Infectious Bronchitis Coronavirus Infection in Chickens: Multiple System Disease with Immune Suppression

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.

Keywords: chicken; infectious bronchitis coronavirus; molecular epidemiology; pathogenesis; tissue tropism.

Figure 1

Phylogenetic tree based on the S1 nucleotide sequences (from the ATG start codon to the cleavage site of the spike protein). The phylogeny contains a total of 21 infectious bronchitis virus (IBV) strains from different countries around the world. The IBV strain and GenBank accession number are given for each strain. The sequences were aligned using Clustal Omega, and the phylogenetic tree was constructed using the maximum likelihood method available in RAxML with 1000 bootstrap replicates for branch support (the numbers on the nodes represent the bootstrap values). The analyses were constructed using Geneious^® v10.2.6 (https://www.geneious.com/).

Figure 2

Clinical and pathological manifestations of IBV infection. The schematic diagram shows the entry, the route of dissemination of the virus to visceral organs and the pathogenesis of various IBV strains in different body systems. All the IBV strains primarily infect the respiratory tract, and based on the genotypes, the IBV infection can extend to various tissues, either persisting or leading to clinical and pathological manifestations. The solid arrows indicate paths that have been confirmed. The empty arrows indicate paths that have been suggested. The text boxes with continuous borders summarize histological changes, and the text boxes with discontinuous borders represent clinical manifestations. SES, shell-less egg syndrome; FLS, false layer syndrome; GIT, gastrointestinal tract.

Figure 3

Immune evasion mechanisms of IBV. IBV replicates in multiple immune organs, such as the bursa of Fabricius (BF), spleen (SP), cecal tonsils (CT) and Harderian gland (HG), enabling it to persist in the host for a longer period. Epithelial cells are the primary target sites of IBV replication, which results in deciliation and destruction, leading to inhibition of the mucociliary escalator mechanism. Certain strains of IBV can inhibit the expression of pathogen recognition receptors such as toll-like receptors (TLRs) or their signaling pathway, leading to reduced expression of proinflammatory cytokines, which eventually interferes with the innate immune response and induction of the adaptive immune response. IBV is also capable of replicating in respiratory tract macrophages, inhibiting their functions and inducing apoptosis. IBV is capable of incorporating CD59 molecules into its envelop during egress from the host cells, shielding it against lysis via complement- and antibody-dependent mechanisms.