Hepatitis E Virus (HEV) is a single-strand positive-sense RNA virus in the family Hepeviridae. Most members of this family belong to the subfamily Orthohepevirinae and circulate in several animals. Orthohepevirinae comprises four genera including Paslahepvirus which is the most relevant to human health (Purdy et al., 2022). Of the eight genotypes currently recognized in this genera, four cause the majority of human hepatitis E infections. HEV genotypes 1 and 2 circulate in humans and spread by fecal-oral transmission. HEV genotypes 3 and 4 circulate in many animals, such as pigs, wild boars, deer, and rabbits. Their transmission to human is zoonotic by the consumption of undercooked infected meat or by close contact with this animal reservoir. Additionally, transmission by blood transfusion has been described for all genotypes (Kamar et al., 2017).

Hepatitis E is usually a self-limiting infection. Therefore, specific treatment is not necessary in the vast majority of patients. However, it could also lead to severe illness, particularly in pregnant women in developing countries infected with HEV genotype 1 or 2 and in individuals with an underlying liver disease infected with HEV genotypes 1–4 (Kamar et al., 2017). Extra-hepatic manifestations including neurological and renal symptoms have also been described (Kamar et al., 2017). A growing number of studies show that HEV can be considered as a re-emerging virus in developed countries (Zahmanova et al., 2023). Hepatitis E infections gained increasing attention as a possible cause of chronic hepatitis and liver cirrhosis in immunocompromised patients such as solid organ transplant recipients, patients living with HIV and patients with hematological malignancies. A reduction in immunosuppressive therapy and/or the use of the antiviral drug ribavirin have been established as effective treatment strategies (Abravanel et al., 2023).

Several serological and molecular assays can be used to diagnose an HEV infection. However, HEV IgM are less frequently positive in the immunocompromised population at the acute phase than in immunocompetent patients (Abravanel et al., 2013a, Abravanel et al., 2019, Abravanel et al., 2022). Therefore, molecular assays should be used to screen HEV infection in this population (Abravanel et al., 2013a, Abravanel et al., 2019, Abravanel et al., 2022). Viral RNA can be found both in plasma and in stool. Chronic HEV infection is defined as persistent HEV replication for more than three months (European Association for the Study of the Liver, 2018a, Kamar et al., 2013). One third of immunosuppressed patients spontaneously eliminate their infection. Therefore, the persistence or elimination of the virus should be assessed by molecular assay 3 months after diagnosis. Quantitative molecular assays are also useful to determine the efficacy of any therapeutic strategies (European Association for the Study of the Liver, 2018b). While a decrease of 0.5 log IU/ml or greater in HEV RNA in blood 7 days after initiation of ribavirin therapy is predictive of a response (Kamar et al., 2015), HEV RNA detected in feces despite a negative blood HEV RNA is a strong predictor of a relapse in immunocompromised subjects (Abravanel et al., 2015). Therefore, monitoring HEV fecal excretion could help to determine the optimal duration of ribavirin therapy and has been recommended for managing chronic HEV infections in solid-organ transplant recipients (European Association for the Study of the Liver, 2018b, Marion et al., 2019). However, the presence of PCR inhibitors in this particular matrix can make detecting HEV RNA difficult (Abravanel et al., 2018).

We evaluated the performance of the AltoStar® HEV RT-PCR Kit 1.5 on the AltoStar® Automation System AM16 by Altona Diagnostics. We compared the results obtained with this system with those obtained previously using a commercial quantitative RT-PCR, on a panel of plasma and stool specimens.