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Morphine reduces mortality in mice following ocular infection with HSV-1

N C Alonzo1, D J Carr

  • 1Louisiana State University Medical Center, Department of Pharmacology, Microbiology, Immunology and Parasitology, New Orleans 70112-1393, USA.

Immunopharmacology
|July 31, 1999
PubMed

Insights

Chronic opioid treatment with morphine in mice reduced herpes simplex virus type 1 (HSV-1) spread in the central nervous system, decreasing the incidence of viral encephalitis and improving survival rates.

Area of Science:

  • Neurovirology
  • Immunopharmacology

Background:

  • Opioid use is common, and herpes simplex virus type 1 (HSV-1) can cause serious neurological complications.
  • The impact of chronic opioid administration on HSV-1 infection and subsequent encephalitis is not well understood.

Purpose of the Study:

  • To investigate the effects of chronic morphine treatment on HSV-1 infection and encephalitis in a mouse model.
  • To determine if morphine influences viral load, host immune response, or neurological spread of HSV-1.

Main Methods:

  • Female ICR mice received daily subcutaneous injections of morphine or saline for five days prior to corneal inoculation with HSV-1.
  • Viral load, cytokine expression, and viral transcript levels were assessed in various tissues (eyes, trigeminal ganglia, brain stem, cerebellum) at different time points post-infection.
  • Survival rates were monitored.

Main Results:

  • Morphine-maintained mice exhibited higher cumulative survival rates compared to saline-treated or morphine-deprived mice.
  • No significant differences in viral load or cytokine expression were observed between morphine-maintained and saline-treated groups during acute infection.
  • Reduced expression of HSV-1 infected cell polypeptide 27 was noted in the brain stem of morphine-maintained mice, suggesting attenuated viral spread in the CNS.

Conclusions:

  • Chronic morphine administration appears to antagonize HSV-1 central nervous system spread in mice.
  • Morphine treatment may reduce the incidence of HSV-1-induced encephalitis, potentially through mechanisms independent of acute immune responses or viral replication in peripheral tissues.

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