5 years ago

Genotype 4 hepatitis E virus is a cause of chronic hepatitis in renal transplant recipients in Hong Kong

Sydney C.W. Tang, Chuan Huang, Desmond Y.H. Yap, Kwok-Yung Yuen, Patrick C. Y. Woo, Jasper F.W. Chan, Siddharth Sridhar, Susanna K. P. Lau, Jade L.L. Teng, Ivan F.N. Hung, Cyril C.Y. Yip
There are two genotypes of swine hepatitis E causing foodborne zoonotic infections in humans – genotype 3 (HEV-3), which is prevalent in Europe and Japan, and genotype 4 (HEV-4) prevalent in China. HEV-3 has been established as a cause of chronic hepatitis in immunocompromised patients. However, the outcomes of HEV-4 infection, the most common cause of viral hepatitis in China, in immunocompromised patients is unknown. The aim of this study is to establish whether HEV-4 infection progresses to chronic hepatitis in immunocompromised transplant recipients. This was an observational study conducted in Hong Kong, China. We identified renal transplant recipients diagnosed with acute hepatitis E and followed up patients who progressed to chronic infection identifying dietary risk factors, immunosuppressant used, clinical features and ultrasonographic findings. Genotyping of all HEV isolates was performed. Ribavirin treatment response was recorded for all patients. Four renal transplant recipients with acute hepatitis E were identified at a prevalence of 0.9%. Of the four patients, three progressed to develop chronic hepatitis due to HEV-4. Ribavirin treatment was initiated in all three cases. Infection was ribavirin refractory in one case with a K1383N mutation identified in the RdRp gene. The other two cases showed good treatment response. This study establishes for the first time that HEV-4 can cause chronic hepatitis in solid organ transplant recipients. This is a highly significant finding given the high population of immunocompromised patients in HEV-4 enzootic regions. Such infection can be refractory to ribavirin, the only available antiviral for chronic hepatitis E. This article is protected by copyright. All rights reserved.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1111/jvh.12799

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