A COMPARATIVE-STUDY OF AVIAN REOVIRUS PATHOGENICITY - VIRUS SPREAD AND REPLICATION AND INDUCTION OF LESIONS

Authors
Citation
Yw. Ni et Mc. Kemp, A COMPARATIVE-STUDY OF AVIAN REOVIRUS PATHOGENICITY - VIRUS SPREAD AND REPLICATION AND INDUCTION OF LESIONS, Avian diseases, 39(3), 1995, pp. 554-566
Citations number
33
Categorie Soggetti
Veterinary Sciences
Journal title
ISSN journal
00052086
Volume
39
Issue
3
Year of publication
1995
Pages
554 - 566
Database
ISI
SICI code
0005-2086(1995)39:3<554:ACOARP>2.0.ZU;2-B
Abstract
This study examined the relationship of avian reovirus spread and repl ication to induction of lesions and the relevant role of the S1 segmen t encoding a virus-neutralizing antigen. One-day-old broiler chickens were infected via footpad or orally with two virus strains (883 and 17 6) that differ greatly in virulence and a reassortant (R44) that has t he S1 segment from 176 and the remaining genome segments from 883. Vir us replication and histological lesions in Various tissues (heart, liv er, spleen, kidney, bursa, hock joint, and bone marrow) were measured at 2-day intervals until day 8 postinoculation. The virulent strain 17 6 spread to and replicated efficiently in all tissues examined and cau sed extensive and severe lesions, whereas the mild strain 883 was dete cted only in tissues near inoculation sites and caused only minimal le sions. The appearance of lesions correlated with the presence of viral replication in each tissue tested. Together, these results indicate t hat induction of lesions, or pathogenicity, is directly related to vir us spread and replication. Reassortant R44 behaved like strain 176 in chicken embryo fibroblasts (CEFs), i.e., both replicated much faster a nd produced larger plaques than strain 883. In broiler chickens, howev er, R44 behaved like strain 883, replicating and inducing lesions to a n extent that was far lower than that of strain 176. These results sug gest that the S1 segment alone is capable of determining Viral replica tion and plaque formation in cultured CEFs but is not sufficient to de termine the virus spread and replication and the pathological change i n broiler chickens.