IgE responses to bluetongue virus (BTV) serotype 11 after immunization with inactivated BTV and challenge infection

Citation
Ac. Odeon et al., IgE responses to bluetongue virus (BTV) serotype 11 after immunization with inactivated BTV and challenge infection, COMPAR IMM, 22(2), 1999, pp. 145-162
Citations number
48
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES
ISSN journal
01479571 → ACNP
Volume
22
Issue
2
Year of publication
1999
Pages
145 - 162
Database
ISI
SICI code
0147-9571(199904)22:2<145:IRTBV(>2.0.ZU;2-N
Abstract
To test the hypothesis that development of a BTV-specific IgE response play s a role in clinical disease manifestation, the humoral immune response of cattle to inactivated and virulent BTV was studied. Three calves received t hree sensitizing immunizations of inactivated BTV, 3 weeks apart. The BTV-s ensitized animals, two non-sensitized BTV-seropositive and 4 BTV-seronegati ve control cattle, were challenge-exposed with BTV-11, UC8 strain. All catt le inoculated with inactivated BTV developed group-specific nonneutralizing and serotype-specific neutralizing antibodies. The development of post. ch allenge-exposure neutralizing antibody titers was inversely correlated with protective immunity. None of the BTV-challenged animals showed clinical di sease. The levels of IgE were greatest in the sensitized calves after virus challenge in comparison with control groups. The sequential development, s pecificity and intensity of virus protein-specific humoral responses were e valuated using immunostaining. After challenge exposure of BTV sensitized a nd non-sensitized cattle, total and IgE antibodies reacted consistently wit h BTV structural proteins VP2, VP5 and VP7. Although no correlation was fou nd between clinical disease and IgE, results add support to the hypothesis that IgE may be involved in the pathogenesis of clinical disease, since inf ection with BTV causes an increase in serum IgE levels. However, these resu lts suggest that the levels of virus-specific reactivity may be an importan t factor in determining whether or not clinical disease manifestation occur s. (C) 1999 Elsevier Science Ltd. All rights reserved.