Studies on influenza viruses H10N4 and H10N7 of avian origin in mink

Authors
Citation
L. Englund, Studies on influenza viruses H10N4 and H10N7 of avian origin in mink, VET MICROB, 74(1-2), 2000, pp. 101-107
Citations number
26
Categorie Soggetti
Veterinary Medicine/Animal Health",Microbiology
Journal title
VETERINARY MICROBIOLOGY
ISSN journal
03781135 → ACNP
Volume
74
Issue
1-2
Year of publication
2000
Pages
101 - 107
Database
ISI
SICI code
0378-1135(20000522)74:1-2<101:SOIVHA>2.0.ZU;2-U
Abstract
An influenza A virus, A/mink/Sweden/84 (H10N4), was isolated from farmed mi nk during an outbreak of respiratory disease, histopathologically character ised by severe interstitial pneumonia. The virus was shown to be of recent avian origin and closely related to concomitantly circulating avian influen za virus. Serological investigations were used to link the isolated virus t o the herds involved in the disease outbreak. Experimental infection of adu lt mink with the virus isolate from the disease outbreak reproduced the dis ease signs and pathological lesions observed in the field cases. The mink i nfluenza virus also induced an antibody response and spread between mink by contact. The same pathogenesis in mink was observed for two avian influenz a viruses of the H10N4 subtype, circulating in the avian population. When m ink were infected with the prototype avian H10 influenza virus, A/chicken/G ermany/N/49, H10N7, the animals responded with antibody production and mild pulmonary lesions but neither disease signs nor contact infections were ob served. Detailed studies, including demonstration of viral antigen in situ by immunohistochemistry, of the sequential development of pathological lesi ons in the mink airways after aerosol exposure to H10N4 or H10N7 revealed t hat the infections progress very similarly during the first 24 h, but are d istinctly different at later stages. The conclusion drawn is that A/mink/Sw eden/84, but not A/chicken/Germany/N/49, produces a multiple-cycle replicat ion in mink airways. Since the viral distribution and pathological lesions are very similar during the initial stages of infection we suggest that the two viruses differ in their abilities to replicate and spread within the m ink tissues, but that their capacities for viral adherence and entry into m ink epithelial cells are comparable. (C) 2000 Elsevier Science B.V. All rig hts reserved.