Characteristics of Bursal T Lymphocytes Induced by Infectious Bursal Disease Virus

Abstract

Infectious bursal disease virus (IBDV) is an avian lymphotropic virus that causes immunosuppression.When specific-pathogen-free chickens were exposed to a pathogenic strain of IBDV (IM), the virus rapidly destroyed B cells in the bursa of Fabricius. Extensive viral replication was accompanied by an infiltration of T cells in the bursa. We studied the characteristics of intrabursal T lymphocytes in IBDV-infected chickens and examined whether T cells were involved in virus clearance. Flow cytometric analysis of single-cell suspensions of the bursal tissue revealed that T cells were first detectable at 4 days postinoculation (p.i.). At 7 days p.i., 65% of bursal cells were T cells and 7% were B cells. After virus infection, the numbers of bursal T cells expressing activation markers Ia and CD25 were significantly increased (P < 0.03). In addition, IBDV-induced bursal T cells produced elevated levels of interleukin-6-like factor and nitric oxide-inducing factor in vitro. Spleen and bursal cells of IBDV-infected chickens had upregulated gamma interferon gene expression in comparison with virus-free chickens. In IBDV-infected chickens, bursal T cells proliferated in vitro upon stimulation with purified IBDV in a dose-dependent manner (P < 0.02), whereas virus-specific T-cell expansion was not detected in the spleen. Cyclosporin A treatment, which reduced the number of circulating T cells and compromised T-cell mitogenesis, increased viral burden in the bursae of IBDV-infected chickens. The results suggest that intrabursal T cells and T-cell-mediated responses may be important in viral clearance and promoting recovery from infection.Infectious bursal disease virus (IBDV), an avian B-lymphotropic virus, causes an acute productive infection in actively dividing immunoglobulin M-expressing (IgM ϩ ) B cells (16,28). The bursa is the principal reservoir of virus replication, and peak virus titers in the bursa can be detected between 3 to 5 days after IBDV infection (20,38). The bursa of Fabricius is a unique, primary lymphoid organ in avian species, where B lymphocytes maturate and differentiate (14). The bursal follicles consist of B lymphocytes (85 to 95%), T cells (Ͻ4%), and other nonlymphoid cells (4,10,21,31). In the bursae of chickens infected with IBDV, productive viral replication is often associated with necrosis, apoptosis of lymphoid cells, inflammatory change, atrophy, and hemorrhages (16,25,38,42). Chickens infected with IBDV experience suppression in both humoral (8,13,32,39) and cellular (5, 23, 32) immunity. Humoral immunosuppression appears to be associated with IBDV-induced B-cell destruction, while the mechanism of cellular immunosuppression is largely elusive.Because viral replication is self-limiting, birds recover from the pathogenic effects of the virus. After the acute phase of the infection subsides, the bursal follicles become repopulated with B cells and immune competence is reestablished (24). The mechanisms that limit virus replication and promote recovery are not known and may involve virus-spe...

Comparison ofin ovoand post‐hatch vaccination with particular reference to infectious bursal disease. A review

“…In a 51Cr-release cytotoxicity assay, non-specific cytotoxic cell reactivity was detected both after in ovo and/or at hatch vaccinated chicks against In IBDV infected chickens during the peak infiltration of T-cells noted at 7 days post infection, CD8+ T-cells were relatively higher in number than CD4+ T-cells (49,99). T-cell aggregates may be important in bursal recovery and follicular repopulation after IBDV infection.…”

Enhanced immunopathology induced by very virulent infectious bursal disease virus

“…The mechanisms underlying the pathology caused by classical virulent and variant IBDV and of those relating to the immune clearance of the virus have begun to be elucidated. Tanimura & Sharma (1997) and Kim et al (2000) have suggested that T cells are induced during an IBDV infection in the bursa, but phenotypic characterization is still required. Rodenberg et al (1994) studied changes in the T-cell subsets within the blood, bursa, spleen and thymus after infection with classical virulent IBDV and suggested that, although the number of immunoglobulin (Ig)M ' cells in the bursa and spleen decreased significantly, the relative proportions of CD4 ' and CD8 ' T cells did not change.…”

Changes in the Cytokine and Toll-Like Receptor Gene Expression Following Infection of Indigenous and Commercial Chickens With Infectious bursal disease virus

“…One of the genes (TLR3) was also subjected to RT-PCR that confirmed the results of microarray. Microarray analysis and qRT-PCR were performed on day 3 post-infection to correspond with the known peak of IBDV acute phase [10,11]. The basal expression levels of IL15 and IL16 were different between mock-infected indigenous Vs commercial chickens with inherent increased IL-16 expression in indigenous chickens indicating inherent genetic differences between these two groups of chickens.…”