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Bhuiyan, M.S. Antiviral Response Against Infectious Bronchitis Virus in Poultry. Encyclopedia. Available online: (accessed on 29 November 2023).
Bhuiyan MS. Antiviral Response Against Infectious Bronchitis Virus in Poultry. Encyclopedia. Available at: Accessed November 29, 2023.
Bhuiyan, Md. Safiul. "Antiviral Response Against Infectious Bronchitis Virus in Poultry" Encyclopedia, (accessed November 29, 2023).
Bhuiyan, M.S.(2021, November 26). Antiviral Response Against Infectious Bronchitis Virus in Poultry. In Encyclopedia.
Bhuiyan, Md. Safiul. "Antiviral Response Against Infectious Bronchitis Virus in Poultry." Encyclopedia. Web. 26 November, 2021.
Antiviral Response Against Infectious Bronchitis Virus in Poultry

Infectious bronchitis virus (IBV) is the causative agent of multi-systemic infection in the respiratory, reproductive and renal systems, which is similar to the symptoms of various viral and bacterial diseases reported in chickens. Currently, the live attenuated and killed vaccines are applied for the control of IBV infection; however, the continual emergence of IB variants with rapidly evolving genetic variants increases the risk of outbreaks in intensive poultry farms.

infectious bronchitis virus vaccination immune system

1. Introduction

Infectious Bronchitis Virus (IBV) is an acute and highly contagious respiratory pathogen of chicken that has a major economic impact on poultry stakeholders. The mutable tissue tropism and continuous emergence in various serotypes or genotypes of IBV are prevalent across various geographic regions. As a consequence of the severity and highly contagious nature of IBV infection, it has been implicated in higher economic loss in breeders and layer chickens attributed to reproductive disorders and renal dysfunction. Long-term impacts on the reduction in egg production (up to 20–70%) and loss of egg quality for trade and hatching are observed [1]. IBV infection can cause up to 10–60% mortality over 4–6 weeks of age and poor weight gain in broilers [2][3]. Several studies confirmed that IBV could persist over the long term in tissues and can be transmitted via the faeces of virus-infected chickens at 163–227 days post-infection [1][4][5].
IBV belongs to gammacoronavirus (γCoV) or Group-3 coronavirus (order Nidovirales, family Coronaviridae) with a positive-sense single-stranded RNA, (+) ssRNA and genome of approximately 27 kb with gene organization: 5′UTR-1a/1ab-S-3a-3b-E-M-5a-5b-N-3′UTR [6]. On the basis of their antigenic cross-reactivity and phylogenetic analysis, CoVs are classified into three major groups [7]: major antigenically related Group-1 of CoVs includes porcine transmissible gastroenteritis virus (TGEV), Feline coronavirus (FCoV) and Canine coronavirus (CCoV). Group-2 comprises Bovine coronavirus (BCoV), Equine coronavirus (ECoV), Murine hepatitis virus (MHV) and Rat coronavirus (RtCoV). Group-3 includes IBV, Turkey Coronavirus (TCoV) and Pheasant Coronavirus [8]. The family Coronaviridae is further divided into two subfamilies: Coronavirinae and Torovirinae. The Coronavirinae subfamily comprises four genera of viruses such as Alphacoronavirus (αCoV), Betacoronavirus (βCoV), γCoV and Deltacoronavirus (δCoV) based on morphology and genome structure [9][10][11]. The first two genera αCoV and βCoV are confined to mammalian CoVs and human CoVs, which are highly pandemic, possess overwhelming spillovers in current history and have raised the significance of public health such as SARS-CoV-2 (etiological agent of COVID-19) and Middle East respiratory syndrome coronavirus (MERS-CoV) [12][13][14]. On the other hand, the other two genera such as γCoV or δCoV usually infects in all kinds of avian species, including chicken, pheasants and galliformes [15]

2. Vaccination

Vaccination is the most effective method for the prevention and control of IBV. Several commercially developed vaccines are available, and their delivery techniques vary depending on vaccine and countrywide local situations. The ideal characteristics of IBV vaccines are as follows: (1) vaccine immunity must be long-term, otherwise re-vaccination is necessary; (2) the selection of the correct antigenic type of vaccination that is specified for wide antigenic variation in order to cover the maximum virulent serotypes; and (3) timing, technique and applications of vaccine according to flock’s status. Expression and delivery systems of various kinds of IBV vaccine with their existing features are shown in Table 1.
Table 1. Routes of delivery of various IBV vaccines with their associated characteristics.
Name of the Vaccine Route of Delivery Characteristics
1. Live attenuated IBV or Aero nasal spray Serial attenuation of virulent IB strain for weakened
Live IBV vaccines In Ovo route virulence [16][17].
  Subcutaneous (S/C)  
2. Killed or inactivated IM injection Inactivated by chemical treatment or heat treat to kill the
IB vaccines S/C virulence of strain [18].
3. Viral Vector vaccine In ovo route Recombinant rNDV/APMV-2 expressing the S protein of
    IBV strain Mass-41 (rNDV/APMV-2/IBV-S) [19].
4. DNA vaccine Mucosal/Orally IBV-DNA vaccine carrying S1-protein and/or N-protein constructs
  IM injection the respective vector [20][21][22][23].
  In ovo route  
5. Recombinant protein
IM injection
Water-in-oil emulsified recombinant S-ectodomain protein [24].
    Second heptad repeat (HR2) region of S protein were
    repeatedly co-displayed in the Self-assembling
    Protein Nanoparticle (SAPN) [25].
6. Multi-epitope-based Oral Using attenuated S enterica serovar Typhimurium strain [26].
peptide vaccine Mucosal Recombinant DNA: The EpiC gene was presented in
(Lactococcus lactis bacterial
Intranasal Lactococcus lactis NZ3900 with 3 recombinant strains
expressing EpiC gene [27].
7. VLP-based IBV vaccine or IM immunized Efficient mucosal immune response [28]
chimeric VLP vaccine  

Currently, IBV vaccination programs have gained more attention with respect to the use of low-virulent, live or inactivated killed vaccines with the aim of booster shots at certain times to increase immunity and reduce the antagonistic response of epithelial cells in the respiratory region [29]. However, there is a significant limitation in applying live IBV vaccines because the attenuation of the vaccine is naturally deficient with respect to its capability in stimulating a mucosal immune response [30][31], which is a critical part of controlling IBV infection since killed vaccine can be an option [32][33]. Nonetheless, it was possible that inactivated killed vaccines can be applied to stimulate t mucosal immune responses once combined with several nanoparticles [32]. Different types of IBV vaccines are available in the market, which may vary in vaccine strains, and in nature based on local isolate and recombination in strains isolated from different countries with special legal legislation (Figure 1). Bijlenga et al. [34] described the earlier development of the H strain of IBV containing both the H52 and H120 due to its better capability of heterologous cross-protection against different serotypes of IBV. Further studies have revealed that heterologous IBV vaccines are also more effective for immunizing the 793B-type of variant that has been evidenced to be long lasting with live attenuated IB vaccines and are effectively applied against Italy 02 and QX stain [35][36][37]. The modified live vaccines and inactivated oil emulsions are available for a few serotypes such as Massachusetts, Connecticut and Arkansas in North America. The California strains and Georgia 98 vaccines are collected from the USA. 

Figure 1. Different types of IBV vaccines are manufactured in the world based on the specific strain.

3. Immune Response against IBV

Various defense mechanisms have shown to neutralize a virus for the sake of building up the immune system in the chicken body against IBV. Primarily, the virus enters the body system and is detected and neutralized by the non-specific immune response [38]. Various types of specialized cells are engaged in the immune system that is a critical contributor to the innate and adaptive immune responses shown in Figure 1. Innate immunity is the first line of defense that is involved with physical and chemical barriers and cellular machinery, e.g., phagocytic cells [39], complement [40] and natural killer cells [41]. In contrast, adaptive immunity is characterized with a highly specific response facilitated by T (helper or cytotoxic cells) and B cells (humoral immunity), resulting in a response against infection and the activation of memory cell for recurrent exposure to similar viruses [38][42]. Several innate immune factors, such as heterophils, macrophages, natural killer cells, complement and pattern recognition receptors (PRRs), have been proposed to play a vital role in the induction of immune response against IBV; nevertheless, some factors have yet to be identified [28].

3.1. Local Immune System

A vaccine requires a certain period of time in order to elicit a protective immune response in avian hosts. Moreover, passive immunization can induce immunity from maternal derivative’s antibody (MDA), which is particularly supportive during the early stages of life [43]. The structure and function of birds’ immune systems are distinctly different from human immune systems due to their virtue of possessing extra lymphatic organs such as the bursa of Fabricius and the thymus responsible for humoral and cellular immunity, respectively. Furthermore, the birds have carried the secondary peripheral organs of the lymphatic system, for example, the Harderian gland (HG), conjunctiva associated lymphoid tissue (CALT), head associated lymphoid tissue (HALT), gut-associated lymphoid tissue (GALT) and bronchus associated lymphoid tissue (BALT), spleen and cecum tonsils, respectively [44], showed in Figure 2. These assemblies are regularly enmeshed in a chicken’s immune response, especially in the respiratory mucosal system during IBV infection.
Figure 2. The primary and secondary lymphoid organs enmeshed in the immune complex where the mature B and T cells are transferred from primary or lymphoid tissue for the development stage term as immune movement or immune peripheralization.

3.2. Adaptive Immune System

3.2.1. Humoral Immunity

The humoral immune response is triggered by the activation of IBV-specific antibodies to inhibit viral replication and virus circulation in the blood steam or hinders viremia from the trachea, kidneys and oviduct [28][45]. The main function of humoral immunity is to generate antibodies at a certain level through plasma cells with or without the response of T helper cells. Long-term protection against IBV infection might need stimulation of an effector that is memory cell-mediated, which has been described in several studies on the systemic and local humoral immune response to IBV vaccination [3]. However, naive B cells carry surface immunoglobulin and MHC class II molecules on the surface of their antigen-presenting cells (APCs) to form a membrane-spanning bond in order to stimulate the antigen-specific immune response [46]. The immunoglobulins have been identified at days 4–5 after post infection and reached their potential peak at days 21 [47]. Generally, the detection of humoral response to IBV infection is measured by ELISA, HI or VN serological tests by using serum [48].

3.2.2. Cell-Mediated Immunity (CMI)

In chickens, CMI is one of the essential immunoregulatory weapons during IBV infection, especially for aiding the clearance of viruses, decline of infection and reducing virus shedding and vaccine development [49]. The evaluation of cellular arms is performed by lymphocytic transformation assays, cytotoxic lymphocyte activity [50], delayed-type hypersensitivity [51] and natural killer cell activity [52]. Histological lesions of CMI responses are performed by T-cell infiltration in the respiratory and renal tissues of IBV-infected chickens [53]. The experimental studies have shown a positive relationship between lymphoproliferative responses and resistance to challenge infection [23]. Alternative studies have been published on mouse monoclonal antibodies (mAbs) that differentiate between T-lymphocytes and are used to evaluate the role of T-cells in viral clearance [54]. N and S genes have a specific protein response associated with the stimulated virus-specific protective immunity of CTLs, which is characterized by the reduction in viral load and clearance of the virus from circulation [55][56]. A marked increase in CD4+ and CD8+ T-cells has been described as the recombinant S1-gene associated with the induction of cellular immunity of specific IBV vaccines [57]. Guo et al. [58] reported that IB vaccination with N gene-based DNA vaccine significantly increased the number of CD4+ and CD8 + T cells in peripheral blood mononuclear cells (PBMCs). The existence of CD8+ cytotoxic T lymphocytes (CTL) signifies an essential relationship for reducing infection and resembles a decrease in clinical signs by the action of major histocompatibility complex (MHC), and lysis is facilitated by CD8+CD4 cells [59]. Consequently, the major histocompatibility complex organized cytotoxic T lymphocytes (CTL), and the cytokine activities of chickens participated during the early stages of IBV infections [60]. Several studies have been conducted on tracheal immunity induced by live vaccines, and they found that all vaccines induced significantly higher expression of CD4+ and CD8+ compared with unvaccinated birds using a nephron-pathogenic IBV strain [28]. In the following year, other studies have reported that CD4+ cells are recruited into the trachea earlier than CD8+ on 5 dpi (days of post-infection) [61], which agrees with the findings by Kotani et al. [62] who recognized that the frequency of CD4+ and CD8+ cell numbers significantly peaked at 5 dpi when using a virulent IBV strain. In contrast, studies reported that CD8+ cells were recruited into the trachea earlier than CD4+ cells after infection with virulent 793B [63] or live attenuated IBV vaccine [28] or a combination of live attenuated vaccine with a booster dose of an inactivated vaccine [64]. CD8+ memory T cells have greatly protected the newborn chicks from acute IBV infection at 4 dpi and mild clinical symptoms show at 5 dpi [59]. Even though the adoptive transfer of CD4 + T cells could not be significantly protected in the early stage of IBV infection, primed αβ T cells carrying CD8+ T cells are critical in protecting chicks from IBV infection [55]. Chhabra et al. [28] reported that the protection against Q1-IBV strain changes the quantity of CD4+ and CD8+ cells in the trachea using immunohistochemistry. The results showed that the overall patterns of CD8+ cells are dominant compared to those of CD4+ cells in the two vaccinated groups. The kinetics of CD4+, CD8+ and the IgA-carrying B lymphocytes in the trachea are shown in Figure 3B–D) compared with control Figure 3A in vaccinated groups as differences may have a close relationship with the IBV-specific strains.
Figure 3. Immunohistochemically found in Tracheal mucosa as control (A), CD4+ cells (B), CD8+ cells (C) and IgA-bearing B cells in (D) at day 28 of age. Chickens vaccinated with live H120 or combination with CR88 at day 1 and subsequently with booster vaccinations. Arrows specify the positive immune cells (Magnification ×400) (Reprinted with permission from ref. [28]. Copyright 2021 American Society for Microbiology).


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