apologize for giving the wrong Rojkind reference. For historical interest, we used the 1976 (3) publication, but by error, referred to the 1979 one ( 1). Dr. W. J. Lindblad makes an excellent point. The methods section was markedly abbreviated and the paper, as published, does give the misleading i
High levels of viral replication during acute hepatitis B infection predict progression to chronicity
✍ Scribed by Tse-Ling Fong; Adrian M. Di Bisceglie; Robin Biswas; Jeanne G. Waggoner; Leonard Wilson; Janet Claggett; Jay H. Hoofnagle
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 481 KB
- Volume
- 43
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
To assess the pattern of development of serologic markers during acute hepatitis B, levels of HBsAg, HBeAg, and hepatitis B virus (HBV) DNA were assayed in stored serum samples obtained sequentially from 12 subjects infected with HBV during experimental studies conducted in the 1950s. Six patients developed acute self‐limited hepatitis, three developed chronic hepatitis, and three had an asymptomatic infection without HBsAg. HBsAg was the first serologic marker detected (mean = 52 days after exposure), followed by HBeAg (62 days) and HBV DNA (72 days). Peak HBsAg levels occurred before onset of symptoms and correlated with peak titers of HBeAg and HBV DNA. Patients who developed chronic hepatitis had higher peak levels of viral markers than those with self‐limited disease: HBsAg (30 versus 5.4 μg/ml), HBeAg (1:2,000 versus 1:60 titer) and HBV DNA (3,192 versus 444 pg/ml). Thus, chronic HBV infection is characterized by high levels of viral replication appearing early during the acute phase of infection. © 1994 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
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