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Experimental hepatitis E: pathogenesis in cynomolgus macaques (Macaca fascicularis)

C F Longer1, S L Denny, J D Caudill

  • 1Dept. of Virus Diseases, WRAIR, Washington DC, 20307-5100.

The Journal of Infectious Diseases
|September 1, 1993
PubMed
Summary

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This study details experimental hepatitis E in macaques, revealing an early phase of virus replication and liver damage, followed by an antibody response and persistent pathology. Understanding hepatitis E virus (HEV) pathogenesis is crucial.

Area of Science:

  • Hepatology
  • Virology
  • Immunology

Background:

  • The pathogenesis of experimental hepatitis E remains incompletely understood.
  • Accurate documentation of disease progression is essential for developing effective interventions.

Purpose of the Study:

  • To meticulously document the chronological events in experimental hepatitis E.
  • To elucidate the interplay between hepatitis E virus (HEV) replication, host immune response, and liver pathology.

Main Methods:

  • Intravenous inoculation of cynomolgus macaques with HEV-containing material (bile or feces).
  • Comprehensive analysis of serum, bile, and liver specimens using light microscopy, immune electron microscopy, immunofluorescence microscopy, EIA, and PCR.
  • Monitoring of histopathologic changes, HEV antigen (HEVAg), HEV RNA, alanine aminotransferase (ALT) levels, and antibody to HEV (anti-HEV).

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Main Results:

  • Histopathologic changes, HEV antigen (HEVAg) in the liver, HEV in bile, and elevated ALT levels were observed by the third week post-inoculation.
  • Widespread pathologic changes occurred in the fourth week, with peak ALT values and the appearance of anti-HEV noted in the fifth or sixth week.
  • HEVAg diminished by the sixth week, while pathological changes persisted, indicating a protracted disease course.

Conclusions:

  • Experimental hepatitis E exhibits a biphasic course: an initial phase of HEV replication and hepatitis onset, followed by a later phase characterized by anti-HEV production and progressive liver damage.
  • The findings support a model where viral replication drives initial hepatitis, and the subsequent immune response correlates with disease progression.