Hepatitis E in post‐liver transplantation: is it time to routinely consider it?

Borg, Brian B.; Feng, Zongdi; Earl, Truman M.; Anderson, Christopher

doi:10.1111/ctr.12777

Cited by 3 publications

(1 citation statement)

References 22 publications

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“…HEV is mainly transmitted via the fecal-oral route through contaminated water or food. Hepatitis E is usually a self-limiting acute disease; however, chronic HEV infection has recently become a major clinical problem in immunocompromised patients, especially in organ transplant recipients (13) and in patients with HIV infection, leukemia, or lymphoma (14). The chronic HEV infections are almost exclusively caused by the zoonotic genotype 3 HEV strains (14).…”

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confidence: 99%

ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication

Sooryanarain

Rogers

Cao

et al. 2017

J Virol

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Hepatitis E virus (HEV), a single-stranded positive-sense RNA virus, generally causes self-limiting acute viral hepatitis, although chronic HEV infection has recently become a significant clinical problem in immunocompromised individuals, especially in solid-organ transplant recipients. Innate immunity, via the type I interferon (IFN) response, plays an important role during the initial stages of a viral infection. IFN-stimulated gene 15 (ISG15), an IFN-induced ubiquitin-like protein, is known to have an immunomodulatory role and can have a direct antiviral effect on a wide spectrum of virus families. In the present study, we investigated the antiviral effect as well as the potential immunomodulatory role of ISG15 during HEV replication. The results revealed that HEV induced high levels of ISG15 production both (Huh7-S10-3 liver cells) and (liver tissues from HEV-infected pigs); however, ISG15 is not required for virus replication. We also demonstrated that ISG15 silencing potentiates enhanced type I IFN-mediated signaling, resulting in an increase in the type I IFN-mediated antiviral effect during HEV replication. This observed enhanced type I IFN signaling correlated with an increase in IFN-stimulated gene expression levels during HEV replication. Furthermore, we showed that PKR and OAS1 played important roles in the ISG15-mediated type I IFN sensitivity of HEV. Taken together, the results from this study suggest that ISG15 plays an important immunomodulatory role and regulates HEV sensitivity to exogenous type I IFN. Hepatitis E virus (HEV) infection typically causes self-limiting acute viral hepatitis. However, chronic HEV infection has recently become a significant clinical problem in immunocompromised patients. Pegylated interferon (IFN) has been used to treat chronic HEV infection in solid-organ transplant patients with some success. However, the mechanism behind the type I IFN-mediated antiviral effect against HEV remains unclear. This report demonstrates that ISG15 induced by HEV replication in Huh7-S10-3 human liver cells plays an immunomodulatory role by negatively regulating type I IFN signaling and, thus, HEV sensitivity to type I IFN. Our results also show that PKR and OAS1 play important roles in the ISG15-mediated type I IFN sensitivity of HEV.

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confidence: 99%

ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication

Sooryanarain

Rogers

Cao

et al. 2017

J Virol

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Chronic Graft Injury

Hartleif¹,

Sturm²

2021

Pediatric Liver Transplantation

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Hepatitis E virus infection in liver transplant recipients: a descriptive literature review

Perisetti

Laoveeravat

Inamdar

et al. 2020

European Journal of Gastroenterology &Amp; Hepatology

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Hepatitis E virus infection has been recognized as a rising hepatotropic viral infection in the developing countries but overlooked in the developed countries, due to its lower prevalence. However, hepatitis E virus prevalence is on rise in the liver transplant recipients due to immunosuppression, which needs prompt recognition by healthcare practitioners. Hepatitis E virus infection is commonly believed to be transmitted via an animal host; but in the post-liver transplant patients, it can also be acquired via blood and blood products transfusion and autochthonous route. Previous studies have shown the significance of hepatitis E virus infection in post-liver transplant, as the patients at a high risk of progressing to chronic hepatitis and cirrhosis. Pediatric patients are at higher risk of hepatitis E virus infection post-liver transplant. Specific hepatitis E virus genotypes have the potential for greater severity. The clinical manifestation of hepatitis E virus can also present as extrahepatic features which need high level of suspicion for early recognition and treatment. Treatment options of hepatitis E virus range from immunosuppressive drug minimization, ribavirin therapy to novel direct-acting antiviral regimens. Herein, we aim to explore epidemiology, prevalence, risk factor, diagnosis, and management of hepatitis E virus infection giving special attention to liver transplant recipients.

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Hepatitis E in post‐liver transplantation: is it time to routinely consider it?

Cited by 3 publications

References 22 publications

ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication

ISG15 Modulates Type I Interferon Signaling and the Antiviral Response during Hepatitis E Virus Replication

Chronic Graft Injury

Hepatitis E virus infection in liver transplant recipients: a descriptive literature review

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