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Peer-reviewedCC BY-NC-NDNature Communications

Dairy cows infected with influenza A(H5N1) reveals low infectious dose and transmission barriers

13 more authors
10 affiliations
  1. 1Department of Animal Sciences, College of Food, Agriculture and Environmental Sciences, The Ohio State University, Wooster, OH, USA
  2. 2Department of Veterinary Preventive Medicine, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA
  3. 3Department of Animal Sciences, College of Food, Agriculture and Environmental Sciences, The Ohio State University, Wooster, OH, USA; Department of Veterinary Preventive Medicine, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA
  4. 4Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA
  5. 5Comparative Pathology and Digital Imaging Shared Resource, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
  6. 6Department of Host-Microbe Interactions, St. Jude Children's Research Hospital, Memphis, TN, USA
  7. 7Department of Veterinary Biosciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA. [email protected]
  8. 8Department of Animal Sciences, College of Food, Agriculture and Environmental Sciences, The Ohio State University, Wooster, OH, USA. [email protected]
  9. 9Department of Veterinary Preventive Medicine, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA. [email protected]
  10. 10Department of Veterinary Preventive Medicine, College of Veterinary Medicine, The Ohio State University, Columbus, OH, USA. [email protected]

Abstract

The discovery that highly pathogenic avian influenza A(H5N1) virus exhibits a strong tropism for the bovine mammary gland1–4 represents a major shift in our understanding of influenza A virus host range and tissue specificity. We conducted a comprehensive series of experimental studies with influenza A(H5N1) B3.13 genotype in lactating dairy cattle to address several key questions related to the viral dose required to establish infection, routes of exposure that lead to transmission, and factors contributing to the morbidity and mortality observed on farms. We demonstrate that intramammary exposure to as few as 10 TCID50 is sufficient to establish robust infection, shedding of high viral titers in milk, and clinical mastitis. Despite evidence of such a low infectious dose, we were unable to recapitulate transmission to sentinel cows via contaminated milking equipment and close contact with infected animals under experimental conditions. High-dose intramammary exposure to influenza A(H5N1) drives severe clinical outcomes and mortality observed in dairy cows on-farm, while respiratory and oral exposure are less likely to establish productive infection and associated morbidity. This study challenges current hypotheses of influenza A(H5N1) transmission on dairy farms5,6, raising important questions about potential agent, host, or environmental cofactors that contribute to the spread of the virus.

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BibTeX
@article{lee2026dairy,
  title = {{Dairy cows infected with influenza A(H5N1) reveals low infectious dose and transmission barriers}},
  author = {Carolyn M. Lee and Natalie N. Tarbuck and Hannah J. Cochran and Bryant M. Foreman and Patricia A. Boley and Saroj Khatiwada and Alok Dhakal and Khadijat O. Adefaye and Jennifer Schrock and Mohammad Jawad Jahid and Thamonpan Laocharoensuk and Raksha Suresh and Olaitan Comfort Shekoni and Erika Stevens and Sara Dolatyabi and Christina G. Sanders and Elizabeth Ohl and Devra D. Huey and Juliette Hanson and Kara Corps and Gourapura J. Renukaradhya and Richard J. Webby and Cody J. Warren and Scott P. Kenney and Andrew S. Bowman},
  journal = {Nature Communications},
  year = {2026},
  month = may,
  doi = {10.1038/s41467-026-73490-6},
  url = {https://doi.org/10.1038/s41467-026-73490-6},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Dairy cows infected with influenza A(H5N1) reveals low infectious dose and transmission barriers
AU  - Carolyn M. Lee
AU  - Natalie N. Tarbuck
AU  - Hannah J. Cochran
AU  - Bryant M. Foreman
AU  - Patricia A. Boley
AU  - Saroj Khatiwada
AU  - Alok Dhakal
AU  - Khadijat O. Adefaye
AU  - Jennifer Schrock
AU  - Mohammad Jawad Jahid
AU  - Thamonpan Laocharoensuk
AU  - Raksha Suresh
AU  - Olaitan Comfort Shekoni
AU  - Erika Stevens
AU  - Sara Dolatyabi
AU  - Christina G. Sanders
AU  - Elizabeth Ohl
AU  - Devra D. Huey
AU  - Juliette Hanson
AU  - Kara Corps
AU  - Gourapura J. Renukaradhya
AU  - Richard J. Webby
AU  - Cody J. Warren
AU  - Scott P. Kenney
AU  - Andrew S. Bowman
PY  - 2026
DA  - 2026/05/24
JO  - Nature Communications
DO  - 10.1038/s41467-026-73490-6
UR  - https://doi.org/10.1038/s41467-026-73490-6
AB  - The discovery that highly pathogenic avian influenza A(H5N1) virus exhibits a strong tropism for the bovine mammary gland1–4 represents a major shift in our understanding of influenza A virus host range and tissue specificity. We conducted a comprehensive series of experimental studies with influenza A(H5N1) B3.13 genotype in lactating dairy cattle to address several key questions related to the viral dose required to establish infection, routes of exposure that lead to transmission, and factors contributing to the morbidity and mortality observed on farms. We demonstrate that intramammary exposure to as few as 10 TCID50 is sufficient to establish robust infection, shedding of high viral titers in milk, and clinical mastitis. Despite evidence of such a low infectious dose, we were unable to recapitulate transmission to sentinel cows via contaminated milking equipment and close contact with infected animals under experimental conditions. High-dose intramammary exposure to influenza A(H5N1) drives severe clinical outcomes and mortality observed in dairy cows on-farm, while respiratory and oral exposure are less likely to establish productive infection and associated morbidity. This study challenges current hypotheses of influenza A(H5N1) transmission on dairy farms5,6, raising important questions about potential agent, host, or environmental cofactors that contribute to the spread of the virus.
SN  - 2041-1723
ER  -