In patients with chronic hepatitis B and C virus (HBV, HCV) infection, an inverse relationship in the replicative activity of the two viruses has been reported. In the present study the genotype of HCV was evaluated in 34 consecutive cases found with hepatitis B surface antigen (HBsAg) and anti-HCV
Molecular characterization and functional analysis of occult hepatitis B virus infection in Chinese patients infected with genotype C
✍ Scribed by Yong Fang; Xu Teng; Wei-Zhen Xu; Di Li; Hong-Wei Zhao; Li-Juan Fu; Feng-Min Zhang; Hong-Xi Gu
- Publisher
- John Wiley and Sons
- Year
- 2009
- Tongue
- English
- Weight
- 155 KB
- Volume
- 81
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
Occult HBV infection is defined as the persistence of HBV DNA in individuals negative for HBV surface antigen (HBsAg), and many different mechanisms have been reported in different countries. However, in China, one of the endemic areas for HBV infection, no reports have been published on occult HBV infection. The present study investigated the virological features and the mechanism of occult HBV infection in China. Full‐length HBV DNA from eight patients with occult HBV infection (S1–S8) and three HBsAg‐positive cases (SWT1–SWT3) was cloned and sequenced. Additionally, four entire linear HBV genomes from occult cases were transfected transiently into HepG2 cells. The sequencing results showed two major mutations in patients with occult HBV infection as follows: deletions in the pre‐S1 (S3, S4, and S7) and X (S1, S2, and S5) regions. Such deletions covered the S promoter and the basal core promoter (BCP), and function analysis of these variants also showed a decrease in DNA replication and antigen expression. Two patients with occult infection (S6 and S8) had no mutations capable of interfering with viral replication and gene expression in the major viral population. Thus, the deletions in the S promoter and the BCP regions that disable the regulatory elements may be the reason for the absence of HBsAg, and multiple mechanisms may be responsible for occult HBV infection. J. Med. Virol. 81:826–835, 2009. © 2009 Wiley‐Liss, Inc.
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