ULTRASTRUCTURAL-STUDY OF TURKEY RHINOTRACHEITIS VIRUS-INFECTION IN TURBINATES OF EXPERIMENTALLY INFECTED CHICKENS

Citation
N. Majo et al., ULTRASTRUCTURAL-STUDY OF TURKEY RHINOTRACHEITIS VIRUS-INFECTION IN TURBINATES OF EXPERIMENTALLY INFECTED CHICKENS, Veterinary microbiology, 52(1-2), 1996, pp. 37-48
Citations number
27
Categorie Soggetti
Microbiology,"Veterinary Sciences
Journal title
ISSN journal
03781135
Volume
52
Issue
1-2
Year of publication
1996
Pages
37 - 48
Database
ISI
SICI code
0378-1135(1996)52:1-2<37:UOTRVI>2.0.ZU;2-2
Abstract
Ultrastructural changes associated with turkey rhinotracheitis virus i nfection were studied in turbinates of chickens experimentally infecte d with the isolate CVL 14/86/1. Chickens were sacrificed at 3, 5 and 7 days after inoculation and samples of the middle turbinate were taken , fixed, dehydrated and embedded in an hydrophilic resin. An immunoflu orescence technique on semithin sections was carried out and viral ant igen was observed in the cytoplasm and associated to cilia of the turb inate epithelial cells, on days 3 and 5 after inoculation. Ultrastruct urally, gold stained intracytoplasmic nucleocapsid aggregates of turke y rhinotracheitis virus were observed in ciliated and non-ciliated epi thelial cells, as well as budding virus particles, at days 3 and 5 pos tinoculation. Different ultrastructural abnormalities, including cytop lasmic blebs, clumping and loss of cilia were observed in the apical c ell membrane of many infected cells, associated with the presence of i ntracytoplasmic inclusions. On day 5 after inoculation, substitution o f ciliated and non-ciliated epithelial cells was noted and many desqua mated epithelial cells were observed within the lumina. Regenerative c hanges in the ciliated epithelium were observed by day 7 postinoculati on. These results indicate that turkey rhinotracheitis virus is able t o replicate in ciliated and non-ciliated epithelial cells causing seve re alterations to the cell surface and ciliary apparatus of the turbin ate epithelium. Viral-induced damage to the turbinate epithelium could enhance the susceptibility of epithelial cells to secondary bacterial infection.