We previously demonstrated susceptibility of pheasants to infection with influenza A viruses of 15 HA subtypes: 13/23 viruses tested were isolated for >/=14 days, all in the presence of serum-neutralizing antibodies; one virus (H10) was shed for 45 days post-infection. Here we confirmed that 20% of pheasants shed low-pathogenic influenza viruses for prolonged periods. We aimed to determine why the antibody response did not clear the virus in the usual 3 to 10 days, because pheasants serve as a long-term source of influenza viruses in poultry markets. We found evidence of virus replication and histological changes in the large intestine, bursa of Fabricius, and cecal tonsil. Virus isolated 41 days post-infection was antigenically distinct from the parental H10 virus with corresponding changes in the hemagglutinin (HA) and neuraminidase. Ten amino acid differences were found between the parental H10 and the pheasant H10 virus; four were in potential antigenic sites of the HA molecule. Prolonged shedding of virus by pheasants results from a complex interplay between the diversity of virus variants and the host response. It is often argued that vaccination pressure is a mechanism that contributes to the generation of antigenic drift variants in poultry. This study provided evidence that drift variants can occur naturally in pheasants after prolonged shedding of virus thus strengthening our argument for removal of pheasants from live bird retail markets.