T-Cell Mediated Immunosuppression And Its Impact On Avian Infectious Bronchitis Virus Persistence In Chickens

Abstract

Although infectious bronchitis (IB) is regarded as an acute respiratory disease of chicken, caused by Infectious Bronchitis Virus (IBV), long-term persistent infection with IBV in experimentally infected tissues such as kidney, caecal tonsil and rectum has been reported by Cook (1968) and Alexander et al (1978). A similar persistence of infection has been observed in fungal infections, where immune modulation, particularly in T-cell responses, plays a critical role in pathogen clearance or persistence (Pathakumari et al., 2022). El Houadfi et al (1986) also reported long-term persistence infection with IBV strain G (IBVG) in intestine of the chicken but not in respiratory tract. Day old chicken infected with IBVG did not excreted virus in their faeces until before 35-day post infection. However, re-excretion occurred when chicken reached their sexual maturity (Jones and Ambali 1987).
Treatment of chickens with oestrogen and progesterone after infection with IBV could not induced viral re-excretion (Ambali and Jones, 1990) but it did occur after T-cell suppression by cyclosporin (CSA) (Bhattacharjee et al., 1995 and Dhinakar Raj and Jones, 1997). This drug (CSA) has been extensively used to study the importance of cellular immunity in a variety of infectious diseases affecting avian species such as turkey haemorrhagic enteritis (Suresh and Sharma 1995), marble spleen disease virus of pheasants (Fitzgerald et al., 1995), reovirus (Hill et al 1989), and avian infectious bronchitis virus (Bhattacharjee et al.,1994; Dhinakar Raj and Jones 1997) CSA has been used as a means of inhibiting the cell-mediated immune response in order to determine the role of T-cells in protective responses to infectious pathogens of chickens (Fitzgerald et al 1996; Hill et al 1989; Isobe et al., 2000; Lillehoj et al., 1987). CSA selectively suppressed T-lymphocyte activity and cell-mediated immunity (Larsson, 1980; hill et al 1989; Ziprin et al 1989). As a consequence, all cell-mediated immune responses driven by cytokines, especially IL-2-dependent functions, which include T-helper activities, cytotoxicity, natural killer cell activity and antibody-dependent cell cytotoxicity, would be deleted after CSA treatment (Schreiber and Crabtree 1992).
The aim of this study was to repeat similar work done in this laboratory (Bhattacharjee et al., 1994; Dhinakar Raj and Jones, 1997), whereby CSA was used to induce re-excretion of IBV after the acute phase of the infection had finished, to attempt to confirm that the kidney is the site of persistence, and to examine re-activated virus for evidence of mutation in the hypervariable region of the S1 spike gene. This was a short –term experiment which might suggest whether a longer-term infection would result in the generation of a genotypically different virus or viruses.