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.
Abstract:
Infectious bronchitis virus (IBV) causes respiratory disease leading to loss of egg and meat production in chickens. Although it is known that macrophage numbers are elevated in the respiratory tract of IBV infected chickens, the role played by macrophages in IBV infection, particularly as a target cell for viral replication, is unknown. In this study, first, we investigated the ability of IBV to establish productive replication in macrophages in lungs and trachea in vivo and in macrophage cell cultures in vitro using two pathogenic IBV strains. Using a double immunofluorescent technique, we observed that both IBV Massachusetts-type 41 (M41) and Connecticut A5968 (Conn A5968) strains replicate in avian macrophages at a low level in vivo. This in vivo observation was substantiated by demonstrating IBV antigens in macrophages following in vitro IBV infection. Further, IBV productive infection in macrophages was confirmed by demonstrating corona viral particles in macrophages and IBV ribonucleic acid (RNA) in culture supernatants. Evaluation of the functions of macrophages following infection of macrophages with IBV M41 and Conn A5968 strains revealed that the production of antimicrobial molecule, nitric oxide (NO) is inhibited. It was also noted that replication of IBV M41 and Conn A5968 strains in macrophages does not interfere with the induction of type 1 IFN activity by macrophages. In conclusion, both M41 and Con A5968 IBV strains infect macrophages in vivo and in vitro resulting productive replications. During the replication of IBV in macrophages, their ability to produce NO can be affected without affecting the ability to induce type 1 IFN activity. Further studies are warranted to uncover the significance of macrophage infection of IBV in the pathogenesis of IBV infection in chickens.
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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