In vitro Infection of Fractionated Chicken Lymphocytes by Infectious Bursal Disease Virus

Nakai, T; Hirai, Katsuya

doi:10.2307/1590057

Cited by 27 publications

(13 citation statements)

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“…It is therefore assumed that the bursa is the target organ of IBD. Differences in the susceptibility of B-and T-cells to pathogenic IBDV support this view (Hirai and Calnek, 1979;Nakai andHirai, 1981, 1984). However, Lucio and Hitchner (1980) have challenged this following their demonstration that chickens treated with a synthetic androgen (mibolerone) developed bursal atrophy and had more severe IBD than the untreated.…”

Section: Introductionmentioning

confidence: 90%

Pathogenesis of infectious bursal disease in embryonally bursectomised chickens

Okoye

Uzoukwu

1990

Avian Pathology

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Section: Introductionmentioning

confidence: 90%

Pathogenesis of infectious bursal disease in embryonally bursectomised chickens

Okoye

Uzoukwu

1990

Avian Pathology

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“…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).…”

mentioning

confidence: 99%

Characteristics of Bursal T Lymphocytes Induced by Infectious Bursal Disease Virus

Kim¹,

You

Kim

et al. 2000

J Virol

119

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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...

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“…The disease is clinically characterized by dullness, depression, loss of appetite, white watery diarrhoea, soiled vent, ruffled feathers, severe prostration followed by death. The virus infects dividing IgM+ B lymphocytes and the main site of viral replication is the bursa of Fabricius, where B cells are produced (Nakai and Hirai, 1981; …”

Section: Introductionmentioning

confidence: 99%