#19,238
Until 28 months ago conventional wisdom held that cattle, sheep, goats and other mammalian livestock were not susceptible to HPAI H5Nx infection (see A Brief History Of Influenza A In Cattle/Ruminants).
Isolated spillovers weren't impossible, but had never been confirmed outside of the lab, and thought highly unlikely.
All that changed abruptly in the spring of 2024 when we saw goats die from H5N1 in Minnesota, followed by a multi-state outbreak of H5N1 in dairy cattle. Since then more than 1,150 U.S. cattle herds in 20 states have been affected, and we've seen sporadic reports from the UK, Europe, and Asia.
At first, the assumption was that only the B3.13 `Bovine' genotype of H5N1 could infect cattle, but in early 2025 genotype D1.1 was discovered in dairy cows in 3 states, and the European and Asia spillovers were from different genotypes as well.
While we've seen evidence that cattle and other ruminants could serve as mixing vessels for avian influenza, the bigger concern has always been HPAI spillovers into pigs, which have a history of generating pandemic viruses.
Although detections in swine have been limited, we've seen scattered evidence that H5N1 can infect pigs, albeit often asymptomatically. A few past reports include:- WHO H5N1 detected in pigs in China (2004)
- EID Journal: Asymptomatic H5N1 In Pigs (2010)
- An Unusual Report Of H5N1 in Pigs (Indonesia 2016)
- Sci. Rpts.: Evidence Of H5N1 Exposure In Domestic Pigs - Nigeria (2018)
Followed only days later by a report out of Italy confirming an H5N1 spillover event at a `mixed species' farm (poultry & swine), and the subsequent seroconversion of the majority of the pigs tested on that farm (see Study: Seroconversion of a Swine Herd in a Free-Range Rural Multi-Species Farm against HPAI H5N1 2.3.4.4b Clade Virus).
In late 2024, we saw two pigs infected with a new, recently emerged genotype (D1.2) in Oregon (see USDA Confirms 2nd Pig on Oregon Farm Tested Positive for H5N1).
And last fall, in Transboundary & Emerg Inf: Serological Evidence of HPAI (H5N1) in Invasive Wild Pigs in Western Canada, we looked at a study which found (limited) serological evidence of HPAI H5 infection in wild pigs in western Canada.
The lack of reports of HPAI H5 in pigs is comforting, but surveillance and testing for the virus in the United States is quite limited.
The USDA further notes:The $64 question remains; are pigs - like cattle - more susceptible the newer HPAI viruses currently circulating in the United States?
Due to the voluntary nature of this surveillance, the information in this report cannot be used to determine regional and/or national incidence, prevalence, or other epidemiological measures, but it may help identify IAV-S trends.
While it doesn't completely answer the question, today's study tested the infectivity and replication of 4 different influenza viruses (Bovine H5N1, LPAI H5N1, Swine H1N2, and Human H1N1) across an array of porcine cell lines (primary nasal turbinate, trachea, lung and mammary gland epithelial cells).
They report that porcine mammary epithelial cells contain both SA-α2,3 avian‑type and SA-α2,6 human‑type receptor cells and can support replication of bovine H5N1 B3.13 to relatively high titers, suggesting lactating pigs are a plausible host for this genotype.
The caveat being, this study was done in vitro using tissues and cells from a single porcine donor, tested against a limited array of (4) viruses. While it shows that pig udder cells can be infected, it's a long way from proving that infections are common in the field.
That said, these results suggest that - given what we've already seen with cattle - we might be better served by escalating the surveillance and testing of swine - and increasing biosecurity on pig farms - before it becomes a bigger issue.
Due to its length and technical details, I've only posted the abstract and a few excerpts. Follow the link to read it in its entirety.
Receptor profiling and growth assessment of influenza A virus in porcine mammary and non-mammary tissues and derived cells
Ulises Barron-Castillo , Nathalie Berube1, Cynthia L. Swan1, M. Afzal Javed1, Lauren Aubrey1, Jill Trann1,2, Makenzie Gidych1, Sauhard Shrivastava1,2, Kaushal Baid1, Arinjay Banerjee ,2, Yan ZhouReceived 17 April 2026 Accepted 8 June 2026 Published 6 July 2026
Highly pathogenic avian influenza (HPAI) virus clade 2.3.4.4b genotype B3.13 infected the mammary gland of dairy cattle; the new tissue tropism and host heightened concern about its ability to cross species barriers with zoonotic potential. Pigs play a key role in influenza A virus (IAV) adaptation, serving as a “mixing vessel” for the emergence of reassortants. The susceptibility of porcine mammary gland to HPAI infection remains unexplored.
In this study, we profiled IAV receptors in porcine mammary gland as well as respiratory tract tissues. Additionally, we evaluated the binding capacity of IAVs to these tissues. Furthermore, we isolated primary cells from porcine mammary gland and respiratory tract, and immortalized them. We examined the growth potential of IAV isolates from bovine, avian, swine, and human on these cells.
We showed that porcine mammary gland displays both SA-α2,3 and SA-α2,6, and that IAVs bind to mammary gland tissues with variable affinities. While bovine H5N1 virus replicates efficiently in mammary gland and respiratory tract cells, replication of other IAVs in mammary epithelial cells is moderate but is efficient in respiratory cells.
These findings suggest that porcine mammary gland could support the infection by HPAI 2.3.4.4b genotype B3.13.
(SNIP)
Pigs are known as mixing vessels for IAVs due to the presence of both SA-α2,3 and SA-α2,6 receptors in their respiratory tract, allowing co-infection by avian, human, and swine IAV strains (13, 14). The expression of both receptors facilitates viral reassortment, enabling the emergence of novel viruses with pandemic potential, such as the 2009 H1N1, a quadruple-reassortant strain (15).
Given the recent evidence of HPAI H5N1 replication in bovine mammary gland tissue, it is important to assess whether the porcine mammary gland could similarly support influenza viral infection. This will provide insights into whether it serves as a potential site for viral adaptation and reassortment. Meanwhile, it is also equally important to assess the potential replication of bovine H5N1 in porcine respiratory tract in comparison to other IAV strains.
Here, we characterized IAV receptors on porcine mammary gland and respiratory tract tissues. Additionally, we tested the binding capacity of IAV to these tissues. Furthermore, we isolated primary cells from both porcine mammary gland and respiratory tract tissues and immortalized them. The growth potential of a panel of IAV isolates from bovine, swine, human, and avian sources was examined in these cells.
We report that porcine mammary gland expresses both SA-α2,3 and SA-α2,6 receptors, and IAVs bind to mammary gland tissues with variable levels. HPAI H5N1 bovine isolate replicates efficiently in epithelial cells derived from the mammary gland and respiratory tract. In contrast, non-HPAI isolates exhibited moderate replication in mammary gland cells but efficient replication in respiratory tract cells. These findings suggest that porcine mammary gland tissues could support infection by HPAI H5N1 clade 2.3.4.4b genotype B3.13.
