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Low HBV‐DNA levels in end‐stage renal disease patients with HBeAg‐negative chronic hepatitis B
Author(s) -
Moutinho Renata S.,
Perez Renata M.,
MedinaPestana José O.,
Figueiredo Mauro S.,
Koide Sandra,
Alberto Fernando Lopes,
Silva Antonio Eduardo B.,
Ferraz Maria Lucia G.
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20691
Subject(s) - hbeag , medicine , virology , coinfection , hepatitis b virus , hbsag , viral load , hepatitis b , hemodialysis , immunology , virus
Abstract In end‐stage renal disease patients treated by hemodialysis with HBeAg‐negative chronic hepatitis B virus (HBV) infection, the evaluation of the presence of viral replication is essential in the assessment for renal transplantation. Data on HBV viral load, prevalence of precore mutations, as well as the influence of HCV coinfection on HBV‐DNA levels in this group of patients is scarce. The aim of this study was to determine the HBV viral load in HBsAg‐positive/HBeAg‐negative hemodialysis patients; to compare HBV‐DNA levels between isolated HBV infection carriers and HBV‐HCV coinfected patients, and to evaluate the prevalence of precore mutations in these patients. Fifty hemodialysis patients with chronic HBeAg‐negative HBV infection were studied. Viral load was determined by PCR (Amplicor HBV Monitor‐Roche). The detection of precore mutations was made by sequencing. Of a total of 50 patients, 76% were male, with a mean age of 44 ± 11 years. Anti‐HCV was positive in 56% of patients. HBV‐DNA was undetectable in 58% of patients; 24% had HBV‐DNA <10,000 copies/ml, 12% between 10,000–100,000 copies/ml, and only 6% had HBV‐DNA >100,000 copies/ml. There was no difference in the viral load of patients infected only by HBV and HBV‐HCV co‐infected patients ( P = 0.96). Precore mutations were detected in only 8% of cases. In conclusion, hemodialysis patients with HBeAg‐negative HBV infection had a low viral load. Precore mutations were infrequent and the presence of anti‐HCV has not influenced the levels of HBV‐DNA. J. Med. Virol. 78:1284–1288, 2006. © 2006 Wiley‐Liss, Inc.