[Rapid differentiation between very virulent and classical infectious bursal disease viruses isolated in Iran by RT-PCR/REA]

This study was conducted to characterize infectious bursal disease virus [IBDV] isolates collected from different parts of Iran during 2005-2006. Pooled bursal samples from 49 broiler and layer pullet flocks suspected to IBD infection were collected and processed. A reverse transcriptase-polymerase chain reaction [RT PCR] procedure was used to amplify a VP2 gene fragment [743 bp] from IBDV field isolates. Amplified VP2 fragments were further characterized by two restriction enzymes, BspMI and Sad. From 49 field samples, 37 [75.5%] samples were IBDV positive by RT PCR. Digestion with two restriction enzymes, BspMI and SacI, showed patterns compatible with very virulent IBDV and classical IBDV strains in 34 [91.9%] and 3 [8.1%] IBDV-positive samples, respectively. The restriction enzyme analysis of this study was comparable to that of other isolates and reference strains with available nucleotide sequence data in the GenBank. The procedure followed in this study is a useful method to rapidly differentiate the very virulent IBDV and classical IBDV isolates

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.