Protective immunity against infectious bursal disease virus in chickens in the absence of virus-specific antibodies.
The role of cell-mediated immunity (CMI) in pathogenesis of infectious bursal disease virus (IBDV) was investigated. One-day-old specific pathogen-free chickens were treated with 3mg of cyclophosphamide (Cy) per chicken for 4 consecutive days and, 3 weeks later, infected with the IBDV-IM strain. Chickens were examined for: (a) mitogenic response of splenocytes to ConA, as an indicator of T-cell functions in vitro, (b) antibody against IBDV by ELISA, (c) IBDV genome in various tissues by RT-PCR and (d) immunological memory. At the time of IBDV infection, Cy-treated chickens had depleted bursal tissue (an avian primary B-cell lymphoid organ), severely compromised antibody-producing ability, but normal T-cell response to ConA. In primary infection, no detectable antibody against IBDV antigen in Cy-treated, IBDV-infected chickens was observed up to 28 days post-infection (PI), while IBDV genome was detected by RT-PCR in spleen, thymus, liver and blood until 10 days PI. Like intact control chickens infected with IBDV, Cy-treated, IBDV-infected chickens suppressed splenocytes responses to ConA from 5 to 10 days PI, suggesting that intact control as well as Cy-treated chickens responded similarly to IBDV infection in the early phase. Following re-infection with IBDV, no detectable secondary antibody response to IBDV as well as IBDV genome in tissues were observed in Cy-treated chickens, while intact control chickens developed vigorous secondary antibody response. Similar to intact control chickens infected with IBDV, Cy-treated chickens after second infection with IBDV did not suppress splenocyte response to ConA. These results suggested that in the absence of detectable anti-IBDV antibodies, protection of Cy-treated chickens from IBDV infection may occur via immunological memory mediated by CMI. We concluded that under normal conditions, IBDV induces a protective antibody response, however, in the absence of antibody, CMI alone is adequate in protecting birds against virulent IBDV.
Yeh
Hung-Yueh
HY
Department of Veterinary PathoBiology, University of Minnesota, 1971 Commonwealth Avenue, St Paul, MN 55108, USA.
Rautenschlein
Silke
S
Sharma
Jagdev M
JM
D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis* / Q000276:immunology; D000918:Antibody Specificity; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology; D018175:Birnaviridae Infections / Q000276:immunology* / Q000517:prevention & control / Q000662:veterinary; D002645:Chickens / Q000276:immunology* / Q000821:virology*; D003208:Concanavalin A / Q000276:immunology; D003520:Cyclophosphamide / Q000276:immunology / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D007166:Immunosuppressive Agents / Q000276:immunology / Q000494:pharmacology; D007243:Infectious bursal disease virus / Q000276:immunology*; D011201:Poultry Diseases / Q000276:immunology* / Q000517:prevention & control / Q000821:virology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013047:Specific Pathogen-Free Organisms; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors
D000914:Antibodies, Viral; D007166:Immunosuppressive Agents; D003208:Concanavalin A; D003520:Cyclophosphamide