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The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Hepatitis B surface antigen, (HBsAg) is the common antigen on the surface of each form of the virus particles. HBsAg is found in great excess in infected subjects and therefore is used in diagnostic tests for the virus infection. The major structural core protein (C protein or hepatitis B core antigen) is a 21 kD basic phosphoprotein that contains viral DNA and a polymerase called P protein. The pre-S1-region of the viral genome encodes the L protein. This protein is a minor component of proteins produced, but is an important component of the infectious Dane particle and is important in virus assembly. L proteins are thought to contain receptor recognition domains. The S protein makes up the majority of the HBsAg and is produced in abundance.
Liver Diseases
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
In the development of viral hepatitis immunologic mechanisms appear to play a significant role. Among the hepatitis viruses (hepatitis A, hepatitis B, or other viruses), the immunologic features associated with hepatitis B virus infection have been studied extensively. Two phases have been distinguished in the course of chronic hepatitis B infection. In the early replicative phase, the hepatitis B virus DNA in episomal form reacts with the hepatocyte nuclei and infectious viral particles are formed. Simultaneously hepatitis B core antigen (HBcAg) is produced and becomes detectable in serum. This replicative phase is associated with chronic active hepatitis. In the later, nonreplicative phase, the hepatitis B virus DNA is in integrated form and anti-HBc and noninfectious hepatitis B surface (HBsAg) antigens are present in the serum. This nonreplicative phase of the virus is accompanied by inactive liver disease. Hepatitis B virus is not cytotoxic, but leads to immunologically mediated liver injury. Cytotoxic T cells are formed and their action is directed against the core antigen. The cytotoxic action of T cells is expressed on the hepatocyte membrane resulting in liver cell necrosis. Differences in the progress and severity of the chronic hepatitis may depend partly on the modulatory factors which include circulating antibodies to HBcAg, immune mediators, and lymphoid cells.
Rheumatology and immunology
Published in Michael McGhee, A Guide to Laboratory Investigations, 2019
The diagnosis of acute hepatitis is made by detecting HbsAg and IgM antibody to hepatitis B core antigen (anti-HbcAg) in a patient with other biochemical evidence of acute hepatitis.
Risk of hepatitis B virus reactivation following ruxolitinib treatment in patients with myeloproliferative neoplasms
Published in Hematology, 2021
Ming-hui Duan, Xin-Xin Cao, Long Chang, Dao-bin Zhou
Certain therapies for hematologic malignancies, including anti-CD20 monoclonal antibodies and ibrutinib, have been associated with an increased risk of HBV reactivation in patients previously infected with hepatitis B virus (HBV) [1–4]. In general, the risk of HBV reactivation is different in patients with chronic HBV (hepatitis B surface antigen, i.e. HBsAg positive) and resolved HBV (HBsAg negative and antibody to hepatitis B core antigen, i.e. HBcAb positive) [4]. Ruxolitinib, a potent Janus kinase (JAK) inhibitor, was the first targeted drug approved for treating myelofibrosis (MF) based on the results of two pivotal phase III controlled myelofibrosis study with oral JAK inhibitor treatment (COMFORT-I and COMFORT-II)[5,6] and hydroxyurea-resistant and refractory polycythemia vera (PV) based on the results of the randomized study on efficacy and safety in polycythemia Vera with JAK inhibitor INCB018424 versus best supportive care (RESPONSE study)[7,8]. Ruxolitinib impairs dendritic cell and T-cell functions, leading to reduced cytokine production that results in impaired control of silent infections and an increased risk of reactivation of viruses, such as herpes zoster and hepatitis B [9–14]. A few patients were reported to experience hepatitis B reactivation after ruxolitinib treatment [11,15,16]. Nevertheless, the actual incidence of HBV reactivation in patients with myeloproliferative neoplasms (MPN) and chronic or resolved HBV infection during and after ruxolitinib treatment remains unclear. Therefore, this retrospective analysis was performed to assess the incidence of HBV reactivation among such patients.
Light-chain amyloidosis with renal involvement: renal outcomes and validation of two renal staging systems in the Chinese population
Published in Amyloid, 2019
Zixuan Zhu, Cai Yue, Ying Sun, Xuemei Li, Mingxi Li
Methods used in the processing of renal biopsies included light microscopy, immunofluorescence, and electron microscopy. All patients had renal biopsy-confirmed diagnosis of AL amyloidosis by positive Congo red staining and electron microscopy [15] and further typing by immunofluorescence [15–17]. All tissue biopsy samples were fixed in formalin and embedded in paraffin wax. Light microscopy evaluation of the renal biopsies included staining with haematoxylin and eosin (H&E), periodic acid-sliver methenamine (PASM) and Congo red [18]. Electron microscopy and standard immunofluorescence staining for IgG, IgM, IgA, C3, C4, C1q, fibrinogen, albumin, hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), kappa chain (κ) and lambda chain (λ) were performed for all patients.
Safety of biologic agents for psoriasis in patients with viral hepatitis
Published in Journal of Dermatological Treatment, 2018
Nawaf AlMutairi, Hesham Alaadin Abouzaid
Viganò et al. (29) revised the mechanisms of action of TNF in hepatitis B and C, the endorsements for managing HBV and HCV-infected patients receiving anti-TNF drugs, their safety and anti-TNF hepatotoxicity. They recommended that in hepatitis B surface antigen (HBsAg) carriers experiencing anti-TNF therapy, either anti-HBV treatment or prophylaxis is compulsory to inhibit hepatitis reactivation. Whereas, HBsAg-negative antibody to hepatitis B core antigen (anti-HBc) seropositive patients require observant monitoring only. On the contrary, they indicated that in HCV-infected patients, TNF-α inhibition therapy is safe and could be even valuable, as TNF-α pathways are elaborated in sustaining liver inflammation and fibrosis progression in HCV. HBV or HCV-infected patients should be referred to a hepatologist for professional clinical management whenever antiviral therapy is compulsory or hepatitis reactivation ensues (29).