Infectious bursal disease virus of chickens: pathogenesis and immunosuppression

Citation
Jm. Sharma et al., Infectious bursal disease virus of chickens: pathogenesis and immunosuppression, DEV COMP IM, 24(2-3), 2000, pp. 223-235
Citations number
52
Categorie Soggetti
Animal Sciences",Immunology
Journal title
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
ISSN journal
0145305X → ACNP
Volume
24
Issue
2-3
Year of publication
2000
Pages
223 - 235
Database
ISI
SICI code
0145-305X(200003/04)24:2-3<223:IBDVOC>2.0.ZU;2-F
Abstract
Infectious bursal disease virus (IBDV) is an important immunosuppressive vi rus of chickens. The virus is ubiquitous and, under natural conditions, chi ckens acquire infection by the oral route. IgM + cells serve as targets for the virus. The most extensive virus replication takes place in the bursa o f Fabricius, The acute phase of the disease lasts for about 7-10 days. With in this phase, bursal follicles are depleted of B cells and the bursa becom es atrophic. Abundant viral antigen can be detected in the bursal follicles and other peripheral lymphoid organs such as the cecal tonsils and spleen. CD4(+) and CD8(+) T cells accumulate at and near the site of virus replica tion. The virus-induced bursal T cells are activated, exhibit upregulation of cytokine genes, proliferate in response to in vitro stimulation with IBD V and have suppressive properties. Chickens may die during the acute phase of the disease although IBDV induced mortality is highly variable and depen ds, among other factors, upon the virulence of the virus strain. Chickens t hat survive the acute disease clear the virus and recover from its patholog ic effects. Bursal follicles are repopulated with IgM(+) B cells. Clinical and subclinical infection with IBDV may cause immunosuppression. Both humor al and cellular immune responses are compromised. Inhibition of the humoral immunity is attributed to the destruction of immunoglobulin-producing cell s by the virus. Other mechanisms such as altered antigen-presenting and hel per T cell functions may also be involved. Infection with IBDV causes a tra nsient inhibition of the in vitro proliferative response of T cells to mito gens. This inhibition is mediated by macrophages which are activated in vir us-exposed chickens and exhibit a marked enhancement of expression of a num ber of cytokine genes, We speculate that T cell cytokines such as interfero n (IFN)-gamma may stimulate macrophages to produce nitric oxide (NO) and ot her cytokines with anti-proliferative activity. Additional studies are need ed to identify the possible direct immunosuppressive effect of IBDV on T ce lls and their functions. Studies are also needed to examine effects of the virus on innate immunity. Earlier data indicate that the virus did not affe ct normal natural killer (NK) cell levels in chickens. (C) 2000 Published b y Elsevier Science Ltd. All rights reserved.