Protective immunity against Newcastle disease: The role of antibodies specific to Newcastle disease virus polypeptides

Citation
Dl. Reynolds et Ad. Maraqa, Protective immunity against Newcastle disease: The role of antibodies specific to Newcastle disease virus polypeptides, AVIAN DIS, 44(1), 2000, pp. 138-144
Citations number
31
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
AVIAN DISEASES
ISSN journal
00052086 → ACNP
Volume
44
Issue
1
Year of publication
2000
Pages
138 - 144
Database
ISI
SICI code
0005-2086(200001/03)44:1<138:PIANDT>2.0.ZU;2-M
Abstract
Studies were performed to determine if passive immunization with hyperimmun e sera generated to specific Newcastle disease virus (NDV) proteins conferr ed protection against virus challenge. Six groups of S-wk-old chickens were passively immunized with antiserum against either hemagglutinin-neuraminid ase/fusion, (HN/F) protein, nucleoprotein/phosphoprotein (NP/P), Matrix (M) protein, a mixture of all NDV proteins (ALL), intact ultraviolet-inactivat ed NDV (UVNDV), or negative sera. Blood samples were collected 2 days posti mmunization, and the birds were challenged with Texas GB strain of NDV. Ant ibody titers were detected from those recipient birds that had received the antisera against the HN/F ALL, or UVNDV by a hemagglutination inhibition t est, an enzyme-linked immunosorbent assay (ELISA), and a virus neutralizati on test. Antibodies were detected only by the ELISA from the birds that had received antisera against NP/P and M protein. Antibody titers in the recip ient birds dropped by two dilutions (log(2)) after 2 days postinjection. Bi rds passively immunized with antisera against HN/F, ALL, and UVNDV were pro tected from challenge, whereas chickens passively immunized with antisera a gainst NP/P and M protein and specific-pathogen-free sera developed clinica l signs of Newcastle disease. The challenge virus was recovered from the tr acheas of all passively immunized groups. The presence of neutralizing anti bodies to NDV provided protection from clinical disease bur was unable ro p revent virus shedding from the trachea.