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Hepatitis B infection of the liver in chronic hepatitis C without detectable hepatitis B virus DNA in serum
✍ Scribed by Luisa Fernanda Mariscal; Elena Rodríguez-Iñigo; Javier Bartolomé; Inmaculada Castillo; Nuria Ortiz-Movilla; Cristina Navacerrada; Margarita Pardo; Arturo Pérez-Mota; Javier Graus; Vicente Carreño
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 327 KB
- Volume
- 73
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Hepatitis B virus (HBV) DNA may persist in the liver in the absence of serum HBV–DNA after a self‐limited acute hepatitis B. This may also occur in patients with chronic hepatitis C virus (HCV) infection but its prevalence and its impact on liver histology is unknown. HBV–DNA was tested by polymerase chain reaction (PCR) and by in situ hybridisation in liver biopsies from 98 patients with chronic hepatitis C who were hepatitis B surface antigen negative and serum HBV–DNA negative by PCR. HBV–DNA resulted positive in the liver of 37/98 (37.7%) patients without serum HBV–DNA. To test whether these patients had serum HBV–DNA levels under the detection limit of the PCR assay used in this study (50 copies/ml), PCR products in which HBV–DNA was undetectable after visualization of agarose gels were analysed by dot‐blot hybridisation. With this method, HBV–DNA was positive in serum of 12/37 patients with liver HBV–DNA. Thus, 25/98 (25.5%) patients have HBV–DNA detectable only in liver. This was confirmed by in situ hybridisation, the percentage of infected hepatocytes ranging from 0.1% to 12%. In patients in whom the HCV infection was shorter than 20 years, HBV infected patients had higher (P = 0.01) fibrosis score (1.64 ± 1.21) than HBV negative cases (0.53 ± 0.66). In conclusion, a significant proportion of patients with chronic HCV infection have HBV–DNA in the liver in the absence of viral DNA in serum. The impact of this finding on liver histology deserves further research. J. Med. Virol. 73:177–186, 2004. © 2004 Wiley‐Liss, Inc.
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