Nipah virus Malaysia and Bangladesh strain-induced pathogenesis in mice lacking type I interferon receptor signaling

Lucia Amurri1, Olivier Reynard1, Ilona Ronco1

  • 1CIRI, Centre International de Recherche en Infectiologie, INSERM U1111, CNRS, UMR5308, Univ Lyon, Université Claude Bernard Lyon 1, École Normale Supérieure de Lyon, Lyon, France.

Insights

Nipah virus (NiV) infection outcomes were studied in type I interferon receptor-deficient (IFNAR KO) mice. These mice showed susceptibility to NiV strains, suggesting a potential model for comparative Nipah virus pathogenesis research.

Area of Science:

  • Virology
  • Immunology
  • Pathogenesis

Background:

  • Nipah virus (NiV) is a highly pathogenic zoonotic virus causing severe encephalitis and Acute Respiratory Distress Syndrome (ARDS).
  • Two main strains, NiV-Malaysia (NiV-Mal) and NiV-Bangladesh (NiV-Ban), exhibit different transmission routes, symptoms, and lethality.
  • Lack of approved therapeutics necessitates further understanding of NiV pathogenesis.

Purpose of the Study:

  • To investigate the susceptibility of type I interferon receptor knockout (IFNAR KO) mice to NiV-Mal and NiV-Ban infections.
  • To evaluate the impact of different inoculation routes (intraperitoneal and intranasal) on NiV infection in IFNAR KO mice.
  • To assess the potential of IFNAR KO mice as a model for comparative studies of NiV strains' immunopathogenesis.

Main Methods:

  • Inoculation of IFNAR KO mice with NiV-Mal and NiV-Ban via intraperitoneal and intranasal routes.
  • Monitoring of infection progression, including clinical signs, viral dissemination, and organ involvement.
  • Assessment of host antiviral response, including the production of neutralizing antibodies.

Main Results:

  • IFNAR KO mice were susceptible to NiV-Ban via intraperitoneal route, though less so than to NiV-Mal, developing encephalitis and pulmonary syndrome.
  • Viral dissemination to multiple organs was observed in infected mice.
  • Intranasal inoculation with both NiV strains resulted in subclinical infections with viral replication in the brain and lungs, and antibody production in some animals.

Conclusions:

  • IFNAR KO mice are susceptible to NiV infection, with varying outcomes depending on the viral strain and route of administration.
  • The study highlights the potential of IFNAR KO mice as a valuable model for comparative research on the immunopathogenesis of different NiV strains.
  • Further research using this model could aid in developing effective therapeutic strategies against Nipah virus.

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