Retrospective analysis of hepatitis B virus chronic infection in 247 patients: clinical stages, response to treatment and poor prognostic factors

Abstract Hepatitis B virus (HBV) infection occurs worldwide and is an important cause of acute and chronic viral hepatitis in the US. In this review, I describe the virus, risk factors for infection, clinical features of infection, results of laboratory tests during infection, and standard and emerging treatment for chronic infection. Although 95% of adult patients recover completely from HBV infection, 90% of children ≤4 years of age develop chronic infection. Active vaccination is highly efficacious.

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Risk of Reactivation of Hepatitis B Virus Infection in Psoriasis Patients Treated With Biologics: A Retrospective Analysis of 20 Cases From the BIOBADADERM Database

Actas Dermo-Sifiliográficas (English Edition) ◽

10.1016/j.adengl.2015.05.013 ◽

2015 ◽

Vol 106 (6) ◽

pp. 477-482 ◽

Cited By ~ 2

Author(s):

J. Sanz-Bueno ◽

F. Vanaclocha ◽

I. García-Doval ◽

R. Torrado ◽

G. Carretero ◽

...

Keyword(s):

Hepatitis B Virus ◽

Virus Infection ◽

Hepatitis B ◽

Retrospective Analysis ◽

Hepatitis B Virus Infection ◽

B Virus

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Estimation of hepatitis B virus cccDNA persistence in chronic infection using within-host evolutionary rates

10.1101/2020.02.04.20020362 ◽

2020 ◽

Cited By ~ 3

Author(s):

Katrina A. Lythgoe ◽

Sheila F. Lumley ◽

Jane A. McKeating ◽

Philippa C. Matthews

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

Chronic Infection ◽

Standard Of Care ◽

Evolutionary Rates ◽

Mathematical Framework ◽

Novel Approach ◽

B Virus ◽

Order Of Magnitude ◽

Progressive Liver Disease

AbstractHepatitis B virus (HBV) infection is a major global health problem with over 240 million infected individuals at risk of developing progressive liver disease and hepatocellular carcinoma. HBV is an enveloped DNA virus that establishes its genome as an episomal, covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocytes. Currently available standard-of-care treatments for chronic hepatitis B (CHB) include nucleos(t)ide analogues (NA) that suppress HBV replication but do not target the cccDNA and hence rarely cure infection. There is considerable interest in determining the lifespan of cccDNA molecules to design and evaluate new curative treatments. We took a novel approach to this problem by developing a new mathematical framework to model changes in evolutionary rates during infection which, combined with previously determined within-host evolutionary rates of HBV, we used to determine the lifespan of cccDNA. We estimate that during HBe-antigen positive (HBeAgPOS) infection the cccDNA lifespan is 61 (36-236) days, whereas during the HBeAgNEG phase of infection it is only 26 (16-81) days. We found that cccDNA replicative capacity declined by an order of magnitude between HBeAgPOS and HBeAgNEG phases of infection. Our estimated lifespan of cccDNA is too short to explain the long durations of chronic infection observed in patients on NA treatment, suggesting that either a sub-population of long-lived hepatocytes harbouring cccDNA molecules persists during therapy, or that NA therapy does not suppress all viral replication. These results provide a greater understanding of the biology of the cccDNA reservoir and can aid the development of new curative therapeutic strategies for treating CHB.

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