Guest guest Posted April 4, 2008 Report Share Posted April 4, 2008 http://www3.interscience.wiley.com/cgi-bin/abstract/117947223/ABSTRACT?CRETRY=1 & SRETRY=0 Original Articles Chronic hepatitis E virus infection in liver transplant recipients B. Haagsma 1 *, Arie P. van den Berg 1, J. Porte 2, Cornelis A. Benne 3, Harry Vennema 4, Johan H. J. Reimerink 4, n P. G. Koopmans 4 1Department of Gastroenterology and Hepatology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands2Department of Hepatobiliary Surgery and Liver Transplantation, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands3Laboratory for Infectious Diseases, Groningen, The Netherlands4Laboratory for Infectious Diseases and Screening, National Institute of Public Health and the Environment, Bilthoven, The Netherlands email: B. Haagsma (e.b.haagsma@...) *Correspondence to B. Haagsma, Department of Gastroenterology and Hepatology, University Medical Center Groningen, Hanzeplein 1, P.O. Box 30.001, 9700 RB Groningen, The Netherlands Telephone: 0031-50-3616161; FAX: 0031-50-3613151 Abstract Hepatitis E virus (HEV) infection is known to run a self-limiting course. Sporadic cases of acute hepatitis due to infection with HEV genotype 3, present in pig populations, are increasingly recognized. Zoonotic transmission seems infrequent. The entity of unexplained chronic hepatitis after liver transplantation has been recognized. Detection of HEV in 2 liver transplant recipients triggered a review of these cases. Freeze-stored sera were available for retrospective analysis. HEV antibodies were determined. For virus detection and identification, a fragment of the gene encoding the major capsid protein (open reading frame 2) was amplified by reverse-transcription polymerase chain reaction and sequenced to identify the genotype. Two months after liver transplantation, case A developed unexplained chronic hepatitis, which developed into cirrhosis. Retransplantation followed 7 years later, after which chronic hepatitis recurred. In retrospect, HEV RNA was present in serum 3 weeks after the first transplantation and remained present afterwards. HEV RNA was also present in retransplant liver tissue. HEV antibodies appeared late after retransplantation. Case B developed unexplained chronic hepatitis 7 years after transplantation. Retransplantation was needed 5 years later, after which no signs of hepatitis recurred. In retrospect, the period of chronic hepatitis up to the retransplantation coincided with HEV RNA in serum. In case B, antibodies developed, the viral load was much lower than in case A, and the virus seemed to be cleared after retransplantation. Genotyping in both cases revealed 2 unique strains of genotype 3. In conclusion, chronic HEV infection may develop in immunosuppressed patients, who may then serve as long-term carriers of the virus. We hypothesize that HEV may be the cause of chronic hepatitis in liver transplant recipients. Liver Transpl 14:547-553, 2008. © 2008 AASLD. Received: 22 January 2008; Accepted: 25 February 2008 Digital Object Identifier (DOI)10.1002/lt.21480 Quote Link to comment Share on other sites More sharing options...
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