Clinical Information

Hepatitis E virus (HEV) is a causative agent of acute self-limited or fulminant hepatitis. HEV has been responsible for large outbreaks of disease in developing countries, primarily through waterborne transmission. Hepatitis E also can occur in industrialized countries, usually as sporadic cases due to zoonotic infection transmitted by the fecal-oral route. A major natural reservoir of HEV is pigs.

In immunocompetent individuals, hepatitis E is mainly a self-limited infection, frequently nonsymptomatic, and does not result in chronic infection. However, in otherwise healthy pregnant patients, hepatitis E can be severe, resulting in significant morbidity and mortality. In individuals who are immunocompromised, such as organ transplant recipients, hepatitis E can be chronic with detectable HEV RNA levels in serum and plasma beyond 3 months after infection. HEV-specific IgM antibody is detectable by serologic testing by 4 weeks after infection in immunocompetent individuals, but it may not be detectable until 6 months after infection in patients who are immunosuppressed.

HEV RNA levels in serum or plasma are usually detectable in all infected individuals by 3 weeks after infection and become undetectable by 7 weeks in immunocompetent individuals. Due to the limitations of HEV serologic testing in patients who are immunosuppressed, molecular testing (eg, real-time reverse-transcriptase polymerase chain reaction assay) for HEV RNA in serum or plasma is an increasingly important tool in the diagnosis of acute or chronic HEV infection in these patients.

Currently, ribavirin is used as the antiviral agent of choice for organ transplant recipients with chronic HEV, and monitoring of HEV RNA levels in serum or plasma is used to assess response to such antiviral therapy. Significant decreases in HEV viral load or clearance of HEV RNA may be important predictors of virologic response during antiviral therapy.