Page 165 - Avian Virology: Current Research and Future Trends

158 | Liu et al.

the growth of IBV (Cavanagh, 2003). The site of virus multiplica- al., 2001), and secondly, to activate TIR-domain-containing
tion in these tissues was not confirmed, but it was postulated to be adapter-inducing-interferon-β (TRIF) adaptor protein-mediated
in the epithelial cells. In the lower gut, IBV replication has been pathway (Kawai and Akira, 2010). TLR7, on the other hand,
reported in the lymphoid and histocytes-resembling cells in the responds to single-stranded RNA and activates the myeloid
caecal tonsils (Gross, 1990), and in apical epithelial cells of the differentiation primary response gene 88 (MyD88) mediated-
villi of the intestines as demonstrated by IF (Ambali and Jones, pathway (Watters et al., 2007). In a study which compared the
1990). immune response genes in the tracheal samples following chal-
Despite the enterotropic nature of some IBV strains, histo- lenge with Brazilian field isolates, a suppressive effect on the
logical changes reported following IBV infection were limited. activation of TLR7 was observed (Okino et al., 2017). It may
Recently, an IBV-like CoV isolated from the intestines of broiler result in insufficient pro-inflammatory response and increased
chicks displayed clinical signs of runting stunting syndrome severity of renal lesions in chicken observed. Collectively,
(Hauck et al., 2016). This new IBV strain, which may have through the actions of the dual signalling pathways activated
merged from the California 99 and Arkansas strains, causes pale by TLR3 and TLR7, this would lead to the production of type
and distended small intestines on post-mortem examination. I IFN and pro-inflammatory cytokines (Guillot et al., 2005).
Histopathology revealed changes on the epithelial surface of the Among them, IL-1β plays an important role in chemotaxis to
intestines, including increased cellularity of the lamina propria, recruit immune cells, such as macrophages, to the site of infec-
blunting of villi, and cystic changes in the crypts. tion (Babcock et al., 2008; Amarasinghe et al., 2018).
Besides TLRs, retinoic acid-inducible gene I (RIG-I) and
Muscular system melanoma differentiation-associated gene 5 (MDA5) are also
The presence of pectoral myopathy in birds has been associ- pattern-recognition receptors (PRRs) that function as viral detec-
ated with an IBV strain known as 793/B. It was first reported in tors in non-immune cells and contribute to type I IFN production
England in the early 1990s, where affected chickens kept in the (Barber, 2011). MDA5 is a functional compensate for RIG-I in
slaughterhouse were presented with both superficial and deep chickens (Barber et al., 2010). It is a cytoplasmic DExD/H-box
bilateral pectoral myopathy. The pectoral lesions are also marked helicase. Upon binding of dsRNA to the helicase domain, the sig-
by atrophy, occasional fascial haemorrhages and oedema over nalling cascades in MDA5 are then initiated through homotypic
its surface (Gough et al., 1992), but did not cause severe clini- caspase activation and recruitment domain (CARD) interactions
cal issues in chickens (Bijanzad et al., 2013). Several studies have with interferon promoter-stimulating factor 1 (IPS-1) adaptor
been conducted to examine the relationship between this group proteins to activate downstream interferon-regulatory factors
of IBV with myopathy in chickens, but the findings have not (IRFs) (Kawai et al., 2005; Potter et al., 2008). MDA5 can recog-
been conclusive (Brentano et al., 2005; Gomes and Brito, 2007; nize CoV RNA products in virus-infected cells to induce IFN-α
Trevisol et al., 2009). It appears that the virus is involved in the and -β signalling (Yoneyama and Fujita, 2007; Züst et al., 2011).
formation and deposition of immune complexes in the capillary This process can be regulated by nsp16 methyltransferase (Yoney-
walls of the muscle, which may have contributed to the develop- ama and Fujita, 2007; Züst et al., 2011). MDA5-mediated innate
ment of this strange lesion (Dhinakar and Jones, 1997). immune responses are implicated in several CoV infections,
including MHV (Zalinger et al., 2015) and SARS-CoV (Yoshi-
kawa et al., 2010). In cells infected with IBV, MDA5 expression is
Immune responses up-regulated, as demonstrated in a number of studies (Cong et al.,
2013; Kint et al., 2015; He et al., 2016).
Innate immunity Macrophages and DCs are important cells of the immune
The innate and adaptive immunity to viral infections in chickens system, facilitating the presentation of antigens to develop
are interconnected, with the innate immunity response being antigen-specific innate and adaptive immune response through
more rapid. The innate immunity comprises of an assortment of PRRs (Akira et al., 2006; Trinchieri and Sher, 2007). While
factors which aim to protect the body against foreign pathogens. IBV can infect the blood-derived monocytes/macrophages and
It includes physical barriers provided by the skin and mucous induce apoptosis (Zhang and Whittaker, 2016), no studies have
membranes, soluble factors such as lysozymes and complement reported that IBV infection could impair the bactericidal or
proteins and immune cells such as phagocytic leucocytes, den- phagocytic activity of macrophages. NK cells are rapidly activated
dritic cells and natural killer (NK) cells. These immune cells, upon M41 infection (Vervelde et al., 2013). On the other hand,
as well as cells on the mucosal surface, detect evolutionarily CD59 is also reported to be down-regulated in IBV-infected cells
conserved structures on pathogens, termed pathogen associated and is found to be associated with IBV virions, protecting IBV
molecular patterns (PAMPs). PAMPs are recognized upon bind- from complement-mediated lysis (Wei et al., 2017).
ing to membrane associated or intra-cellular Toll-like receptors
(TLRs) (Akira, 2001). Adaptive immunity
In chickens, TLR3 and TLR7 are most extensively Adaptive immunity involves the activation of antigen-specific
studied in viral infection. TLR3 serves two roles in viral infec- B-cells (humoral), T-cells (cellular), macrophages and memory
tion: first, to recognize and bind to double-stranded RNA cells (Chaplin, 2010). The cross-neutralization test developed by
(dsRNA) produced during viral replication (Alexopoulou et Fabricant (1951) has enabled the detection and quantification