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Published on: June 26, 2020
Clinical implications of chronic hepatitis E virus infection in heart transplant recipients
Ludi Koning1, Suzan D Pas, Robert A de Man
1Department of Gastroenterology and Hepatology, Erasmus Medical Center, Rotterdam, The Netherlands.
Insights
Chronic hepatitis E virus (HEV) infection in heart transplant recipients can cause rapid liver fibrosis. Early HEV RNA screening and reduced immunosuppression are recommended for solid-organ transplant patients with elevated liver enzymes.
Area of Science:
- Hepatology
- Transplant Medicine
- Virology
Background:
- Hepatitis E virus (HEV) infection can lead to chronic disease in solid-organ transplant (SOT) recipients.
- Clinical consequences of chronic HEV in SOT recipients are not well-established.
Purpose of the Study:
- To investigate the clinical, biochemical, and virologic presentation of chronic HEV infection in heart transplant (HTx) recipients.
- To understand the outcomes and management strategies for chronic HEV in this patient population.
Main Methods:
- In-depth study of 6 chronic HEV-infected heart transplant recipients.
- Analysis of clinical data, liver enzymes, viral load, and histology.
- Evaluation of treatment responses to immunosuppression modification and ribavirin therapy.
Main Results:
- Chronic HEV genotype 3 identified in 6 HTx patients (2.3%) on tacrolimus-based immunosuppression.
- All patients had elevated liver enzymes; 33% had positive IgM antibodies.
- 67% showed advanced fibrosis within 2 years; one patient cleared infection spontaneously, one after immunosuppression dose reduction, and three with ribavirin.
Conclusions:
- Chronic HEV infection in HTx recipients can cause rapid liver fibrosis.
- Recommend HEV RNA screening for SOT recipients with elevated liver enzymes due to delayed antibody response.
- Suggest initial immunosuppression dose reduction, followed by ribavirin therapy for persistent HEV infection.
Background:
Recent reports have shown that hepatitis E virus (HEV) infection can become chronic in solid-organ transplant recipients, but few studies have systematically investigated the clinical consequences of this chronic HEV infection in solid-organ transplant (SOT) recipients.
Methods:
We have undertaken an in-depth study of 6 chronic HEV-infected heart transplant recipients to gain further insight into the clinical, biochemical and virologic presentation of this disorder.
Results:
In 6 patients (2.3%) chronic HEV infection, genotype 3, was identified. Immunosuppression in these patients was tacrolimus-based, combined with either everolimus or prednisolone and/or mycophenolate mofetil. Median follow-up after case detection was 26 months (range 21 to 40 months). All chronic HEV cases had elevated liver enzyme values. IgM antibodies at presentation were positive in 2 of 6 (33%) patients. Liver histology in 4 of 6 (67%) patients showed advanced fibrosis within 2 years after infection. One patient spontaneously cleared the HEV infection: 1 after dose reduction of immunosuppressive therapy and 3 during ribavirin therapy. One patient has yet to clear the virus and remains on ribavirin therapy.
Conclusions:
Chronic HEV infection in heart transplant (HTx) recipients may lead to rapid fibrosis of the liver. We advise additional HEV RNA screening in solid-organ transplant recipients with elevated liver enzymes, because antibody production is often delayed, as demonstrated in these patients. Dose reduction of immunosuppressive therapy should be the first intervention strategy to achieve viral clearance in chronic HEV-infected immunocompromised patients. Ribavirin treatment should be considered in cases of chronic HEV.
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