Hepatitis E virus (HEV) is a hepatotropic infectious agent that generally causes self-limiting acute hepatitis in healthy adults and chronic hepatitis in immunocompromised individuals [
1]. Annually, there are an estimated 20 million HEV infections, 3.3 million symptomatic hepatitis E cases, and 60,000 deaths worldwide [
1,
2]. In addition to hepatic manifestations, extrahepatic manifestations, including pancreatitis, neurological symptoms, hematological disorders, glomerulonephritis, and mixed cryoglobulinemia have been associated with HEV infection [
1,
3]. HEV is classified into 8 major genotypes, with genotypes 1–4 being the predominant strains involved in human infections. Genotypes 1 (HEV-1) and 2 (HEV-2) infect only humans and are transmitted via the fecal-oral route [
1,
4], whereas genotypes 3 (HEV-3) and 4 (HEV-4) are zoonotic and are contracted through the consumption of undercooked pork and wild boar meat [
5]. Although swine are the most commonly implicated source of HEV-3 and HEV-4, other animals including shellfish, deer, and rabbits can serve as a source of infection [
4,
6‐
9]. Therefore, HEV-1 and HEV-2 are often associated with epidemics in developing countries due to poor hygiene and sanitation. In contrast, HEV-3 and HEV-4 are prevalent in industrialized countries and are associated with sporadic and clustered cases of hepatitis E in these regions [
1,
4]. In recent years, the transmission of HEV-3 and HEV-4 through blood transfusions has been increasingly reported in Europe [
1,
4,
10], prompting many countries to consider the screening of blood products for HEV [
11]. For these reasons, HEV is now recognized as a global health problem in both developing and industrialized countries [
1,
12]. Current therapeutics used to treat HEV infection include the nucleoside analog ribavirin and interferon-α (IFN-α). Ribavirin therapy can be fairly efficient in most cases of chronic hepatitis E [
1,
2,
13,
14]. In some specific situations, interferon has also been used successfully [
2]. However, until now, there have been no specific direct-acting antiviral agents against HEV, particularly for pregnant women [
1,
15]. A recombinant hepatitis E vaccine, HEV 239, has been demonstrated to be well tolerated and effective in the prevention of hepatitis E in China; however, it is currently only approved for use in China and is not yet available elsewhere [
2,
16,
17].
HEV infection can cause fulminant hepatitis failure (FHF), especially in pregnant women, with a mortality rate of up to 30% [
1,
18‐
20]. In addition, HEV can be vertically transmitted from infected mothers to their infants, with significant perinatal morbidity and mortality [
20‐
22]. Ribavirin and IFN-α are contraindicated in pregnancy because of the risk of teratogenicity [
23‐
25]. Therefore, only supportive care is provided for pregnant women with HEV infection. In this review, we provide a summary of the current knowledge regarding HEV and highlight HEV infection during pregnancy, which has been poorly understood until now and deserves the utmost attention.