PubMed:11799173 JSONTXT

{"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":87,"end":96},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":140,"end":155},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":195,"end":204},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":384,"end":393},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":889,"end":898},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1062,"end":1071},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1516,"end":1525},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005812"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0018695"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005812"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0000605"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005812"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005812"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0005812"}],"text":"Cooperation between the hemagglutinin of avian viruses and the matrix protein of human influenza A viruses.\nTo analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning."}