The pathogenesis of low pathogenicity H7 avian influenza viruses in chickens, ducks and turkeys

Abstract

BackgroundAvian influenza (AI) viruses infect numerous avian species, and low pathogenicity (LP) AI viruses of the H7 subtype are typically reported to produce mild or subclinical infections in both wild aquatic birds and domestic poultry. However relatively little work has been done to compare LPAI viruses from different avian species for their ability to cause disease in domestic poultry under the same conditions. In this study twelve H7 LPAI virus isolates from North America were each evaluated for their comparative pathogenesis in chickens, ducks, and turkeys.ResultsAll 12 isolates were able to infect all three species at a dose of 106 50% egg infectious doses based on seroconversion, although not all animals seroconverted with each isolate-species combination. The severity of disease varied among isolate and species combinations, but there was a consistent trend for clinical disease to be most severe in turkeys where all 12 isolates induced disease, and mortality was observed in turkeys exposed to 9 of the 12 viruses. Turkeys also shed virus by the oral and cloacal routes at significantly higher titers than either ducks or chickens at numerous time points. Only 3 isolates induced observable clinical disease in ducks and only 6 isolates induced disease in chickens, which was generally very mild and did not result in mortality. Full genome sequence was completed for all 12 isolates and some isolates did have features consistent with adaptation to poultry (e.g. NA stalk deletions), however none of these features correlated with disease severity.ConclusionsThe data suggests that turkeys may be more susceptible to clinical disease from the H7 LPAI viruses included in this study than either chickens or ducks. However the severity of disease and degree of virus shed was not clearly correlated with any isolate or group of isolates, but relied on specific species and isolate combinations.

Role of Poultry in the Spread of Novel H7N9 Influenza Virus in China

“…Wild aquatic birds do not typically show clinical signs of infection with AIVs, and although AIVs can replicate in cells of both the respiratory and intestinal tracts, in ducks they are reported to favor the intestinal tract (43,44). The results of these studies are consistent with those of previous studies indicating that chicken-adapted AIVs replicate better in chickens than in ducks (45,46). The underlining mechanism is not clear, but a shorter neuraminidase protein due to a deletion in the stalk region may be linked to this feature (47)(48)(49).…”

“…Detection of LPAIVs is more difficult than detection of HPAIVs, like H5N1, because testing cannot target sick or dead birds like syndromic surveillance can. Critically, the data from both quail and chickens show high levels of viral replication in the upper respiratory tract and the shedding of much less virus in cloacal swabs, findings which are not unexpected, because poultry-adapted AIVs are typically shed at much higher levels in the respiratory tract in gallinaceous poultry (45,46,(50)(51)(52). The disease pathogenesis of the H7N9 virus was unusual, in that virus replication was primarily restricted to the upper respiratory tract for all the species examined and the virus did not replicate well in lungs.…”

Transmission of H7N9 Influenza Viruses with a Polymorphism at PB2 Residue 627 in Chickens and Ferrets

“…Chickens infected with H7N9 viruses portrayed the typical patterns of early onset and predominant oropharyngeal shedding in chickens following low-pathogenic avian influenza virus infection (45) and were in agreement with other H7N9 studies with chickens (11,41,(46)(47)(48)(49). Importantly, chickens inoculated with H9N2 viruses isolated from China also shed in a similar fashion (50,51).…”

Pathogenicity and Transmission of H5 and H7 Highly Pathogenic Avian Influenza Viruses in Mallards

“…When these gallinaceous adapted viruses infect ducks, the virus usually retains the respiratory-tropic replication pattern (65,66). In our study, the LPAI viruses examined were shed for longer by the CL route than the OP route, although moderate replication in the upper respiratory tract still occurred.…”