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Effect of heat on viral protein production and budding in cultured mammalian cells

P P Herman1, M B Yatvin

  • 1Department of Radiation Oncology, Oregon Health Sciences University, Portland 97201.

International Journal of Hyperthermia : the Official Journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
|September 1, 1994
PubMed

Insights

Hyperthermia affects enveloped virus release and protein processing in host cells. Mild heat shock can increase virus release, while intense heat inhibits it, though released virus remains infectious.

Area of Science:

  • Virology
  • Cell Biology
  • Biophysics

Background:

  • Enveloped virus life cycles depend on host cell membranes.
  • Hyperthermia alters host cell organization, impacting viral processes.
  • Moloney murine leukemia virus (M-MuLV) is an enveloped retrovirus.

Purpose of the Study:

  • To investigate the effects of hyperthermia on M-MuLV release, protein production, and processing.
  • To determine if hyperthermia-induced changes affect viral infectivity.
  • To explore thermotolerance in virus-producing cells after heat exposure.

Main Methods:

  • Cultured murine C9CL98 cells chronically infected with M-MuLV were subjected to different hyperthermia treatments (44°C/45 min, 42.8°C/135 min, 42.8°C/25 min).
  • Viral env protein levels, virus release, and intracellular protein processing (Pr65 gag to p30 gag) were measured post-heating.
  • Infectivity of released virus was assessed using NIH/3T3 cells.
  • Thermotolerance was evaluated by applying a second heat shock at varying intervals after the initial exposure.

Main Results:

  • High-intensity hyperthermia (44°C/45 min or 42.8°C/135 min) decreased cell-free viral env protein levels for up to 48 hours.
  • A milder heat shock (42.8°C/25 min) increased virus release and cellular viral protein content.
  • Proteolytic processing of the Pr65 gag precursor to p30 gag was inhibited for at least 8 hours after 44°C/45 min treatment.
  • Virus released from heated cells retained infectivity for NIH/3T3 cells.
  • Cells surviving 42.8°C/135 min exhibited thermotolerance, showing reduced viral release upon a second heating event.

Conclusions:

  • Hyperthermia differentially impacts M-MuLV release and protein processing based on intensity and duration.
  • While severe hyperthermia can block viral protein processing, the released virus remains infectious.
  • Cells can develop thermotolerance, influencing subsequent viral release after repeated heat stress.
  • The precise mechanisms underlying hyperthermia-induced inhibition of virus release require further investigation.

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