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Viral hepatitis.
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
Eleanor Barnes, George Webster, Geoffrey M Dusheiko
Antepartum haemorrhage and ingestion or inoculation of maternal blood causes perinatal transmission of HBV. The neonatal route of transmission is particularly important in areas of high prevalence such as China. The risk of perinatal infection is highest for children born to HBeAg-positive mothers with high concentrations of virus in blood.
Prevention, Screening, and Treatment of Sexually Transmitted Infections
Published in James M. Rippe, Lifestyle Medicine, 2019
Diagnosis is made by serologic testing. Hepatitis B surface antigen (HBsAg) is the marker for current infection, either acute or chronic. Antibody status to Hepatitis B core (HBc) can differentiate acute from chronic disease. IgM anti-HBc indicates an acute infection and IgG anti-HBc indicates chronic infection. Hepatitis B e antigen (HBeAg) is a marker of high infectivity seen with peak viral loads. Patients with anti-HBs, anti-HBe, and/or anti-HBc without a positive HBsAg have cleared the disease and are immune by prior infection. One would expect a vaccinated patient to have an isolated anti-HBs antibody.32
Infectious diseases (and tropical medicine and sexually transmitted diseases)
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
It is important to remember a few key ‘background’ facts: Surface antigen (HBsAg) is the first marker to appear and causes the production of anti-HBs antibody.HBsAg normally implies acute disease (present for 1–6 months).If HBsAg is present for >6 months then this implies chronic disease (i.e. infective).Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease.Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months.HbeAg results from breakdown of core antigen from infected liver cells and is therefore a marker of infectivity.
Developments in pharmacotherapeutic agents for hepatitis B – how close are we to a functional cure?
Published in Expert Opinion on Pharmacotherapy, 2023
Naoshin Khan, Mohamed Ramzi Almajed, Mary Grace Fitzmaurice, Syed-Mohammed Jafri
Entecavir (ETV) is another agent used to treat chronic hepatitis B with similar efficacy to tenofovir [23]. ETV is a cyclopentyl guanosine analog, and like other analogs, ETV is phosphorylated to its active triphosphate form. It has potent selective inhibition of the three main functions of the HBV polymerase: priming, DNA-dependent synthesis, and reverse transcription. ETV is typically administered at 0.5 mg daily and has shown efficacy in both HBeAg positive and negative patients. In HBeAg-positive patients, a significant reduction in HBV DNA was seen. HBeAg seroconversion was also seen in 20% of patients that have not been previously treated with other analogs; this was demonstrated after three years of continuous ETV therapy [29]. In HBeAg-negative patients, patients achieved undetectable HBV DNA by PCR, ALT normalization, and a decrease in inflammation, especially when compared to older agents such as lamivudine [30]. Special considerations need to be made for patients previously treated with lamivudine due to lower efficacy and increased risk of developing ETV resistance. ETV should be avoided in patients with prior lamivudine monotherapy. Prior studies have shown approximately 50% of patients developed ETV resistance after 5 years of treatment in lamivudine-treated patients. In the setting of patients previously treated with other analogs or with decompensated liver disease, ETV can be used, but the dose is increased to 1 mg daily.
Pharmacotherapy options for managing hepatitis B in children
Published in Expert Opinion on Pharmacotherapy, 2021
Haruki Komatsu, Ayano Inui, Sachiyo Yoshio, Tomoo Fujisawa
PEG-IFN was approved for children with chronic HBV infection in 2017, and thus the number of studies of PEG-IFN therapy for children with chronic HBV infection is not large (Table 4) [80–83]. These pediatric studies obtained conflicting results. In the randomized controlled pediatric trial, HBeAg-positive children with chronic HBV infection were treated with PEG-IFN alfa 2a, and the rates of HBeAg loss and HBsAg loss were 25.7% and 8.9% at 24 weeks after the cessation of treatment, respectively [80]. Contrary to expectations, the study showed that the rate of HBeAg loss was slightly lower in children than in adults. The authors suggested that children infected with difficult-to-treat HBV genotype D, which accounted for 31% of the treated patients, could have lowered the rate of HBeAg loss in that study. Lower baseline HBeAg levels and HBV DNA levels were predictors of HBeAg seroconversion. Although children individually infected with HBV genotype A, B, C, or D were included in the study, genotype A was not a significant predictor of HBeAg seroconversion [80].
CDR-H3 loop ensemble in solution – conformational selection upon antibody binding
Published in mAbs, 2019
Monica L. Fernández-Quintero, Johannes Kraml, Guy Georges, Klaus R. Liedl
The first antibody selected is an anti-hepatitis B antibody, which binds the e6-antigen (HBeAg). HBeAg is a clinical marker for disease severity, and is a variant of the core c-antigen. HBeAg is not required for virion production, but it is involved in developing immune tolerance and chronic infection.24 For the anti-hepatitis B antibody-binding fragment (Fab) e6, two different X-ray structures are available in the Protein Data Bank (PDB),25 crystallized in complex with the antigen (3V6Z) and without the antigen (3V6F). Comparison of the two crystal structures reveals binding-related differences in the CDR-H3 and CDR-L3 loop conformations. The structures crystallized without antigen present, sometimes also called “apo structures”, will be referred to as “AGless”. Within the AGless antibody crystal structure 3V6F, we find two substantially differing conformations of the CDR-H3 loop in the asymmetric unit. These two CDR-H3 loop states will be referred to as AGless 1 and AGless 2, respectively. The anti-hepatitis B antibody Fab e6 is the only system in our study that has a CDR-L3 loop that cannot be assigned to a canonical structure model. As shown in SI Figure S1 the CDR-L3 loop adopts the same conformation for AGless 1 and AGless 2 but a different conformation in the complex structure, while the CDR-H3 loop exists in three different conformations.