Whilst remarkable progress in elucidating the mechanisms governing interspecies transmission and pathogenicity of highly pathogenic avian influenza viruses (AIVs) has been made, similar studies focusing on low-pathogenic AIVs isolated from the wild waterfowl reservoir are limited. We previously reported that two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues. To further substantiate these observations, we infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all of the tested strains replicated poorly and were nonpathogenic for chickens. In contrast, most of the strains having human signatures replicated well in the lungs of mice, and one of these strains caused severe illness in mice and induced lung injury that was characterized by a severe accumulation of polymorphonuclear leukocytes. These results suggest that some strains tested in this study may have the potential to infect mammalian hosts directly without adaptation, which might possibly be associated with the possession of human signature residues. Close monitoring and evaluation of host-associated signatures may help to elucidate the prevalence and emergence of AIVs with potential for causing zoonotic infections.
AnimalsAnimals, WildChickensDisease Models, AnimalFemaleHumansInfluenza A Virus, H3N8 SubtypeInfluenza in BirdsInfluenza, HumanLungMiceMice, Inbred BALB CNeutrophilsZambia
Structured evidence records
Evidence records
5 total
Host Range Experiment2 records
Host Range ExperimentExtraction confidence 0.95
Key finding
Avian influenza virus strains from wild waterfowl in Zambia replicated poorly in chickens but replicated efficiently and caused disease in mice, indicating greater susceptibility of mice compared to chickens to these avian isolates.
We infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all of the tested strains replicated poorly and were nonpathogenic for chickens. In contrast, most of the strains having human signatures replicated well in the lungs of mice.
Method
experimental infection
Sample type
lungs
Experimental system
in vivo animal experiment
Host Range ExperimentExtraction confidence 0.95
Key finding
Avian influenza virus strains isolated from wild waterfowl in Zambia replicated poorly and were nonpathogenic in experimentally infected chickens.
We infected chickens and mice intranasally with AIV strains of various subtypes (H3N6, H3N8, H4N6, H6N2, H9N1 and H11N9) isolated from wild waterfowl in Zambia. Although some strains induced seroconversion, all of the tested strains replicated poorly and were nonpathogenic for chickens.
Method
experimental infection
Experimental system
in vivo animal experiment
Molecular Adaptation2 records
Molecular AdaptationExtraction confidence 0.95
Key finding
Avian influenza viruses H6N2 and H3N8 from wild waterfowl in Zambia carried human signature amino acid residues linked to enhanced replication and morbidity in mice, indicating partial molecular adaptation to mammalian hosts.
Two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues.
Mechanism types
pathogenicity; replication_efficiency
Molecular AdaptationExtraction confidence 0.95
Key finding
Avian influenza virus H3N8 from wild waterfowl in Zambia contained human signature amino acid residues linked to increased replication and morbidity in mice, suggesting molecular adaptation toward mammalian hosts.
Two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues preferentially associated with human influenza virus proteins (so-called human signatures) and replicated better in the lungs of infected mice and caused more morbidity than a strain lacking such residues.
Mechanism types
pathogenicity; replication_efficiency
Zoonotic Surveillance1 records
Zoonotic SurveillanceExtraction confidence 0.95
Key finding
Avian influenza virus subtypes H3N6, H3N8, H4N6, H6N2, H9N1, and H11N9 were isolated from wild waterfowl in Zambia as part of surveillance of the wild bird reservoir.
Two AIV strains (subtypes H6N2 and H3N8) isolated from wild waterfowl in Zambia harbored some amino acid residues ... To further substantiate these observations, we infected chickens and mice ... with AIV strains ... isolated from wild waterfowl in Zambia.
