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The ABCs of viral hepatitis that define biomarker signatures of acute viral hepatitis

Duffy, Darragh; Mamdouh, Rasha; Laird, Melissa; Soneson, Charlotte LU ; Le Fouler, Lenaig; El-Daly, Mai; Casrouge, Armanda; Decalf, Jeremie; Abbas, Amal and Eldin, Noha Sharaf, et al. (2014) In Hepatology 59(4). p.1273-1282
Abstract
Viral hepatitis is the leading cause of liver disease worldwide and can be caused by several agents, including hepatitis A (HAV), B (HBV), and C (HCV) virus. We employed multiplexed protein immune assays to identify biomarker signatures of viral hepatitis in order to define unique and common responses for three different acute viral infections of the liver. We performed multianalyte profiling, measuring the concentrations of 182 serum proteins obtained from acute HAV- (18), HBV- (18), and HCV-infected (28) individuals, recruited as part of a hospital-based surveillance program in Cairo, Egypt. Virus-specific biomarker signatures were identified and validation was performed using a unique patient population. A core signature of 46 plasma... (More)
Viral hepatitis is the leading cause of liver disease worldwide and can be caused by several agents, including hepatitis A (HAV), B (HBV), and C (HCV) virus. We employed multiplexed protein immune assays to identify biomarker signatures of viral hepatitis in order to define unique and common responses for three different acute viral infections of the liver. We performed multianalyte profiling, measuring the concentrations of 182 serum proteins obtained from acute HAV- (18), HBV- (18), and HCV-infected (28) individuals, recruited as part of a hospital-based surveillance program in Cairo, Egypt. Virus-specific biomarker signatures were identified and validation was performed using a unique patient population. A core signature of 46 plasma proteins was commonly modulated in all three infections, as compared to healthy controls. Principle component analysis (PCA) revealed a host response based upon 34 proteins, which could distinguish HCV patients from HAV- and HBV-infected individuals or healthy controls. When HAV and HBV groups were compared directly, 34 differentially expressed serum proteins allowed the separation of these two patient groups. A validation study was performed on an additional 111 patients, confirming the relevance of our initial findings, and defining the 17 analytes that reproducibly segregated the patient populations. Conclusions: This combined discovery and biomarker validation approach revealed a previously unrecognized virus-specific induction of host proteins. The identification of hepatitis virus specific signatures provides a foundation for functional studies and the identification of potential correlates of viral clearance. (Hepatology 2014;59:1273-1282) (Less)
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published
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Hepatology
volume
59
issue
4
pages
1273 - 1282
publisher
John Wiley & Sons
external identifiers
  • wos:000333249800013
  • scopus:84896494711
ISSN
1527-3350
DOI
10.1002/hep.26901
language
English
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yes
id
5e098880-77c0-4105-adb9-b55a7a0fb3e5 (old id 4559374)
date added to LUP
2014-07-16 10:15:42
date last changed
2017-11-12 03:38:05
@article{5e098880-77c0-4105-adb9-b55a7a0fb3e5,
  abstract     = {Viral hepatitis is the leading cause of liver disease worldwide and can be caused by several agents, including hepatitis A (HAV), B (HBV), and C (HCV) virus. We employed multiplexed protein immune assays to identify biomarker signatures of viral hepatitis in order to define unique and common responses for three different acute viral infections of the liver. We performed multianalyte profiling, measuring the concentrations of 182 serum proteins obtained from acute HAV- (18), HBV- (18), and HCV-infected (28) individuals, recruited as part of a hospital-based surveillance program in Cairo, Egypt. Virus-specific biomarker signatures were identified and validation was performed using a unique patient population. A core signature of 46 plasma proteins was commonly modulated in all three infections, as compared to healthy controls. Principle component analysis (PCA) revealed a host response based upon 34 proteins, which could distinguish HCV patients from HAV- and HBV-infected individuals or healthy controls. When HAV and HBV groups were compared directly, 34 differentially expressed serum proteins allowed the separation of these two patient groups. A validation study was performed on an additional 111 patients, confirming the relevance of our initial findings, and defining the 17 analytes that reproducibly segregated the patient populations. Conclusions: This combined discovery and biomarker validation approach revealed a previously unrecognized virus-specific induction of host proteins. The identification of hepatitis virus specific signatures provides a foundation for functional studies and the identification of potential correlates of viral clearance. (Hepatology 2014;59:1273-1282)},
  author       = {Duffy, Darragh and Mamdouh, Rasha and Laird, Melissa and Soneson, Charlotte and Le Fouler, Lenaig and El-Daly, Mai and Casrouge, Armanda and Decalf, Jeremie and Abbas, Amal and Eldin, Noha Sharaf and Fontes, Magnus and Abdel-Hamid, Mohamed and Mohamed, Mostafa K. and Rafik, Mona and Fontanet, Arnaud and Albert, Matthew L.},
  issn         = {1527-3350},
  language     = {eng},
  number       = {4},
  pages        = {1273--1282},
  publisher    = {John Wiley & Sons},
  series       = {Hepatology},
  title        = {The ABCs of viral hepatitis that define biomarker signatures of acute viral hepatitis},
  url          = {http://dx.doi.org/10.1002/hep.26901},
  volume       = {59},
  year         = {2014},
}