Webster and Pereira identified serological cross-reactions between avian influenza viruses from turkeys and ducks and human A2/57 influenza virus. Using complement fixation and neuraminidase inhibition tests, they detected antigenic relationships not apparent in hemagglutination-inhibition assays. The cross-reactions were specifically attributed to the neuraminidase surface antigen, as demonstrated using antiserum specific to A2/57 neuraminidase. Four avian viruses from geographically distant sources (USA and Italy) possessed neuraminidase antigens closely related to the human virus. A similar relationship was found between an avian turkey virus and an equine strain. The authors discuss three possible explanations: that the human A2/57 subtype derived from avian viruses through host-range mutation, that antigenic similarity resulted from independent mutations by chance, or that recombination between avian and human influenza viruses occurred naturally. Given the ease of producing antigenic hybrids in laboratory settings, the authors suggest natural recombination as a plausible mechanism, highlighting the potential reservoir of animal influenza viruses that could recombine with human strains to generate pandemic variants.

Key findings

• Four avian influenza viruses from turkeys and ducks possess neuraminidase antigens antigenically indistinguishable from human A2/57 virus neuraminidase
• Cross-reactions between avian and human influenza viruses were detected by complement fixation and neuraminidase inhibition tests but not by hemagglutination-inhibition tests
• The common antigen shared between avian and human viruses is the neuraminidase surface protein, not the hemagglutinin
• Avian and human influenza viruses may have arisen through natural recombination rather than independent mutation or host-range adaptation