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Published on: June 26, 2020
The histology of acute autochthonous hepatitis E virus infection
P Malcolm1, H Dalton, H S Hussaini
1Department of Pathology, Royal Cornwall Hospital, Truro, UK. jack-and-paul@medix-uk.com
Insights
Histological examination of liver biopsies reveals distinct features of autochthonous hepatitis E virus (HEV) infection. These findings aid in diagnosing HEV in acute settings and differentiating it from endemic forms.
Area of Science:
- Hepatology
- Virology
- Pathology
Background:
- Hepatitis E virus (HEV) infection is a significant cause of acute hepatitis globally.
- Understanding the histological manifestations of HEV is crucial for accurate diagnosis and patient management.
Observation:
- This study investigated the liver biopsy findings in four patients with serologically confirmed HEV infection.
- Three patients had autochthonous (locally acquired) HEV, while one had an imported case from China.
Findings:
- Autochthonous HEV cases exhibited severe portal and lobular inflammation with a characteristic geographical distribution of inflammatory cells.
- Key features included interface hepatitis, cholangiolitis, apoptotic hepatocytes, and cholestatic rosettes.
- Absence of steatosis, megamitochondria, Mallory bodies, and iron/copper accumulation was noted in autochthonous cases.
- The imported HEV case showed less intense inflammation and lacked the distinct geographical pattern and cholangiolitis.
Implications:
- The distinct histological features of autochthonous HEV infection can aid in early diagnosis.
- Histopathology may help differentiate locally acquired HEV from imported cases or other forms of hepatitis.
Aim:
To document the histological appearances of liver biopsies in autochthonous hepatitis E virus (HEV) infection.
Methods And Results:
Four patients were serologically positive for HEV; three had no traditional risk factors, the fourth had recently returned from China. All four consumed meat products. Liver histology of the three autochthonous (locally acquired) cases showed portal tracts expanded by a severe mixed polymorph and lymphocytic inflammatory infiltrate, with a geographical distribution of polymorphs at the interface and lymphocytes centrally. Moderate to severe interface hepatitis and cholangiolitis were present. There was a striking acinar mixed inflammatory infiltrate made up of polymorphs, lymphocytes and macrophages; frequent apoptotic hepatocytes, focal necrosis, cholestatic rosettes and zone 3 canalicular and cytoplasmic bilirubinostasis were noted. Significant steatosis, megamitochondria and Mallory bodies were not present. There was no evidence of iron, copper or alpha(1)-antitrypsin accumulation. By contrast, the histology of the imported case of HEV infection showed less intense portal and acinar inflammation, no cholangiolitis and no geographical distribution of the portal inflammatory infiltrate.
Conclusion:
The histological appearances of autochthonous HEV infection are sufficiently distinctive to consider the diagnosis in an acute setting and possibly to differentiate it from the endemic form of the disease.
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