Use this URL to cite or link to this record in EThOS:
Title: Respiratory transmission of maedi-visna virus
Author: McNeilly, Tom N.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 2005
Availability of Full Text:
Access from EThOS:
Full text unavailable from EThOS. Please try the link below.
Access from Institution:
Using an ovine tracheal organ culture model it was found that tracheal mucosa was infectable with MVV, but this infection was inefficient and non-productive, with doses of ≥ 1 x 105 TCID50 required for detectable infection. Virus containing cells were located in a sub-epithelial location within 12 hours post-infection, but never in the tracheal epithelium. In addition, mechanical disruption of the epithelium resulted in a significant increase in virus uptake. These results suggest that tracheal epithelium acts as a barrier to MVV uptake, and is not a primary target for MVV. Immunohistochemical (IHC) analysis of tracheal mucosa identified an extensive network of sub-epithelial dendritic cells in the same location as provirus positive cells, suggesting uptake of MVV by the trachea is mediated by dendritic cells. In vivo tracking of intra-tracheal inocula using patent blue dye demonstrated exposure of both trachea and lower lung. Differential exposure of trachea and lower lung to MVV demonstrated lower lung to be significantly more efficient at MVV uptake. It was shown that virus instilled into the lower lung is taken up by alveolar macrophages (AMs), and that MVV-infected AMs are capable of transferring virus into the body. In vivo tracking of MVV infected AMs with PKH-26 dye failed to demonstrate migration of AMs from the lung airspace, suggesting that during infection, virus is transferred from AMs into the body via an indirect route. It was hypothesised that lower lung inflammation may play a key role in initial MVV entry into the body via recruitment of viral target cells, namely macrophages and dendritic cells, and that infected AMs may play a central role in this inflammation. Histopathological, IHC and real-time PCR analysis of virus treated lung tissue failed to detect an early inflammatory response.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available