Infectious bursal disease virus of chickens: Pathogenesis and immunosuppression

Jagdev M. Sharma, In Jeong Kim, Silke Rautenschlein, Hung Yueh Yeh

Research output: Contribution to journalArticlepeer-review

322 Scopus citations

Abstract

Infectious bursal disease virus (IBDV) is an important immunosuppressive virus of chickens. The virus is ubiquitous and, under natural conditions, chickens acquire infection by the oral route. IgM+ cells serve as targets for the virus. The most extensive virus replication takes place in the bursa of Fabricius. The acute phase of the disease lasts for about 7-10 days. Within this phase, bursal follicles are depleted of B cells and the bursa becomes 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 replication. The virus-induced bursal T cells are activated, exhibit upregulation of cytokine genes, proliferate in response to in vitro stimulation with IBDV and have suppressive properties. Chickens may die during the acute phase of the disease although IBDV induced mortality is highly variable and depends, among other factors, upon the virulence of the virus strain. Chickens that survive the acute disease clear the virus and recover from its pathologic effects. Bursal follicles are repopulated with IgM+ B cells. Clinical and subclinical infection with IBDV may cause immunosuppression. Both humoral and cellular immune responses are compromised. Inhibition of the humoral immunity is attributed to the destruction of immunoglobulin-producing cells by the virus. Other mechanisms such as altered antigen-presenting and helper T cell functions may also be involved. Infection with IBDV causes a transient inhibition of the in vitro proliferative response of T cells to mitogens. This inhibition is mediated by macrophages which are activated in virus- exposed chickens and exhibit a marked enhancement of expression of a number of cytokine genes. We speculate that T cell cytokines such as interferon (IFN)-γ may stimulate macrophages to produce nitric oxide (NO) and other cytokines with anti-proliferative activity. Additional studies are needed to identify the possible direct immunosuppressive effect of IBDV on T cells and their functions. Studies are also needed to examine effects of the virus on innate immunity. Earlier data indicate that the virus did not affect normal natural killer (NK) cell levels in chickens. (C) 2000 Published by Elsevier Science Ltd.

Original languageEnglish (US)
Pages (from-to)223-235
Number of pages13
JournalDevelopmental and comparative immunology
Volume24
Issue number2-3
DOIs
StatePublished - Mar 1 2000

Keywords

  • Bursa of Fabricius
  • Cytokines
  • IBDV
  • Immunosuppression
  • Macrophage
  • Pathogenesis
  • T cells

ASJC Scopus subject areas

  • Immunology
  • Developmental Biology

Fingerprint

Dive into the research topics of 'Infectious bursal disease virus of chickens: Pathogenesis and immunosuppression'. Together they form a unique fingerprint.

Cite this