In pregnant women, especially in the third trimester, the disease is more often severe and is associated with a clinical syndrome called fulminant liver failure, with death rates around 20%.

[18] The virus was discovered in 1983 by researchers investigating an outbreak of unexplained hepatitis among Soviet soldiers serving in Afghanistan.

After a short prodromal phase symptoms may include jaundice, fatigue, and nausea, though most HEV infections are asymptomatic.

Besides signs of an acute infections, adverse effects on the mother and fetus may include preterm delivery, abortion, stillbirth, and neonatal death.

Increased viral replication and influence of hormonal changes on the immune system are currently thought to contribute to worsening the course of infection.

[40] Genotypes 1 and 2 are restricted to humans and often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions.

[41] Genotypes 3 and 4 infect humans, pigs, and other animal species and have been responsible for sporadic cases of hepatitis E in both developing and industrialized countries.

[5][48] It is spread mainly by the fecal–oral route due to contamination of water supplies or food; direct person-to-person transmission is uncommon.

[58][59] Hepatitis E infection appeared to be more common in people on hemodialysis, although the specific risk factors for transmission are not clear.

[62] Replicative virus has been found in the small intestine, lymph nodes, colon, and liver of experimentally infected pigs.

Previous studies showed that ORF3 is bound to viral particles found in patient sera and produced in cell culture.

Although in cultured cells ORF3 has not appeared essential for HEV RNA replication, viral assembly, or infection, it is required for particle release.

[69] The lifecycle of hepatitis E virus is unknown; the capsid protein obtains viral entry by binding to a cellular receptor.

[11][72] In the United States no serologic tests for diagnosis of HEV infection have ever been authorized by the Food and Drug Administration.

[74] Assuming that vaccination has not occurred, tests may show:[5] Sanitation is the most important measure in prevention of hepatitis E; this consists of proper treatment and disposal of human waste, higher standards for public water supplies, improved personal hygiene procedures, and sanitary food preparation.

[59] The amount of virus present in blood products required to cause transfusion-transmitted infection (TTI) appears variable.

The vaccine—called HEV 239 by its developer Xiamen Innovax Biotech—was approved for prevention of hepatitis E in 2012 by the Chinese Ministry of Science and Technology, following a controlled trial on 100,000+ people from Jiangsu Province where none of those vaccinated became infected during a 12-month period, compared to 15 in the group given placebo.

[79] Due to lack of evidence, the World Health Organization has not made a recommendation regarding routine use of the HEV 239 vaccine as of 2015.

[8] Reviews of existing small studies suggest that ribavirin can be considered effective in immunocompromised people who have developed chronic infection.

[8] Pregnant women are particularly at risk of complications due to HEV infection, who can develop an acute form of the disease that is fatal in 30% of cases or more.

[87] In July 2012, an outbreak was reported in South Sudanese refugee camps in Maban County near the Sudan border.

A record number of hepatitis E cases have been diagnosed in Finland so far this year, according to figures released on Tuesday by public health authority THL.

Data from the authority's Infectious Diseases Register showed that a total of 92 lab-confirmed infections have been recorded since the beginning of January until 12 March, with 42 people requiring hospital treatment.