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Related Experiment Videos

Herpesvirus saimiri.

H Fickenscher1, B Fleckenstein

  • 1Institut für Klinische und Molekulare Virologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, Schlossgarten 4, D-91054 Erlangen, Germany. fickenscher@viro.med.uni-elargen.de

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|April 21, 2001
PubMed
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Herpesvirus saimiri, a rhadinovirus, causes T-cell lymphoma in non-natural hosts but persists without disease in squirrel monkeys. Specific viral genes are crucial for its oncogenic potential and transformation of human T cells, offering research applications.

Area of Science:

  • Virology
  • Oncology
  • Immunology

Background:

  • Herpesvirus saimiri (HVS) is a prototype gamma(2)-herpesvirus (rhadinovirus) related to Kaposi's sarcoma-associated herpesvirus.
  • HVS establishes persistent infections in its natural host, Saimiri sciureus (squirrel monkey), without causing disease.
  • Experimentally, HVS induces fatal T-cell lymphoma in other primate species.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying HVS pathogenicity and T-cell transformation.
  • To explore the potential of HVS-transformed cells as tools in immunology and gene therapy.

Main Methods:

  • Isolation of HVS through co-cultivation of infected primate cells.
  • Genomic analysis of HVS, identifying viral genes homologous to cellular counterparts.

Related Experiment Videos

  • Characterization of oncogenic subgroup C strains, including stpC and tip genes.
  • Transformation assays using HVS strains on human T lymphocytes.

    • Main Results:

    • HVS possesses viral genes with functional homology to cellular proteins, contributing to apathogenic persistence.
    • A specific terminal region of the HVS genome is essential for pathogenicity and T-cell transformation.
    • Highly oncogenic subgroup C strains, particularly C488, can transform human T lymphocytes into continuously growing cells.
    • Transformed human T cells retain parental functions and harbor viral genomes as episomes without producing virions.

    Conclusions:

    • The stpC and tip genes in HVS subgroup C are critical for oncogenesis and leukemia induction.
    • HVS-transformed human T cells represent valuable tools for T-cell immunology, gene transfer, and potential adoptive immunotherapy.