV-related hepatocellular carcinoma (HCC). However, the results are still debatable. With an increasing number of studies about this topic, this study employed a meta-analysis to identify the association between HBV preS mutation and HCC risk. We searched for eligible studies from PubMed, ProQuest, CINAHL, ScienceDirect and Springer databases to assess the association between HBV mutation and HCC risk. This meta-analysis was conducted using RevMan 5.3 to provide pooled estimate for odds ratio (ORs) with 95% confidence intervals (95% CIs). Twenty-one clinical studies were included in this meta-analysis study which consisted of 1738 participants with HBV-related HCC and 3740 HBsAg-positive patients without HCC. All studies used samples of Asian population. PreS deletion was the most common mutation found in all studies. We found that ORs of HBV overall preS deletion was associated with HCC (OR = 3.28; 95% CI = 2.32-4.65;P < .00001; random-effects model). Each preS1 and preS2 deletion was associated with increased risk of HCC, with OR 2.42 (95% CI = 1.25-4.68,P = .008) and 3.36 (95% CI = 2.04-5.55,P < .00001), respectively. PreS2 start codon mutation was also significantly associated with HCC risk (OR = 2.47; 95% CI: 1.15-5.27;P = .02; random-effect model). The result of this meta-analysis suggested that HBV preS deletion (all, preS1 and preS2) and preS2 start codon mutation might contribute to the increased risk of HBV-related HCC.
COA
Publication 
Figure 1. Schematic model of Dane particle and HBsAg proteins
Loading ......
