Abstract
In the early 1930s, infectious bronchitis (IB) was first characterized as a respiratory disease in young chickens; later, the disease was also described in older chickens. The etiology of IB was confirmed later as being due to a coronavirus: the infectious bronchitis virus (IBV). Being a coronavirus, IBV is subject to constant genome change due to mutation and recombination, with the consequence of changing clinical and pathological manifestations. The potential use of live attenuated vaccines for the control of IBV infection was demonstrated in the early 1950s, but vaccine breaks occurred due to the emergence of new IBV serotypes. Over the years, various IBV genotypes associated with reproductive, renal, gastrointestinal, muscular and immunosuppressive manifestations have emerged. IBV causes considerable economic impacts on global poultry production due to its pathogenesis involving multiple body systems and immune suppression; hence, there is a need to better understand the pathogenesis of infection and the immune response in order to help developing better management strategies. The evolution of new strains of IBV during the last nine decades against vaccine-induced immune response and changing clinical and pathological manifestations emphasize the necessity of the rational development of intervention strategies based on a thorough understanding of IBV interaction with the host.
Highlights
Infectious bronchitis virus (IBV) belongs to the family Coronaviridae and order Nidovirales [1].IBV infects chickens and pheasants and induces a clinical disease known as infectious bronchitis (IB) [2].The infected chickens may appear depressed with various levels of breathing difficulty and have ruffled feathers [3,4,5,6]
Type 1 IFNs are the main antiviral molecules synthesized in the host in response to viral replication, and, previously, it has been shown that IBV is sensitive to the antiviral activity of type 1 IFNs given as a treatment to prevent IB in chickens [90]
Many studies have been conducted on IBV pathogenesis, there is little specific information on IBV receptors that determine macrophage tropism and tissue tropism, mechanisms that allow IBV dissemination from the respiratory tract to secondary tissues, IBV persistence in the cecal tonsils and kidney and the immunopathogenesis and immunosuppressive mechanisms of different strains of IBV
Summary
Infectious bronchitis virus (IBV) belongs to the family Coronaviridae and order Nidovirales [1]. IBV infects chickens and pheasants and induces a clinical disease known as infectious bronchitis (IB) [2]. The infected chickens may appear depressed with various levels of breathing difficulty and have ruffled feathers [3,4,5,6]. Younger chickens show the most severe clinical manifestations [7]. Certain IBV strains (i.e., Massachusetts (Mass) and Gray) have been found to be capable of replicating in human cell lines [9]. The first IB case caused by the Mass serotype was recorded from North Dakota, USA [10]. High IB-associated losses are recorded in spite of control attempts using live attenuated vaccines. Knowledge of different IBV strains and their pathogenicity is important for establishing sustainable vaccination strategies. Despite several published reviews relevant to IBV pathogenesis [18,19,20,21,22], there is a need for an analysis of information due to the large influx of literature in recent years on the evolving pathogenesis of IBV infection [23,24,25]
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