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Apoptosis markers related to pathogenesis of pediatric chronic hepatitis C virus infection: M30 mirrors the severity of steatosis
Author(s) -
Valva Pamela,
De Matteo Elena,
Galoppo María C.,
Gismondi María I.,
Preciado María V.
Publication year - 2010
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.21699
Subject(s) - steatosis , pathogenesis , virology , hepatitis c virus , virus , apoptosis , medicine , chronic hepatitis , viral disease , immunology , biology , gastroenterology , genetics
Apoptosis involvement in liver damage related to hepatitis C virus (HCV) chronic infection has been suggested. Although liver biopsy represents the gold standard for evaluating disease severity, non‐invasive tests are a growing medical need. The aim of this study was to detect apoptosis markers in liver and serum from pediatric HCV‐infected patients and to assess its utility to predict liver damage progression. Twenty‐three patients were included. Liver biopsies were used for histological analysis as well as for immunodetection of a viral protein (NS3) and apoptosis markers (activated caspase‐3 [casp‐3a], caspase‐generated CK‐18 fragment [M30] and TUNEL). M30 was quantified in paired serum and biopsy samples. NS3 correlated both with casp‐3a (r = 0.83, P < 0.0001) and TUNEL (r = 0.61, P < 0.0017). Casp‐3a and TUNEL also displayed a correlation (r = 0.56, P = 0.005). Both NS3 and casp‐3a were associated with fibrosis stage ( P = 0.03). Serum M30 [median: 122.15 UL‐1 (86.68–794.58)] was higher in patients than in controls [median: 81.44 UL‐1 (41.17–129.30)], ( P < 0.0001). M30 showed a correlation with steatosis, and indeed it was linked to severe grade ( P = 0.004). In children, HCV would be involved in liver damage through apoptosis induction. The apoptosis markers detected reflect liver injury. Serum M30 might be useful as a marker to detect the extent of liver steatosis. J. Med. Virol. 82:949–957, 2010. © 2010 Wiley‐Liss, Inc.