Abstract
Influenza virus A/turkey/Ontario/7732/66 (H 5 N 9), which is highly pathogenic to chickens, is nonpathogenic to quails. After intratracheal or intramuscular inoculation of quails, virus replication was limited to the respiratory tract, genital organs, and pancreas. However, aggravation of the pathogenicity was achieved through adaptation only by several passages of lung homogenates in quails. The adapted virus caused a fatal generalized infection in quails as well as in chickens. The pathogenic change of the virus could not be explained by a change in the proteolytic cleavability of the hemagglutinin, because no difference was found in the cleavability between the original and the adapted viruses. The adapted virus formed larger plaques and grew a little faster than the original one in both chicken embryo and quail embryo cells. The faster multiplication of the adapted virus at the site of infection might be the reason for its change in pathogenicity. The original virus could circulate among quails by a direct contact transmission without causing disease. The shed virus, however, caused a fatal infection in chickens when they were kept in contact with the infected quails. The epidemiological significance of this observation is discussed.
MeSH Terms
Adaptation, Physiological
Animals
Antibodies, Viral/analysis
Antigens, Viral/analysis
Central Nervous System/microbiology
Chickens/microbiology
Coturnix/microbiology
Hemagglutinins, Viral/analysis
Influenza A virus/immunology,pathogenicity
Influenza in Birds/microbiology
Quail/microbiology
Ribonucleoproteins/analysis
Turkeys/microbiology
Virus Replication
Chemicals
Antibodies, Viral
Antigens, Viral
Hemagglutinins, Viral
Ribonucleoproteins
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Tashiro M
Reinacher M
Rott R
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