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Avian - 2003
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| (Print Friendly Version) |
| Project Contact: | Jagdev Sharma | Funding: | $65,000 |
| P. Chary |
District:
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Unknown |
| • The Problem • Background • Objectives • Mid-Year Progress Report • Final Report • |
At least one of every three turkeys raised in Minnesota tests positive for exposure to avian pneumovirus, and recent reports indicate that the virus may be spreading to neighboring states. Turkey flocks exposed to APV undergo immunosuppression and experience an increased incidence of secondary infections, particularly bacterial infections.
Several attenuated virus preparations have been tried as vaccines with variable results. The lack of understanding of vaccine action in APV largely stems from a poor knowledge of how APV develops within an infected bird, the pathogenesis of the virus. Much recent research has focused on the genetic structure and epidemiology of the virus. There is an urgent need to understand the pathogenesis of APV and the nature of protective immunity.
Earlier results suggest that during the acute phase of the disease, the virus localizes in the upper respiratory tract, and that after about the first week of infection, the host clears the virus. This suggests a localized mucosal immunity operating in an unknown manner, and presents a target for research relating to vaccine-induced protection.
A summary of Avian Respiratory Disease Research Progress (1998-2001) is available. See also the project topic page for 2002.
This research will examine the observable and functional characteristics of the immune cells infiltrating the respiratory mucosa of infected turkeys, and attempt to associate this response with disease progression. Strategies will be developed to enhance local immunity induced by APV vaccines, resulting in improved control of the disease.
Specific objective include:
Update – February 2003
This study is providing useful information on the pathogenesis of APV and the importance of local respiratory immunity in protecting turkeys against virulent outbreaks of the virus. It should be helpful in controlling avian pneumovirus (APV).
This project induced acute disease in turkeys by exposing them to pathogenic (APV). Respiratory signs that include difficult breathing, sinus swelling, and runny nose and eyes characterize the acute disease.
Immune cells infiltrated the lining of the respiratory tract. The Harderian gland, a secondary lymphoid structure located near the eye, showed the most dramatic changes. In most of the infected turkeys, this gland became replete with infiltrating lymphoid (immune) cells.
Analysis of cells extracted from these Harderian glands showed both B and T cells present (T and B cells are lymphocytes that serve as important parts of a body’s immune system). Further, those T cells were able to be activated, secreting increased levels of cytokines, following in vitro stimulation with an appropriate compound.
A group of turkeys were treated with Cyclosporin A, a drug that destroys T cells. These turkeys developed a more acute clinical disease, with earlier onset and longer duration, than those not treated. This result provided strong preliminary evidence that T cells were important in defense against APV. But, because both Cyclosporin A-treated and untreated turkeys recovered from the acute disease, clearly T cells alone were not responsible for recovery.
Recovery from acute disease may have been mediated by a number of defense mechanisms, including T cells. Turkeys immunized with a live APV-41 virus by a respiratory route, when challenged with virulent APV, were protected against clinical signs and replication of the challenge virus in the upper respiratory tract and the spleen. A second group of turkeys immunized through their skin were not protected when challenged by the respiratory route. This indicates that local immune response, not circulating antibodies initiated by the live vaccine virus, was critical for protecting the respiratory tract against subsequent exposure to virulent APV.
Researchers then treated a group of turkeys with Cyclosporin A, a drug that destroys T cells. Cyclosporin A-treated turkeys developed a more acute clinical disease that had an earlier onset and longer duration than those not treated with the drug. This result provided strong preliminary evidence that T cells were important in defense against APV. Because both Cyclosporin A-treated and untreated turkeys recovered from the acute disease, clearly T cells alone were not responsible for recovery. Recovery from acute disease may have been mediated by a number of defense mechanisms, including T cells.
Turkeys were then immunized with live APV-41 by the respiratory route (Group 1) or the subcutaneous route (Group 2). Turkeys in both groups developed anti-APV antibodies. Two weeks after vaccination, the turkeys in Groups 1 and 2 were challenged with virulent APV. Results showed that turkeys in Group 1 (vaccinated by the respiratory route), when challenged by the respiratory route or the subcutaneous route, were protected against clinical signs and replication of the challenge virus in the URT and spleen. Turkeys in Group 2 (vaccinated subcutaneously) were not protected when challenged by the respiratory route. This result indicated that local immune response and not circulating antibodies initiated by the live vaccine virus was critical for protection of the respiratory tract against subsequent exposure to virulent APV. Immunization of turkeys with recombinant N and M proteins of APV induced protection against challenge with virulent APV. N provided better protection than M. Immunized turkeys developed memory cells that proliferated in vitro when stimulated with protein N.