Hbsag

Manufactured by Roche

Sourced in Israel, Switzerland

The HBsAg is a laboratory equipment product designed to detect the presence of the hepatitis B surface antigen (HBsAg) in clinical samples. It is a key diagnostic tool used to screen for and monitor hepatitis B virus (HBV) infections.

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Lab products found in correlation

Anti hbe, by Roche (2 mentions) Hbeag, by Roche (2 mentions) Anti hbs, by Roche (1 mentions) Anti hbc, by Roche (1 mentions) Ampliprep cobas taqman, by Roche (1 mentions) Elispot plate, by Merck Group (1 mentions) 3 3 5 5 tetramethylbenzidine (tmb), by Mabtech (1 mentions) Mt78 145, by Mabtech (1 mentions) Streptavidin hrp, by Mabtech (1 mentions) Interleukin 2 (il 2), by Mabtech (1 mentions) Brefeldin a, by Merck Group (1 mentions) Hbeag reagent kit, by Roche (1 mentions) Cobas taqman, by Roche (1 mentions) Cobas 8000, by Roche (1 mentions) Facsaria, by BD (1 mentions) Anti hcv, by DiaSorin (1 mentions)

7 protocols using hbsag

Hepatitis B Infection Profiling

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All subjects who were HBsAg-positive were then tested for Hepatitis e antigen (HBeAg) and anti-HBeAg, anti-HBcAg, and anti-Hepatitis D virus (HDV) antibodies; HBsAg and HBV-DNA were then quantified, and the HBV genotype was assessed. Serum HBV markers were analysed by commercial immunoenzymatic assays (HBsAg, HBeAg, anti-HBe, anti-HBs, and anti-HBc [total and IgM] from Roche Cobas Diagnostics, North Chicago, IL). Plasma HBV-DNA was quantified by real-time polymerase chain reaction (Roche Cobas^® Ampliprep/Cobas^® TaqMan). Most patients included in the study had a single point observation for HBV infection since they were in temporary migrant shelters and they moved to other locations after the first visit.
A liver biopsy was proposed to all patients who had a CHB E genotype infection to histologically evaluate liver damage and to define intrahepatic virological parameters. Nine patients gave written informed consent to undergo liver biopsy. For these 9 patients we had the opportunity to have a second follow-up and to further study HBV intrahepatic parameters and liver histology.

Malagnino V., Salpini R., Maffongelli G., Battisti A., Fabeni L., Piermatteo L., Colagrossi L., Fini V., Ricciardi A., Sarrecchia C., Perno C.F., Andreoni M., Svicher V, & Sarmati L. (2018). High rates of chronic HBV genotype E infection in a group of migrants in Italy from West Africa: Virological characteristics associated with poor immune clearance. PLoS ONE, 13(3), e0195045.

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Comprehensive Hepatitis B Virus Profiling

Cited 1 time

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Demographic (sex, age, self-reported race, continent of birth, presumed mode of HBV transmission, estimated duration of infection), clinical (body mass index, liver enzymes, platelets, aspartate aminotransferase [AST] to platelet ratio index [APRI], history of cirrhosis, HBV therapy) and virologic (HBsAg, HBeAg, and HBV DNA levels, HBV genotype, presence of precure [PC]/basal core promoter [BCP] mutations) characteristics were recorded. Age was categorized as 18 to 29, 30 to <40, and ≥40 years and APRI as <0.5, 0.5 to 1.5, and >1.5.⁹Quantitative HBeAg and HBsAg (Roche Elecsys) assays were performed at the HBRN central virology laboratory at the University of Washington, with lower limits of detection of 0.3 IU/mL for HBeAg and 0.05 IU/mL for HBsAg. HBV DNA testing was performed centrally by real-time polymerase chain reaction (COBAS Ampliprep/COBAS TaqMan Test, v.2.0; Roche Molecular Diagnostics, Branchburg, NJ) with a lower limit of quantification of 20 IU/mL and a lower limit of detection of 10 IU/mL.
HBV genotyping and PC and BCP determination were performed at the Molecular Epidemiology and Bioinformatics Laboratory in the Division of Viral Hepatitis at the Centers for Disease Control and Prevention using mass spectrometry as previously described.^{10 (link),11 (link)}

Feld J.J., King W.C., Ghany M.G., Chang K.M., Terrault N., Perrillo R.P., Khalili M., Hinerman A.S., Janssen H.L, & Lok A.S. (2022). Characteristics of Older Patients With Immunotolerant Chronic Hepatitis B Virus Infection. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 21(6), 1503-1512.e4.

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HBsAg-specific B cell ELISpot

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PBMC were stimulated with 1 µg/mL R848 and 10 ng/mL IL2 (MabTech) at 2x10⁶ cells/mL for 5d at 37°C. ELISpot plates (Merck) were activated and coated ON at 4°C with 2 µg/mL HBsAg (Roche Diagnostics), washed 1x with PBS, and blocked with RPMI for 2h at RT. Stimulated PBMC were added to ELISpot plates at 1-2x10⁵/well in RPMI and incubated for 18h at 37°C. B cells were subsequently removed, and plates were washed 5x with PBS. 1 µg/ml detection antibody MT78/145 (MabTech) was added in PBS+0.5%BSA for 2h at RT. After washing, Streptavidin-HRP (MabTech) in PBS+0.5%BSA was added for 1h at RT, followed by TMB (MabTech). Spot development was stopped by rinsing with H₂O, and spot numbers were quantified with ImmunoSpot Reader (CTL Europe).

Schreiber S., Dressler L.S., Loffredo-Verde E., Asen T., Färber S., Wang W., Groll T., Chakraborty A., Kolbe F., Kreer C., Kosinska A.D., Simon S., Urban S., Klein F., Riddell S.R, & Protzer U. (2024). CARs derived from broadly neutralizing, human monoclonal antibodies identified by single B cell sorting target hepatitis B virus-positive cells. Frontiers in Immunology, 15, 1340619.

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Cytokine Expression Assay in Activated T-cells

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Flat-bottom 96-well non-tissue-plates were coated with HBsAg (2.5 μg/mL in PBS; Roche Diagnostics) or anti-CD3 and anti-CD28 antibodies (10 μg/mL in PBS) for two hours at 37°C and blocked for 30 minutes at 37°C with 2% BSA in PBS. After incubation, transduced T cells, freshly isolated splenocytes or LALs were added in appropriate number (2x10⁵ cells/well) to the plate. Cells were incubated for the indicated time at 37°C. For the analysis of intracellular cytokine expression by ICS, Brefeldin A (1 μg/mL; Sigma-Aldrich) was added to cells two hours after start of stimulation and cells were incubated for additional 14 hours at 37°C.

Klopp A., Schreiber S., Kosinska A.D., Pulé M., Protzer U, & Wisskirchen K. (2021). Depletion of T cells via Inducible Caspase 9 Increases Safety of Adoptive T-Cell Therapy Against Chronic Hepatitis B. Frontiers in Immunology, 12, 734246.

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Quantifying Hepatitis B Virus Response

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Serum HBV DNA was quantified by real-time polymerase chain reaction kit Roche COBAS TaqMan (Roche Molecular Systems, Inc., Branchburg, NJ) with detection limit threshold of 20 IU/mL. HBsAg and HBeAg were quantified using the HBsAg and HBeAg reagent kit (Roche Molecular Systems, Inc., Branchburg, NJ), respectively. Serum biochemical assessments [including alanine aminotransferase (ALT), aspartate aminotransferase (AST)] and serum Cr were measured by biochemistry auto analyzer (Roche Cobas 8000; Roche Diagnostics GmbH, Mannheim, Germany) in the Department of Laboratory Medicine, the First Affiliated Hospital of Anhui Medical University. VR is defined as an HBV DNA concentration of less than 300 IU/mL after 48 weeks of treatment and biochemical response (BR) is defined as normalization of ALT levels after 48 weeks of treatment.

Su Q., Liu Y, & Li J. (2018). Combined effect of pegylated interferon α with adefovir on renal function in Chinese patients with chronic hepatitis B. Medicine, 97(34), e12089.

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Plasma Cell Differentiation from Memory B Cells

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PBMCs were stained as above and sorted into atMBC and cMBC populations using a FACSAria (BD Biosciences). Stringent criteria were applied to identify lymphocytes, based on forward scatter (FSC) versus side scatter (SSC), and to remove doublet contamination. CD10⁺ immature B cells were excluded. Between 5 × 10⁴ and 2 × 10⁵ atMBC were purified using this method; in all cases, a matched number of cMBC were sorted and stimulated as below.
Cells were first activated for 4 days in a 96-well plate using CpG-B (50 ng/ml; TLR9 agonist; ODN-2009; Invivogen) and HBsAg (Roche; ayw, 10 μg/ml) in combination with IL-2 (50 U/ml), IL-10 (50 ng/ml), IL-15 (10 ng/ml), and IL-21 (100 ng/ml), diluted in DMEM (plus 10% FBS, 1% penicillin/streptomycin, and 10% nonessential amino acids). Cells were then switched into DMEM containing IL-2, IL-10, IL-15 (concentrations as above), IL-6 (50 ng/ml), and INF-α (500 U/ml) for a further 3 days to promote their differentiation into Ab-secreting cells. After culture, cells were stained for plasma cell differentiation using BUV805-CD45, BV786-CD19, PE-Cy7-IgD, BUV395-CD27, PE-dazzle-CD38, AF700-CD20, BV711-CD3, and APC-CD138 and analyzed on a Fortessa X20.

Burton A.R., Pallett L.J., McCoy L.E., Suveizdyte K., Amin O.E., Swadling L., Alberts E., Davidson B.R., Kennedy P.T., Gill U.S., Mauri C., Blair P.A., Pelletier N, & Maini M.K. (2018). Circulating and intrahepatic antiviral B cells are defective in hepatitis B. The Journal of Clinical Investigation, 128(10), 4588-4603.

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Serum Biomarkers for Liver Disease and Viral Hepatitis

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Serum levels of biochemical markers of liver function as alanine-aminotransferase (ALT), aspartate-aminotransferase (AST), gama-glutamyltransferase (GGT), direct and indirect bilirubin and alkaline phosphatase (AP) were determined using a photometric technique (ICMA) (Liason, Diasorin, Varceli, Italy).
Serum samples were used for detection of HBV, hepatitis C virus (HCV) and human immunodeficiency virus (HIV) serological markers with commercial tests. The detection of HBsAg (Biokit, Buenos Aires, Argentina), anti-HBc (Biokit, Buenos Aires, Argentina), anti-HBc IgM (Symbiosis Diagnóstica, Leme, Brazil), anti-HBs (Biokit, Buenos Aires, Argentina), anti-HIV (RPC Diagnostic Systems, Yablonevaya, Russia) and anti-HCV (Diasorin, São Paulo, Brazil) were performed using immunoenzymatic commercial methods, according to the instructions of each manufacturer. HBeAg (Roche Diagnostics, Rotkreuz ZG, Switzerland) and anti-HBe (Roche Diagnostics, Rotkreuz ZG, Switzerland) were performed in HBsAg positive samples.

Bezerra C.S., Portilho M.M., Barbosa J.R., de Azevedo C.P., Mendonça A.C., da Cruz J.N., Frota C.C., do Lago B.V, & Villar L.M. (2022). Dried blood spot sampling for hepatitis B virus quantification, sequencing and mutation detection. Scientific Reports, 12, 1651.

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