Effect of T‐cell suppression by cyclosporin on primary and persistent infections of infectious bronchitis virus in chickens
Open Access
- 1 June 1997
- journal article
- research article
- Published by Taylor & Francis in Avian Pathology
- Vol. 26 (2) , 257-276
- https://doi.org/10.1080/03079459708419210
Abstract
Two‐week‐old white leghorn (WL) chickens were inoculated intra‐nasally with 4.51ogio median ciliostatic doses (CD50) of IBV strain M41. Cyclosporin (CSP) (100 mg/kg body weight) was injected intra‐muscularly 3 days before virus infection and every 3 days till day 15 post‐infection (p.i.). Significant reduction in proliferation responses of whole blood lymphocytes to a T‐cell mitogen, concanavalin A were induced, but not to a B and T‐cell mitogen, pokeweed mitogen. Mortality in the IBV + CSP group was 18%, but in the IBV group it was 2%. No significant differences in the total number of virus isolations were seen between the two groups. Virus titres in trachea, lung and kidneys of the T‐cell suppressed chickens were slightly higher and histopathological lesions more severe. Thus it appeared that T‐cells may play a major role in limiting severity and lethality of IBV infections rather than clearing virus. To confirm this, another experiment was performed in which 2‐week‐old brown leghorn (BrL) chickens, relatively resistant to IBV were infected with a pool of IBV strains. Mortality was 43% in the IBV + CSP group and zero with IBV alone. Earlier reports using the same pool of IBV strains have shown a mortality of 47% in line 151 chicks, a line sensitive to IBV infection. Thus, a resistant line was induced to behave like a susceptible line by T‐cell suppression. Virus titres were always 1 to 3 logs higher in the kidneys of T‐cell suppressed BrL chicks. Attempts to induce re‐excretion of virus by CSP treatment of WL chickens infected with the IBV strain M41 when 2 weeks old were unsuccessful, but when chicks were infected with the same strain at day‐old and given CSP injections from 5 weeks p.i., virus re‐excretion was primarily seen from the kidneys and not the caecal tonsil. Thus the kidney appears to be the primary site of IBV persistence. The pathogenesis of the disease in T‐cell suppressed chickens is discussed.Keywords
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