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Increased toxicity of double-stranded ribonucleic acid in virus-infected animals

Infection and Immunity
|February 1, 1973
PubMed

Insights

Virus infections increase susceptibility to double-stranded RNA toxicity. This heightened toxicity in infected mice, observed with synthetic and natural double-stranded RNA, is linked to virus-induced interferon levels.

Area of Science:

  • Immunology
  • Virology
  • Toxicology

Background:

  • Double-stranded ribonucleic acid (RNA) can induce interferon production.
  • Virus infections can modulate the host immune response.
  • Understanding the interplay between viral infections and immune stimulants is crucial.

Purpose of the Study:

  • To investigate the toxicity of double-stranded RNA in virus-infected mice.
  • To determine if other interferon inducers share this enhanced toxicity.
  • To explore the role of interferon in this phenomenon.

Main Methods:

  • Administering synthetic (polyriboinosinic.polyribocytidylic acid) and natural (mycophage) double-stranded RNA to virus-infected and uninfected mice.
  • Comparing mortality rates between infected and uninfected groups.
  • Testing other interferon inducers (tilorone-hydrochloride, chlorite-oxidized oxyamylose) for toxicity in infected mice.
  • Correlating toxicity with systemic and local interferon levels.

Main Results:

  • Virus-infected mice exhibited significantly higher mortality after double-stranded RNA injection compared to uninfected mice.
  • Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV) infections potentiated double-stranded RNA toxicity.
  • Interferon inducers other than double-stranded RNA did not show increased toxicity in infected animals.
  • Increased susceptibility correlated with elevated interferon levels, either systemic (NDV) or local (VSV).

Conclusions:

  • Virus infections enhance the toxic effects of double-stranded RNA.
  • This heightened toxicity is likely mediated by virus-induced interferon.
  • The findings highlight a specific interaction between viral infections and double-stranded RNA immunomodulation.

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