Infectious bronchitis corona virus establishes productive infection in avian macrophages interfering with selected

Aruna Amarasinghe1, Mohamed Sarjoon Abdul-Cader1, Sadiya Nazir1

  • 1Department of Ecosystem and Public Health, Faculty of Veterinary Medicine, University of Calgary, Health Research Innovation Center 2C53, Calgary, Alberta, Canada.

Plos One
|August 2, 2017
PubMed

Insights

Infectious bronchitis virus (IBV) infects avian macrophages, leading to productive replication. This viral infection inhibits nitric oxide (NO) production but not type 1 interferon activity in macrophages.

Area of Science:

  • Avian immunology
  • Virology
  • Poultry disease

Background:

  • Infectious bronchitis virus (IBV) causes significant economic losses in chickens due to respiratory disease.
  • Elevated macrophage numbers are observed in IBV-infected respiratory tracts, but their role remains unclear.
  • The susceptibility of macrophages to IBV replication is a key unknown factor in disease pathogenesis.

Purpose of the Study:

  • To investigate the capacity of pathogenic IBV strains to infect and replicate within avian macrophages.
  • To assess the functional consequences of IBV infection on macrophage antimicrobial and immune-signaling capabilities.

Main Methods:

  • In vivo and in vitro infection models using two pathogenic IBV strains (M41 and Conn A5968).
  • Double immunofluorescence assays to detect viral antigens in macrophages.
  • Electron microscopy to identify viral particles and RT-PCR for viral RNA detection.
  • Measurement of nitric oxide (NO) production and type 1 interferon (IFN) activity in infected macrophages.

Main Results:

  • Both IBV M41 and Conn A5968 strains demonstrated low-level productive replication in avian macrophages in vivo and in vitro.
  • Viral antigens, RNA, and complete viral particles were detected in infected macrophages.
  • IBV infection significantly inhibited the production of nitric oxide (NO) by macrophages.
  • Macrophage-induced type 1 interferon (IFN) activity remained unaffected by IBV replication.

Conclusions:

  • Avian macrophages are susceptible to productive infection by pathogenic IBV strains.
  • IBV replication in macrophages impairs their ability to produce NO, a key antimicrobial molecule.
  • Type 1 IFN induction capacity of macrophages is not compromised by IBV infection.
  • The significance of macrophage tropism in IBV pathogenesis requires further investigation.

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