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Photomicrographs (40x magnification) of H&E stained lung sections from IBV infected and uninfected control chickens at 1, 2, 3, 5 and 7 dpi are shown. Inflammatory cell infiltration and haemorrhage into the parabronchi and parabronchial lumen can be seen in the infected lungs compared to uninfected control Lungs.
Source publication
Infectious bronchitis virus (IBV) infection is a major cause of economic losses to the poultry industry. Due to limitations in current control measures, alternative approaches, based on thorough understanding of the host responses are required. As one of the key component of the avian immune system, the innate immune system has a crucial role in li...
Citations
... Awad et al. (2015) showed that the combined vaccination of H120 and CR88 (a 793B strain) at 1-day-old chicks, followed by CR88 at 14 days old, achieved greater protection against the Middle East isolates (IS/885/00like and IS/1494/06-like); also, Chhabra et al. (2015) suggested great protection for the Q1 IBV strain when using the same vaccine protocol. In addition to the adaptive host response that contributes to the control of IBV in infected chickens, the innate host response is also important and considered the first line of defense against infection (Akira, 2001;Chhabra et al., 2015;Amarasinghe et al., 2018b). As a part of the innate host response, the cytokines are considered critical components, as shown in other host-virus infection models (Amarasinghe et al., 2018b;. ...
... In addition to the adaptive host response that contributes to the control of IBV in infected chickens, the innate host response is also important and considered the first line of defense against infection (Akira, 2001;Chhabra et al., 2015;Amarasinghe et al., 2018b). As a part of the innate host response, the cytokines are considered critical components, as shown in other host-virus infection models (Amarasinghe et al., 2018b;. The information related to the significance of innate immunity in the early time of vaccination and/or infection with IBV in the kidneys of chickens is inadequate. ...
Background
Being a ubiquitous, highly contagious virus with a continuous mutation and a large number of evolutions worldwide, the infectious bronchitis virus (IBV) continues to wreak problems among Egyptian chickens and generate economic losses. The commonly applied IBV vaccination protocols in broilers include alternatives to classic and/or variant attenuated live virus vaccines.
Aim
The current study targeted to assess the protective efficacy of concurrent and successive Ma5 and 4/91 vaccine strain regimens against the field variant II IBV strain (IBV-EGY-ZU/Ck-127/2021) in chickens.
Methods
Commercial broiler chickens were vaccinated with Ma5 and 4/91 strains simultaneously at 1 and 14 days of age. The evaluation parameters included clinical protection and humoral and early innate immunity aspects in the renal tissues of vaccinated and infected birds.
Results
The vaccine regimen ameliorated the clinical and histopathological lesions against variant II IBV and enhanced body gain as well as succeeded in preventing tracheal shedding and minimizing cloacal shedding of the field virus. The IL-1β mRNA gene expression was evident as early as 24 hours, with highly significant upregulation at 48 hours post vaccination and 24 hours post challenge (PC) in vaccinated birds. Remarkable upregulation was observed in oligoadenylate synthetases (OAS) expression 48 hours PC in vaccinated and unvaccinated infected birds. The vaccinated birds developed a significant antibody titer of 704.0 ± 111.98 at 28 days of age, with a consistent antibody titer increase after the challenge.
Conclusion
Overall, a combination of heterologous protectotype commercial vaccines achieved good protection against the Egyptian variant II IBV strain. This vaccine program could be an effective protocol against the threat posed by IBV viruses circulating in the Egyptian field.
... Double immunofluorescence staining for colocalization of IBV-antigen and COX-2 protein was carried out in macrophages as previously described [45,46]. The cells were grown on glass coverslips (VWR International, Radnor, Pennsylvania, USA) in 12-well plates (Corning Incorporated, Corning, New York, USA). ...
... Chicken macrophages play a pivotal role during IBV infection. Not only does IBV target macrophages in vitro and in vivo for replication, but it also alters the host responses induced by macrophages [10,46]. Previous studies examining IBV replication in avian macrophages reveals strain-dependent responses. ...
... Based on the findings of the current study and the observations of others [32,41,46,47], we propose the model of induction of COX-2/PGE2 and pro-inflammatory mediators as illustrated in Fig. 8. Briefly, IBV infection potentially increases the expression of TLR 3 and 7, leading to recognition of IBV RNA molecules in chicken macrophages. This TLR 3 and 7 recognition of IBV RNA activates the downstream signalling molecules, such as MAPK and JAK, leading to the production of COX-2 and mRNA expression of iNOS and IL-6. ...
Infectious bronchitis virus (IBV) is a significant respiratory pathogen that affects chickens worldwide. As an avian coronavirus, IBV leads to productive infection in chicken macrophages. However, the effects of IBV infection in macrophages on cyclooxygenase-2 (COX-2) expression are still to be elucidated. Therefore, we investigated the role of IBV infection on the production of COX-2, an enzyme involved in the synthesis of prostaglandin E2 (PGE2) in chicken macrophages. The chicken macrophage cells were infected with two IBV strains, and the cells and culture supernatants were harvested at predetermined time points to measure intracellular and extracellular IBV infection. IBV infection was quantified as has been the COX-2 and PGE2 productions. We found that IBV infection enhances COX-2 production at both mRNA and protein levels in chicken macrophages. When a selective COX-2 antagonist was used to reduce the COX-2 expression in macrophages, we observed that IBV replication decreased. When IBV-infected macrophages were treated with PGE2 receptor (EP2 and EP4) inhibitors, IBV replication was reduced. Upon utilizing a selective COX-2 antagonist to diminish PGE2 expression in macrophages, a discernible decrease in IBV replication was observed. Treatment of IBV-infected macrophages with a PGE2 receptor (EP2) inhibitor resulted in a reduction in IBV replication, whereas the introduction of exogenous PGE2 heightened viral replication. Additionally, pretreatment with a Janus-kinase two antagonist attenuated the inhibitory effect of recombinant chicken interferon (IFN)-γ on viral replication. The evaluation of immune mediators, such as inducible nitric oxide (NO) synthase (iNOS), NO, and interleukin (IL)−6, revealed enhanced expression following IBV infection of macrophages. In response to the inhibition of COX-2 and PGE2 receptors, we observed a reduction in the expressions of iNOS and IL-6 in macrophages, correlating with reduced IBV infection. Overall, IBV infection increased COX-2 and PGE2 production in addition to iNOS, NO, and IL-6 expression in chicken macrophages in a time-dependent manner. Inhibition of the COX-2/PGE2 pathway may lead to increased macrophage defence mechanisms against IBV infection, resulting in a reduction in viral replication and iNOS and IL-6 expressions. Understanding the molecular mechanisms underlying these processes may shed light on potential antiviral targets for controlling IBV infection.
... The upregulation of four innate immune factors, Interferon (IFN)-α, IFN-β, IL-6 and IL-1B, within the cell lysate of CK cells infected with either BeauR-T16A, BeauR-A26F or Beau-R ( Figure 10) was examined. These factors were selected as they have previously been shown to be upregulated during IBV infection [53][54][55][56]. qRT-PCRs determined comparable levels of IBVderived RNA between samples, suggesting comparable replication kinetics ( Figure 10A). ...
The envelope (E) protein of the avian coronavirus infectious bronchitis virus (IBV) is a small-membrane protein present in two forms during infection: a monomer and a pentameric ion channel. Each form has an independent role during replication; the monomer disrupts the secretory pathway, and the pentamer facilitates virion production. The presence of a T16A or A26F mutation within E exclusively generates the pentameric or monomeric form, respectively. We generated two recombinant IBVs (rIBVs) based on the apathogenic molecular clone Beau-R, containing either a T16A or A26F mutation, denoted as BeauR-T16A and BeauR-A26F. The replication and genetic stability of the rIBVs were assessed in several different cell types, including primary and continuous cells, ex vivo tracheal organ cultures (TOCs) and in ovo. Different replication profiles were observed between cell cultures of different origins. BeauR-A26F replicated to a lower level than Beau-R in Vero cells and in ovo but not in DF1, primary chicken kidney (CK) cells or TOCs. Genetic stability and cytopathic effects were found to differ depending on the cell system. The effect of the T16A and A26F mutations appear to be cell-type dependent, which, therefore, highlights the importance of cell type in the investigation of the IBV E protein.
... The downstream signaling of Toll-like receptors (TLRs) is conducted via MyD88 adaptors, which in turn activates NF-k B and the subsequent expression of downstream cytokines (29). IL-1b, IL-8, and IL-18 are important cytokines regulating the inflammatory responses at the site of infection (30,31). Previous studies reported significant upregulations of IL-1b, IL-8, and IL-18 in the livers of pathogenic FAdV-4 infected chickens, which is consistent with our results (27,32). ...
HHS induced by FAdV-4 has caused huge economic losses to the poultry industry. The key determinants for the different virulence of FAdV-4 have not been fully elucidated.
... The immunofluorescence signal intensity of the target proteins (NF-kB and IFN-g) was quantitatively analyzed, and the target proteins were locally analyzed. The specific procedures are similar to those described by Amarasinghe et al. (Amarasinghe et al., 2018). ...
Nephropathogenic infectious bronchitis virus (NIBV) is one of the most important viral pathogens in the world poultry industry. Here, we used RT–qPCR, WB and immunofluorescence to explore the interaction between NIBV and the host innate immune system of the kidney. Multiple virions were found in the kidney tissues of the disease group under electron microscopy, and pathological changes such as structural damage of renal tubules and bleeding were observed by HE staining. In addition, we found that the mRNA levels of TLR7, TRAF6, and IKKβ were upregulated after NIBV infection. IRF7 mRNA levels decreased significantly at 5 dpi and increased significantly at 11 to 18 dpi. The NF-κB P65 mRNA level increased significantly at 5 to 18 dpi and decreased at 28 dpi. However, NIBV infection-induced NF-κB P65 protein levels were downregulated at multiple time points. Moreover, we demonstrated that the cytokine (IFN-γ, IL-8, and IL-6) mRNA and protein expression levels were increased significantly at multiple time points after NIBV infection. Furthermore, immunofluorescence analysis showed that NF-κB P65 and IFN-γ were mainly located in the nuclear or perinuclear region. The positive signal intensity of NF-κB P65 was significantly lower than that of the normal group at 1 to 5 dpi, and there was no significant change in the subsequent time period. The positive signal intensity of IFN-γ decreased significantly at 5 dpi, and increased significantly at 11 to 28 dpi. In conclusion, we found that NIBV promoted cytokine release through the TLR7/NF-κB signaling axis, thus causing kidney injury.
... Infectious bronchitis (IB) is an acute, highly contagious disease responsible for remarkably significant economic losses in the poultry industry worldwide [1] . The disease was first documented in 1931 in the USA and is caused by the avian infectious bronchitis virus (IBV) [2] , a single-stranded RNA virus belonging to the Coronaviridae family of order Nidovirales [3] . ...
... The disease was first documented in 1931 in the USA and is caused by the avian infectious bronchitis virus (IBV) [2] , a single-stranded RNA virus belonging to the Coronaviridae family of order Nidovirales [3] . IBV primarily causes respiratory infection and can also cause infection according to its strain in the digestive, urinary, and reproductive systems, leading to reduced egg production [1] . The continuous emergence of new antigenic and genetic variants of IBV is due to its high substitution and recombination rate characterizations with heterogeneous biological and immunological properties [4] . ...
... IL-1β has been demonstrated to play an important role in other poultry diseases as well. Infectious bronchitis virus (IBV) infection induces upregulation of IL-1β expression in the trachea and lungs of chickens [36]. Anti-IL-1β neutralizing antibody treatment was found to decrease the mortality rate in chickens after infection with virulent NDV [37]. ...
Hepatitis-hydropericardium syndrome (HHS), caused by fowl adenovirus serotype 4 (FAdV-4), has spread on chicken farms worldwide, causing huge economic losses. Currently, the exact mechanism of pathogenesis of FAdV-4 remains unknown. Despite the severe inflammatory damage observed in chickens infected with pathogenic FAdV-4, few studies have focused on the host immune system-virus interactions and cytokine secretion. Host immunity acts as one of the most robust defense mechanisms against infection by pathogens, and cytokines are important in their elimination. However, excessive inflammatory cytokine secretion could contribute to the pathogenesis of FAdV-4. Understanding of the roles of cytokines produced during FAdV-4 infection is important for the study of pathogenicity and for developing strategies to control FAdV-4. Several previous studies have addressed the immune responses to FAdV-4 infection, but there has not been a systematic review of this work. The present review provides a detailed summary of the current findings on cytokine production induced by FAdV-4 infection to accelerate our understanding of FAdV-4 pathogenesis.
... The number of macrophages in respiratory lavage fluid, embryonic tissues, trachea, and lung was increased after IBV inoculation [25,26]. In respiratory tracts, the increased macrophages were accompanied by reduced IBV viral loads, as well as production of interleukin-1β (IL-1β) [27]. In vitro studies showed a decreased viability and phagocytic ability of HD11 chicken macrophage cells and chicken peripheral blood mononuclear cell-derived macrophages (PBMCs-Mϕ) after infection by the respiratory M41 IBV strain. ...
... Other cytokines and chemokines are also crucial regulators of innate immune responses against viral infection. For instance, correlated with recruited macrophages, production of IL-1β was involved in reducing IBV viral loads in the respiratory tract [27]. In addition, upregulation of IFN-α, IFN-γ, and IL12 at 12 hpi, upregulation of IFN-γ, IL-8, and macrophage inflammatory protein (MIP)-1β at 48 hpi, and upregulation of IFN-γ and IL-6 at 72 hpi were also observed, and the upregulation of these cytokines was associated with inhibition of respiratory IBV Ark99 replication [77]. ...
Avian infectious bronchitis virus (IBV) is an important gammacoronavirus. The virus is highly contagious, can infect chickens of all ages, and causes considerable economic losses in the poultry industry worldwide. In the last few decades, numerous studies have been published regarding pathogenicity, vaccination, and host immunity-virus interaction. In particular, innate immunity serves as the first line of defense against invasive pathogens and plays an important role in the pathogenetic process of IBV infection. This review focuses on fundamental aspects of host innate immune responses after IBV infection, including identification of conserved viral structures and different components of host with antiviral activity, which could provide useful information for novel vaccine development, vaccination strategies, and intervention programs.
... ages and breeds. IBV mainly transmitted through the respiratory tract through droplets coughed by sick chickens, which is extremely contagious, and it is particularly easy to spread quickly through the air [35,36]. Various strains of IBV cause disease that varies in severity from mild respiratory problems to nephropathology and reproductive organ illness [36,37]. ...
Dendritic cells are first guard to defend avian infectious bronchitis virus (IBV) infection and invasion. While IBV always suppress dendritic cells and escape the degradation and presentation, which might help viruses to transfer and migrant. Initially, we compared two IBV's function in activating avian bone marrow dendritic cells (BMDCs) and found that both IBV (QX and M41) did not significantly increase surface marker of avian BMDCs. Moreover, a significant decrease of m⁶A modification level in mRNA, but an increased in the ut RNA were observed in avian BMDCs upon the prevalent IBV (QX) infection. Further study found that both non-structural protein 7 (NSP7) and NSP16 inhibited the maturation and cytokines secretion of BMDCs, as well as their antigen-presentation ability. Lastly, we found that gga-miR21, induced by both NSP7 and NSP16, inhibited the antigen presentation of avian BMDCs. Taken together, our results illustrated how IBV inhibited the antigen-presentation of avian DCs.
... Interleukin 1β, one of the pro-inflammatory cytokines binds to cell surface receptors on infected cells and initiates recruitment of several immune and inflammatory cells including macrophages, dendritic cells, and other antigen-presenting cells (APCs) to the site of infection. Activated macrophages initiate inducible nitric oxide synthases (iNOS), which catalyze the production of nitric oxide (NO), inducing antiviral responses [58]. Macrophages, which are important for phagocytosis, also produces cytokines (Interleukin 1β), and as APCs initiate antigenspecific adaptive immune response. ...
... This is illustrated in Figure 1. Infected macrophages are destroyed through apoptosis [58]. Avian β-defensins (AvBDs), cathelicidins (CATHs) and Prostagladin (PG) E2 (PGE2) are also induced by IBV antigens. ...
Infectious bronchitis (IB) and Newcastle disease (ND) are two important diseases of poultry and have remained a threat to the development of the poultry industry in many parts of the world. The immunology of avian has been well studied and numerous vaccines have been developed against the two viruses. Most of these vaccines are either inactivated vaccines or live attenuated vaccines. Inactivated vaccines induce weak cellular immune responses and require priming with live or other types of vaccines. Advanced technology has been used to produce several types of vaccines that can initiate prime immune responses. However, as a result of rapid genetic variations, the control of these two viral infections through vaccination has remained a challenge. Using various strategies such as combination of live attenuated and inactivated vaccines, development of IB/ND vaccines, use of DNA vaccines and transgenic plant vaccines, the problem is being surmounted. It is hoped that with increasing understanding of the immunological mechanisms in birds that are used in fighting these viruses, a more successful control of the diseases will be achieved. This will go a long way in contributing to global food security and the economic development of many developing countries, given the role of poultry in the attainment of these goals.
Keywords: infectious bronchitis; Newcastle disease; poultry; vaccine; immunity
