Attenuation of Avian Infectious Bronchitis Virus by Cold-Adaptation

Abstract

Avian infectious bronchitis virus (IBV) Arkansas-type DPI strain was passaged 10 times in specific-pathogen-free (SPF) chicken embryos incubated at 28 C and 37 C. Virus grown at 28 C acquired cold-adapted (CA) and temperature-sensitive (TS) characteristics based on more-rapid growth at 28 C and a reduced ability to grown at 41 C, respectively, compared with non-cold-adapted (non-CA) virus grown at 37 C. The pathogenicity and immunogenicity were determined for CA and non-CA IBV in 1-day-old SPF chickens following intratracheal inoculation. The percentage of CA IBV-vaccinated chicks exhibiting respiratory disease exceeded 30% on only 1 day postinoculation (PI) (day 5 PI), compared with 8 days (days 2-9 PI) for birds given non-CA IBV. Mortality was 0% for CA IBV-vaccinated chickens and 6% for non-CA virus-vaccinated chickens. Microscopically, both CA and non-CA IBV caused diffuse tracheal deciliation, although mucosal hyperplasia, necrosis, and heterophil infiltration were more severe with non-CA IBV. Virus was reisolated from kidneys of chickens given CA IBV, suggesting the loss of the TS property. The instability of the TS property was confirmed by growth of the reisolated virus at 41 C. Both CA and non-CA viruses induced complete protection against homologous challenge virus infection of the upper respiratory tract.

Infectious bronchitis virus: Immunopathogenesis of infection in the chicken

“…IBV has been isolated from the Harderian gland (Dhinakar Raj & Jones, 1996a;Gelb et al, 1991b;Toro et al, 1996a) and IBV-positive cells have been shown in the stroma of the gland by IF staining (Toro et al, 1996a). IBV vaccination by eyedrop resulted in a massive infiltration of lymphocytes, increase in plasma cell numbers (Davelaar & Kouwenhoven, 1976;Survashe et al, 1979;Montgomery et al, 1994;Toro et al, 1996a) and desquamation of tubular epithelium in the Harderian gland with restoration from 14 days after vaccination (Toro et al, 1996a).…”

Differential innate immune responses induced by classical and variant infectious bronchitis viruses in specific pathogen free chicks

“…Concurrent circulation of both classic and variant IBVs have been identified in most parts of the world, raising major challenges to global prevention and control efforts. During the past few decades, there have been reports of new virulent field isolates that represent variant strains, which can cause wide tissue tropism and high pathogenicity (Gelb et al, 1991;Jackwood, 2012;Shaw et al, 1996;Zanella et al, 2000). Though the mechanisms behind chickens' varying susceptibility to different IBV infections have been studied, little to no data is available on comparative immunopathogenesis on recently emerged IBVs.…”

Pathogenicity and tissue tropism of infectious bronchitis virus is associated with elevated apoptosis and innate immune responses

“…Current IBV isolates present high antigenic diversity (Hofstad, 1975), and emergent strains that differ in antigenic properties, tissue tropism and pathogenicity are continuously being reported across the world (Gelb et al, 1991;Jackwood, 2012;Shaw et al, 1996;Zanella et al, 2000). While all IBV strains appear to initially infect chickens via the respiratory tract, vireamia enables spread to secondary sites for further replication and persistence.…”