| dc.description.abstract | Proventricular dilatation disease (PDD) is a fatal viral disease that affects mainly psittacine birds, although some non-psittacine species can be affected. Gastrointestinal and/or neurological signs can be seen in PDD-affected birds. These signs are likely a result of non-suppurative inflammation of the central, peripheral and autonomic nervous systems. Parrot bornavirus (PaBV) was discovered as a causative agent of PDD in 2008. The prognosis of PDD is very poor once clinical signs have developed and no specific treatments or commercial vaccines are available to date.
In order to investigate methods of protection, we vaccinated cockatiels using inactivated whole PaBV and/or recombinant PaBV N protein vaccines followed by challenge with virulent PaBV-2. In the first experiment, inactivated PaBV-2-infected cells were administrated via intramuscular (IM) inoculation, three times, followed by one IM injection of recombinant N protein vaccine. In a second experiment, the recombinant N protein vaccine was administered alone, two times, via the IM route. Over 28 weeks post challenge, cloacal swabs were collected and body weights and any clinical signs were noted. Using tissues collected at necropsy, histopathologic examination was used to detect the presence of microscopic lesions characteristic of PDD. Quantitative RealTime PCR (qRT-PCR) and immunohistochemistry (IHC) were used to detect PaBVRNA and antigen respectively. Using western blots assays, we were not able to detect a humoral response after vaccination with the inactivated vaccine. Conversely, the recombinant N protein vaccine stimulated production of anti-N antibodies.
The results of both vaccine studies indicated that the recombinant N protein vaccine was able to protect subsequently challenged birds from lesions associated with PDD. Further, the vaccine protected birds from PDD-related morbidity and mortality. However, the vaccine did not protect "efficiently" against infection, as PaBV- RNA and antigen were detected in organs and cloacal swabs of vaccinated and unvaccinated birds. Moreover, there was no evidence that vaccination, either before or after challenge, increased the severity of the infection. We hypothesized that this protective response was a result of a switch from a type 1 cell-mediated immune response to a type 2 humoral immune response. This hypothesis was supported by a third study which revealed that treatment of cockatiels with cyclosporine A, an immunosuppressant, at the time of challenge with virulent PaBV-2, also conferred complete protection against PDD at the expense of increasing the viral load. This experiment showed that PDD might be an immunologically mediated disease, similar to Borna disease in mammals. | en |
