## Abstract Since hepatitis C virus (HCV) and hepatitis delta virus (HDV) are transmitted by the same routes as hepatitis B virus (HBV), simultaneous or concurrent HCV and HDV infection in patients with chronic HBV infection may occur. To test this hypothesis and to examine the clinicohistological
Distribution of hepatitis B virus in the liver of chronic hepatitis C patients with occult hepatitis B virus infection
✍ Scribed by Elena Rodríguez-Iñigo; Luisa Mariscal; Javier Bartolomé; Inmaculada Castillo; Cristina Navacerrada; Nuria Ortiz-Movilla; Margarita Pardo; Vicente Carreño
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 487 KB
- Volume
- 70
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
Abstract
Although occult hepatitis B virus (HBV) infection (HBV‐DNA in serum in the absence of hepatitis B surface antigen [HBsAg]) is common in chronic hepatitis C, its characteristics are not well known. In this work, the presence of HBV‐DNA (by polymerase chain reaction; PCR) and its distribution (by in situ hybridization) in liver biopsies and peripheral blood mononuclear cells (PBMCs) from 32 patients with chronic hepatitis C and occult HBV infection and in 20 HBsAg chronic carriers were determined. The results showed that serum HBV‐DNA levels were statistically lower (P = 0.001) in patients with occult HBV infection than in HBsAg chronic carriers. The HBV infection pattern in liver cells was identical between patients with occult HBV infection and those with chronic hepatitis B. However, the mean percentage of HBV‐infected hepatocytes was significantly lower (P = 0.001) in patients with occult HBV infection (5 ± 4.44%) than in HBsAg chronic carriers (17.99 ± 11.58%). All patients with chronic hepatitis B have HBV‐DNA in their PBMCs while this occurred in 50% of the cases with occult HBV infection. In conclusion, patients with occult HBV infection have a low number of HBV‐infected hepatocytes and this fact could explain the lack of HBsAg detection and low viremia levels found in these cases. J. Med. Virol. 70:571–580, 2003. © 2003 Wiley‐Liss, Inc.
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