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Morphological changes in HAV-infected Frp/3 cells and immunolocalization of HAAg

A Tinari1, F M Ruggeri, M Divizia

  • 1Department of Ultrastructures, Istituto Superiore di Sanità, Rome, Italy.

Archives of Virology
|January 1, 1989
PubMed

Insights

Hepatitis A virus (HAV) infection causes significant cell damage in Frp/3 cells, marked by changes in the endoplasmic reticulum and the formation of virus particles. Replication appears closely linked to cellular membranes, particularly the RER.

Area of Science:

  • Hepatology
  • Virology
  • Cell Biology

Background:

  • Hepatitis A virus (HAV) is a significant human pathogen.
  • Understanding HAV replication mechanisms is crucial for developing antiviral strategies.
  • HAV infection induces characteristic cytopathic effects in host cells.

Purpose of the Study:

  • To investigate the ultrastructural changes in HAV-infected Frp/3 cells.
  • To elucidate the role of cellular membranes in HAV replication.
  • To localize HAV antigen (HAAg) within infected cells.

Main Methods:

  • Electron microscopy (EM) and immunoelectron microscopy (IEM) were employed.
  • Frp/3 cells were infected with HAV and analyzed at various time points.
  • Indirect immunoperoxidase staining was used for antigen localization.

Main Results:

  • Distinct cytopathic effects (CPE) were observed, including cell detachment.
  • Progressive modifications in the rough endoplasmic reticulum (RER) were noted, such as polyribosome formation, hypertrophy, dilatation, and degranulation.
  • Virus-like particles (24-27 nm) were found in cytoplasmic vesicles and extracellularly.
  • HAV antigen (HAAg) was localized to vesicular inclusion bodies, RER, and myelin-like structures.
  • HAV replication appears associated with cytoplasmic membranes, with a demonstrated involvement of the RER.

Conclusions:

  • HAV infection induces profound ultrastructural alterations in Frp/3 cells.
  • The RER and cytoplasmic membranes are likely critical sites for HAV replication.
  • These findings provide insights into the intracellular lifecycle of HAV.

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