Hepatitis E

An enterically transmitted viral infection similar to, but distinct from, hepatitis A virus (HAV) infection had been suspected for many years before it was first identified in an HAV-immune individual in 1983 on electron microscopy of stool samples.[26] Subsequently, in 1990, a non-enveloped, single-stranded RNA virus 27-34 nanometres in diameter was isolated and cloned and named hepatitis E virus (HEV).[27]

Infection with HEV genotypes 1 and 2 is typically acquired by drinking faecally contaminated water in endemic areas such as Africa and Asia, demonstrated by epidemic peaks during the rainy season.[1][7] HEV genotypes 3 and 4 are acquired by ingestion of contaminated and uncooked or undercooked meat (e.g, pork, wild boar, or deer) or close association with the animal reservoir, such as by farm workers or veterinarians.[1][19][28][29] Genotype 7 (the most recently identified genotype) was detected in a liver-transplant recipient who regularly consumed camel meat and milk.[8]

Although much less common, HEV infection can occur after transfusion of blood products and organ transplantation.[22][30][31][32][33] Note that these risks are not applicable universally: for example, in the UK, blood donations are screened for HEV before transfusion. Vertical transmission is also a less common mode of transmission.[34] People living in crowded camps or temporary housing, such as refugees or people who are internally displaced, are also at greater risk of contracting HEV infection.[1]

Note that many people in the US and Europe will not have a readily identifiable risk factor for HEV infection; any person presenting with an otherwise unexplained acute hepatitis could have HEV infection, as HEV infection is endemic in most high-income countries.[2]

It remains unclear how HEV infection leads to hepatitis. Because HEV infection is often transmitted via contaminated water or by ingestion of infected meat products by the faecal-oral route, intestinal replication of the virus after ingestion has been postulated before travel in the portal circulation to the liver.[35] The virus is not pathogenic, so the hepatitis is presumably a result of the immune response.[3] The incubation period for HEV infection is around 15-60 days.[2]

HEV may affect other areas of the body, including neuronal, kidney, and placental tissue, which may help to explain some of the extrahepatic manifestations of the condition.[9]

HEV genotype

Hepatitis E virus (HEV) is part of the Hepeviridae family, which consists of positive-stranded RNA viruses that affect many species. The Orthohepevirus genus of this family includes all the mammalian and avian HEV isolates and is divided into four subgroups, A-D.[6] Group A is further divided into eight genotypes, with genotype 1 and 2 infecting humans and genotypes 3 and 4 infecting animals such as swine, deer, and non-human primates that can transmit disease to humans through ingestion of meat, direct contact, and other routes. Note that patients are not routinely screened for genotypes as a part of diagnosis.

Genotype 1 is endemic in Africa and Asia. It is transmitted by the faecal-oral route through contaminated water and by person-to-person contact.[1][7]
Genotype 2 is endemic in Mexico and West Africa. It is transmitted by the faecal-oral route through contaminated water.[1][7]
Genotype 3 is found as isolated cases in developed countries, such as the US, France, the Netherlands, and the UK. It is primarily transmitted to humans through ingestion of uncooked or undercooked meat.[1][2]
Genotype 4 is found as sporadic cases in China, Taiwan, and Japan. It is primarily transmitted to humans through ingestion of uncooked or undercooked meat.[1]
Genotype 7 (the most recently identified genotype) was detected in a liver-transplant recipient who regularly consumed camel meat and milk.[8]

Pathophysiology

Classification

HEV genotype