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Epstein-Barr virus and its interaction with the host

H Wolf1, C Bogedain, F Schwarzmann

  • 1Institute of Medical Microbiology and Hygiene, University of Regensburg, FRG.

Intervirology
|January 1, 1993
PubMed
Summary

Epstein-Barr virus (EBV) persists lifelong, causing various diseases. Terminally differentiated epithelial cells are key for EBV replication, while other cells eliminate infected cells, controlling viral production.

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A case of severe chronic active infection with Epstein-Barr virus: immunologic deficiencies associated with a lytic virus strain.

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America·1999

Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Epstein-Barr virus (EBV), a herpesvirus, establishes lifelong infections.
  • EBV causes diseases ranging from infectious mononucleosis to cancers like nasopharyngeal carcinoma and lymphomas.
  • Viral latency and replication are tightly regulated, with epithelial cells playing a crucial role in lytic production.

Purpose of the Study:

  • To elucidate the mechanisms of Epstein-Barr virus (EBV) replication and latency in epithelial cells.
  • To understand why EBV production is restricted in most target cells.
  • To identify factors contributing to EBV-associated oncogenesis.

Main Methods:

  • Investigation of EBV entry routes into epithelial cells (e.g., cell fusion, IgA receptor-mediated uptake).
  • Analysis of molecular mechanisms inhibiting EBV lytic cycle in non-permissive cells.
  • Study of EBV's role in apoptosis suppression and immune evasion (e.g., HLA molecule down-regulation).

Main Results:

  • EBV can enter epithelial cells via CR2 receptor-independent pathways.
  • Viral production is limited by silencer activities and early elimination of infected cells.
  • Terminally differentiated epithelial cells efficiently support EBV lytic replication.
  • EBV suppresses apoptosis and down-regulates HLA molecules, facilitating immune evasion.

Conclusions:

  • EBV replication is tightly controlled, with terminally differentiated epithelial cells being permissive.
  • EBV-associated neoplasias involve viral gene interactions with host factors like p53, alongside genetic and environmental influences.
  • New diagnostic tools and a vaccine offer potential for controlling EBV-related diseases.

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