Abstract
Infection with the hepatitis E virus (HEV) is one of the main ubiquitous causes for developing an acute hepatitis. Moreover, chronification plays a predominant role in immunocompromised patients such as transplant recipients with more frequent severe courses. Unfortunately, besides reduction of immunosuppression and off-label use of ribavirin or pegylated interferon alfa, there is currently no specific anti-viral treatment to prevent disease progression. So far, research on involved immune mechanisms induced by HEV is limited. It is very difficult to collect clinical samples especially from the early phase of infection since this is often asymptomatic. Nevertheless, it is certain that the outcome of HEV-infected patients correlates with the strength of the proceeding immune response. Several lymphoid cells have been identified in contributing either to disease progression or achieving sustained virologic response. In particular, a sufficient immune control by both CD4+ and CD8+ T cells is necessary to prevent chronic viral replication. Especially the mechanisms underlying fulminant courses are poorly understood. However, liver biopsies indicate the involvement of cytotoxic T cells in liver damage. In this review, we aimed to highlight different parts of the lymphoid immune response against HEV and point out questions that remain unanswered regarding this underestimated global threat.
Highlights
Worldwide, an infection with the hepatitis E virus (HEV) is one of the main causes for an acute hepatitis
Studies with HEV-infected patients showed a diminished presence of natural killer (NK) cells in the peripheral blood, whereas activation was strongly increased, indicating a possible migration to affected hepatic tissue, shown by higher NK cell counts in liver biopsies
Studies on HEV-infected Mongolian gerbils showed an enhanced activation of mast cells, a cell population largely associated with allergic reactions, and regarded as a connection between innate and adaptive immune response [135,136]
Summary
An infection with the hepatitis E virus (HEV) is one of the main causes for an acute hepatitis. HEV was described for the first time in 1983 as a new non-A, non-B hepatitis virus when it was possible to detect novel virus-like particles in stool samples via immune electron microscopy [4]. 1955 to 1956 in New Delhi, India, due to contaminated drinking water, though it was yet to be attributed to hepatitis A virus. It took until 1994 to identify HEV as the cause for this outbreak [5,6]. In this review we aimed to outline relevant aspects regarding the versatile lymphoid immune response and point out open questions concerning a globally challenging disease
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