Hepatitis E virus (HEV) is a nonenveloped, single-stranded RNA virus and a leading cause of acute viral hepatitis worldwide. In children, HEV infection is usually self-limited, but certain populations—pregnant girls, malnourished children, and those with preexisting liver disease or immunosuppression—are at risk for severe or chronic disease.
HEV belongs to the family Hepeviridae. Four major genotypes infect humans:
| Genotype | Reservoir | Geographic Distribution | Notes |
|---|---|---|---|
| 1 | Human only | Asia, Africa | Waterborne outbreaks; high mortality in pregnancy |
| 2 | Human only | Mexico, West Africa | Similar to genotype 1 |
| 3 | Pigs, deer, rabbits | Worldwide (industrialized countries) | Zoonotic; chronic infection in immunosuppressed |
| 4 | Pigs, boar | Asia, Europe | Zoonotic; variable severity |
HEV spreads by the fecal–oral route, typically through contaminated water or food. Outbreaks are common in areas with poor sanitation and during rainy seasons. Rarely, HEV may transmit through transfused blood products or organ transplantation.
In children, acute HEV infection often presents with nonspecific prodromal symptoms—anorexia, malaise, low-grade fever, headache—followed by nausea, vomiting, diarrhea, and jaundice. Most children recover completely within 4–6 weeks.
Fulminant hepatic failure is uncommon in children but occurs more frequently in:
Accurate diagnosis relies on serologic and molecular testing:
| Test | Interpretation |
|---|---|
| Anti-HEV IgM | Marker of acute infection |
| Anti-HEV IgG | Indicates past infection; appears later |
| HEV RNA (PCR) | Confirms active infection in serum or feces |
When liver biopsy is performed, characteristic findings include ballooning degeneration of hepatocytes, cholestasis, and gland-like (pseudoacinar) hepatocyte changes.
HEV usually causes an acute, self-limited hepatitis without chronic carrier state. Rarely, immunocompromised children—such as organ transplant recipients or those receiving chemotherapy—develop chronic HEV infection, defined by persistent HEV RNA >3 months.
Chronic HEV in immunocompromised children is treated with:
Ribavirin may be teratogenic—use strict contraception in post-pubertal patients. Side effects include hemolytic anemia and rash.
In children with acute liver failure, management includes intensive supportive care, correction of coagulopathy, and evaluation for liver transplantation.
No HEV vaccine is widely available in most countries (a recombinant vaccine is licensed in China). Prevention focuses on:
HEV genotype 1 and 2 in pregnant girls carries high risk of fulminant hepatitis, fetal loss, and maternal mortality. Management is supportive; early transfer to a liver center is advised for hepatic decompensation.
Chronic HEV may lead to rapid fibrosis in these patients. Routine screening for HEV RNA in unexplained liver enzyme elevations is recommended, and early ribavirin therapy can achieve viral clearance in >80 percent of cases.
Hepatitis E in children is typically an acute, self-limited illness, but carries significant risk in pregnancy and immunosuppressed patients. Diagnosis relies on anti-HEV IgM and RNA detection; treatment is supportive for acute cases and ribavirin-based for chronic infection. Prevention through water sanitation, hygiene, and HBV vaccination in endemic regions remains vital to reducing HEV burden.