Early and transient induction of nitric oxide (NO) in infectious bursal disease virus infection is T-cell dependent: a study in cyclosporin-A treated chicken-model.

The level of nitric oxide (NO) in the supernatants of mitogen (PHA) stimulated lymphocyte cultures from infectious bursal disease (IBD) virus infected T-cell suppressed and immune competent chickens was monitored. The immune competent chickens when infected with IBD virus showed 4-6 folds increased levels of NO as compared to uninfected chickens. The levels of NO in T-cell suppressed chickens were comparable to uninfected control chickens, in spite of markedly increased hemorrhage suggesting that the muscular hemorrhage observed in IBD in not solely and directly related with NO production. The immune suppressed chickens that did not induce NO production after IBD virus infection showed more severe lesions and supported enhanced virus replication. Taken together it may be suggested that NO production after IBD virus infection, may exert antiviral effect since the immune-suppressed chickens that failed to induce NO showed more severe disease and higher magnitude of virus replication, but does not seem to correlate with the hemorrhagic lesions which in fact may be as a result of the net outcome of various host-factors and the determinants responsible for virus virulence and virus clearance.

Infiltration by CD4+ and CD8+ lymphocytes in bursa of chickens infected with Infectious Bursal Disease Virus (IBDV): strain-specific differences.

In order to investigate if there is any definite correlation between the degree of T-cell response in the bursa of Fabricius (BF) and the virulence of Infectious Bursal Disease (IBD) virus strains, chickens were infected with strains of different virulence i.e. mild (Lukert strain), intermediate (Georgia strain) or invasive intermediate (IV-95 strain). At various times post-inoculation, bursal samples were collected to study virus specific histopathological lesions, the distribution of viral antigen and the extent of T-cell infiltration in the bursa. Most severe bursal lesions were induced by IV-95 strain (the invasive intermediate strain), whereas Lukert, the mild strain caused the least severe lesions. The number of virus positive cells in the bursa was highest in chickens infected with IV-95 strain. Substantial infiltration of CD4+ and CD8+ T-cells in the bursal follicles of virus-infected groups was observed from 4 d.p.i. onwards. The magnitude of T-cell response was more in the birds infected with intermediate (Georgia) or invasive intermediate strains of virus than chickens inoculated with mild (Lukert) strain, even when 10-fold higher doses of the inoculums were used. PHA responses to peripheral lymphocytes were found suppressed in all the groups of chickens only transiently. The results indicate that the magnitude of T-cell responses in BF during IBDV infection is influenced more by the virulence of virus strain rather than the quantum of viral load in BF. Over all these studies may have implications in understanding the role of T-cells in pathogenesis and immunity in IBD.