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 January 22, 2008 accepted February 25, 2008.The enterically transmitted human hepatitis E virus (HEV) has long been known as a major cause of acute hepatitis E in developing countries, with occasional travel-related cases in developed countries.1 However, following the discovery of a new lineage of HEV (genotype 3) in the mid 1990s, sporadic cases of acute hepatitis due to infection with this genotype have been increasingly recognized.2,3 Since their discovery, genotype 3 HEV strains have been detected in pig populations worldwide, with very high prevalence in commercially held pigs. 1,4 Studies looking at risk factors of endemic HEV cases in Europe have failed to show evidence for direct zoonotic transmission resulting from contact with pigs, although this has been documented elsewhere.5-9 HEV infection has been documented in other animal species, and transmission via contaminated water and food has been described. 1,6 In addition, persons with HEV infection go through a viremic Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; CMV, cytomegalovirus; CT, point at which the fluorescence cro...

No abstract

No abstract

No abstract

No consensus exists on the tectonic evolution of the western Mediterranean since~35 Ma. Three disparate tectonic evolution scenarios are identified, each portraying slab rollback as the driving mechanism but with rollback starting from strongly different subduction geometries. As a critical test for the validity of each tectonic scenario we employ thermomechanical modeling of the 3-D subduction evolution. From each tectonic scenario we configure an initial condition for numerical modeling that mimics the perceived subduction geometry at~35 Ma. We seek to optimize the fit between observed and predicted slab morphology by varying the nonlinear viscoplastic rheology for mantle, slab, and continental margins. From a wide range of experiments we conclude that a tectonic scenario that starts from NW dipping subduction confined to the Balearic margin at 35 Ma is successful in predicting present-day slab morphology. The other two scenarios (initial subduction from Gibraltar to the Baleares and initial subduction under the African margin) lead to mantle structure much different from what is tomographically imaged. The preferred model predicts slab rotation by more than 180°, east-west lithosphere tearing along the north African margin and a resulting steep east dipping slab under the Gibraltar Strait. The preferred subduction model also meets the first-order temporal constraints corresponding to Mid-Miocene (~16 Ma) thrusting of the Kabylides onto the African margin and nearly stalled subduction under the Rif-Gibraltar-Betic arc since the Tortonian (~8 Ma). Our modeling also provides constraints on the rheological properties of the mantle and slab, and of continental margins in the region.

Hepatitis E virus (HEV) infection is known to run a self-limited course. Recently, chronic hepatitis E has been described in several immunosuppressed patients after solid organ transplantation. The prevalence of HEV infection after transplantation, however, is unknown. We studied HEV parameters [HEV RNA, HEV immunoglobulin M (IgM), and HEV immunoglobulin G (IgG) by enzyme-linked immunosorbent assay and confirmatory immunoblotting] in a cohort of 285 adult liver transplant recipients. The most recent freeze-stored sera were investigated, and if they were positive, a retrospective analysis was performed. Samples from 274 patients (96.1%) tested negative for all HEV parameters. This included a patient described earlier as having experienced an episode of chronic HEV hepatitis in the past. One patient was found positive for HEV RNA without HEV antibodies. She presently suffers from chronic HEV hepatitis and has also been described before. Sera from 9 patients tested positive for HEV IgG without HEV IgM or HEV RNA. Six of these 9 patients (2.1% of the total) were found to have HEV IgG antibodies in retrospect related to an HEV infection at some time pre-transplant as they also tested positive in a pretransplant serum sample. One of these 9 patients suffered in retrospect from a chronic HEV infection with mild hepatitis between 2 and 5 years after liver transplantation on the basis of the course of HEV RNA, IgM, and IgG, aminotransferases, and liver histology. Overall, the prevalence of acquired HEV hepatitis after liver transplantation was 1% in this cohort. We conclude that liver transplant recipients have a risk for chronic HEV infection, but the prevalence is low.

No abstract

No abstract