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Hamster brain tumor cells persistently infected with measles-subacute sclerosing panencephalitis virus

Archives of Virology
|January 1, 1977
PubMed

Insights

Persistent measles virus infection in hamster brain tumor cells reduced tumor growth in vivo. Hydrocortisone treatment restored tumor growth, suggesting an immune response against measles virus antigens contributes to reduced cell transplantability.

Area of Science:

  • Virology
  • Immunology
  • Oncology

Background:

  • Subacute sclerosing panencephalitis (SSPE) is a severe neurological complication of measles virus (MV) infection.
  • Persistent viral infections can alter host cell behavior and immune responses.
  • Hamster brain tumor (HBT) cells provide a model for studying tumor growth and viral interactions.

Purpose of the Study:

  • To investigate the effect of persistent measles virus (HBS strain) infection on the growth and transplantability of hamster brain tumor (HBT) cells in vivo.
  • To determine the role of the host immune response in the altered behavior of virus-infected tumor cells.

Main Methods:

  • Establishment of a persistently infected cell line (HBT-M) from HBT cells and SSPE virus (HBS strain).
  • In vitro growth assays comparing HBT-M and HBT cells.
  • In vivo transplantability studies of HBT-M and HBT cells in weanling hamsters, with and without hydrocortisone treatment.

Main Results:

  • HBT-M cells exhibited similar growth to HBT cells in vitro.
  • Transplantability of HBT-M cells was significantly decreased in weanling hamsters compared to HBT cells.
  • Hydrocortisone treatment of hamsters restored the tumor-producing capacity of HBT-M cells to levels comparable to HBT cells.
  • Decreased in vivo cell growth was attributed to measles virus antigen expression and host immune response.

Conclusions:

  • Persistent measles virus infection in hamster brain tumor cells leads to decreased in vivo transplantability.
  • The host immune response against acquired measles virus antigens plays a critical role in suppressing tumor growth.
  • Modulation of the host immune response, e.g., with hydrocortisone, can overcome viral-induced immunosuppression and restore tumor-forming capacity.

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