Panzootic Bird Flu: A Comprehensive Analysis of the H5N1 Influenza Crisis in the United States (2024–2026)

1. Introduction

1.1 The Emergence of a Modern Plague

The narrative of the Highly Pathogenic Avian Influenza (HPAI) A(H5N1) virus in the early 21st century is one of relentless adaptation and ecological expansion. While the virus has been a known entity in virology since its initial identification in Southern China in 1996, the lineage that confronts the United States in January 2026—clade 2.3.4.4b—represents a fundamentally distinct biological agent in terms of its host range, environmental persistence, and transmission dynamics. This report provides an exhaustive status update on the H5N1 outbreak as it stands in early 2026, analyzing the unprecedented establishment of the virus in mammalian reservoirs, specifically dairy cattle, and its continued devastation of avian populations.

The "panzootic"—a pandemic of animals—has shifted from a seasonal avian phenomenon to a year-round, multi-species crisis. The virus has exploited the ecological interfaces where human agricultural systems intersect with wildlife corridors, creating a complex web of transmission that defies traditional containment strategies. By dissecting the recent historical infections in farmed herds, the cumulative toll on poultry, and the expanding list of wild hosts, this article aims to delineate the spread potential of the virus, contrasting the mechanisms operative in urban agricultural environments with those driving transmission in the wild.

1.2 The 2026 H5N1 Landscape

As of January 2026, the United States faces a tripartite threat. First, the dairy cattle epizootic, which began in early 2024, has not been eradicated; instead, it has evolved into a cryptic, endemic issue in certain regions while sparking new, distinct spillover events in others. Second, the poultry industry continues to suffer attrition from both lateral spread and constant re-introduction from wild birds, with over 166 million birds affected since 2022.¹ Third, the virus has entrenched itself in the continent's wildlife, affecting marine mammals on both coasts and terrestrial scavengers in between, signaling a permanent alteration of the North American viral ecosystem.

The human cost, while statistically low relative to the animal toll, has escalated in severity. With 71 confirmed cases and two fatalities by early 2026, the virus is testing the "species barrier" with increasing frequency.² This report will explore the genomic nuances of these human cases, particularly the emergence of reassortant viruses like H5N5, and the implications for occupational safety in the agricultural sector.

2. Viral Biology and Genomic Evolution in H5N1

2.1 The Architecture of the Virus

To understand the spread potential of H5N1, one must first appreciate the biological machinery driving it. Influenza A viruses are orthomyxoviruses characterized by a segmented negative-sense RNA genome. This segmented nature is the virus's greatest evolutionary asset, allowing for "reassortment"—the swapping of gene segments when two different viruses infect the same cell.

The virus is classified by two surface proteins: Hemagglutinin (HA) and Neuraminidase (NA).

• Hemagglutinin (HA): This protein acts as the key to the host cell's lock. It binds to sialic acid receptors on the cell surface. Avian viruses typically bind to alpha-2,3 sialic acid receptors, which are abundant in the intestinal tract of birds. Human viruses bind to alpha-2,6 receptors, found in the human upper respiratory tract. The "H5" hemagglutinin of clade 2.3.4.4b has proven exceptionally stable but has not yet acquired the mutations necessary for a complete switch to human receptor binding.

• Neuraminidase (NA): This protein acts as the molecular scissors, cleaving the sialic acid receptors to allow newly formed virus particles to exit the cell and spread. The "N1" neuraminidase has been the standard partner in this panzootic, but recent events have seen the virus swap this for "N5," creating the H5N5 subtype detected in Washington State.³

2.2 Clade 2.3.4.4b: The Dominant Lineage

The current outbreak is driven by clade 2.3.4.4b. Unlike previous H5N1 lineages that caused high mortality in wild birds and thus limited their own spread (dead birds do not migrate), clade 2.3.4.4b struck an evolutionary balance. It causes variable pathogenicity in wild waterfowl—often asymptomatic or mild enough to allow migration—while remaining highly lethal to poultry and raptors. This "Trojan horse" phenotype allowed the virus to hitchhike across the Atlantic and Pacific oceans, seeding North American flyways in late 2021.

2.3 Genomic Divergence: Genotypes B3.13 and D1.1

A critical development in the 2024-2026 period is the divergence of the virus into distinct genotypes, each telling a different epidemiological story.

Genotype B3.13 (The Bovine Specialist):

This genotype emerged from a reassortment event between the Eurasian H5N1 and North American wild bird viruses. It is the strain responsible for the initial and widespread outbreak in U.S. dairy cattle starting in late 2023/early 2024.

• Key Mutation: PB2 M631L. The Polymerase Basic 2 (PB2) protein is part of the viral replication complex. In avian cells, it relies on the host protein ANP32A. Mammalian ANP32A is shorter and less effective for avian viruses. The M631L mutation adapts the viral polymerase to function efficiently with mammalian ANP32A, effectively "unlocking" the mammalian cell for replication.⁴ This mutation is a hallmark of the cattle-adapted strain.

Genotype D1.1 (The Wild Challenger):

This genotype represents a separate, more recent introduction from the wild bird reservoir. It was detected in spillover events in dairy cattle in Nevada, Arizona, and Wisconsin in late 2025 and early 2026.

• Key Mutation: PB2 D701N. This mutation serves a similar function to M631L but operates through a different mechanism. It enhances the nuclear import of the viral polymerase in mammalian cells by altering its interaction with the host's importin-alpha protein.⁵ The independent acquisition of mammalian adaptations (M631L in B3.13, D701N in D1.1) represents convergent evolution—the virus is finding multiple genetic pathways to conquer the mammalian host.

2.4 Reassortment and the H5N5 Emergence

The plasticity of the viral genome was further demonstrated in November 2025 with the detection of H5N5 in a human case in Washington State. This virus possesses the H5 hemagglutinin of clade 2.3.4.4b but a neuraminidase (N5) acquired from low-pathogenic North American avian influenza viruses. Such reassortants are "wild cards." While the H5 protein dictates the host range (mostly birds), the new N5 protein could alter the virus's stability, transmissibility, or sensitivity to antiviral drugs.³

3. The Mammalian Breach: Dairy Cattle Infections

3.1 Historical Context of the Bovine Outbreak

Until 2024, the scientific consensus held that cattle were not a significant host for influenza A viruses. The detection of H5N1 in Texas dairy herds in March 2024 shattered this paradigm. Retrospective analysis suggests the spillover likely occurred in late 2023, with the virus circulating undetected for months. By January 2026, the virus had spread to 19 states, establishing a recalcitrant reservoir in the U.S. dairy herd.⁸

3.2 Mechanism of Transmission: The "Milking Machine" Vector

The spread of H5N1 in cattle defies the standard respiratory model of influenza. In humans and pigs, flu spreads via coughing and sneezing. in cattle, the virus exhibits an extreme tropism for the mammary gland. Viral loads in milk are orders of magnitude higher than in nasal secretions.

• Fomite Transmission: The primary vector of transmission is not the cow, but the milking equipment. The teat cups of milking machines, if not perfectly sanitized, transfer the virus from the infected udder of one cow to the teats of the next. This mechanical transmission explains the rapid intra-herd spread despite the lack of efficient aerosol transmission.

• The "Dried Cow" Anomaly: Serological studies have found antibodies in non-lactating ("dry") cows, suggesting that while the udder is the amplifier, some level of respiratory or environmental transmission may still occur, possibly through shared water troughs or direct contact.⁹

3.3 The D1.1 Spillover Events (2025-2026)

While the B3.13 genotype became endemic in cattle, maintained by cattle movements, the D1.1 genotype represents de novo spillover from nature.

• The Wisconsin Case (Dec 2025): A dairy herd in Wisconsin tested positive for H5N1 genotype D1.1. Crucially, this herd showed no clinical signs of illness. The infection was only detected because of the USDA's National Milk Testing Strategy (NMTS), which mandates testing of bulk milk silos.¹⁰

• Implication: The existence of asymptomatic infection with D1.1 suggests that reliance on clinical surveillance (looking for sick cows) is insufficient. The virus can circulate silently, potentially exposing farm workers who are unaware of the risk.

3.4 Milk Safety and Public Health

The presence of H5N1 in milk raised immediate food safety concerns. Studies conducted throughout 2024 and 2025 consistently confirmed that standard commercial pasteurization (High-Temperature Short-Time, or HTST) effectively inactivates the virus. While viral RNA fragments (genetic debris) are often detected in store-bought milk by PCR, infectious virus is not.¹² However, the risk remains acute for farm families and workers who consume raw (unpasteurized) milk. The "raw milk" movement has thus become a significant public health vector for H5N1 exposure.

4. The Avian Reservoir: Wild Spread Dynamics

4.1 The Flyway Superhighway

The United States is intersected by four major migratory flyways: the Pacific, Central, Mississippi, and Atlantic. These corridors act as the arteries of viral dissemination.

• The Pacific Flyway: In late 2025, this flyway became the epicenter for the novel D1.1 genotype and the H5N5 reassortant. The mixing of birds from Alaska (where Asian and American flyways overlap) creates a "melting pot" for viral diversity.¹³

• The Central and Mississippi Flyways: These corridors, which overlay the nation's densest poultry and dairy regions (Iowa, Minnesota, Texas), facilitate the "rain" of virus from migrating waterfowl onto farms below.

4.2 Species Vulnerability and Mortality

The impact of H5N1 on wild birds varies dramatically by species.

• Waterfowl (Ducks/Geese): Often the primary carriers. They shed virus into wetlands where it remains infectious in cold water for weeks. While many survive, the 2025-2026 season saw significant mortality events, such as the death of 200 Canada geese in Iowa ¹⁴, indicating that the virus retains lethality even for its reservoir hosts.

• Raptors and Scavengers: Eagles, hawks, and owls are highly susceptible. They contract the virus by preying on sick waterfowl. These infections are almost invariably fatal and often present with severe neurological symptoms (torticollis, tremors).

• The "Scavenger Cycle": A disturbing ecological feedback loop has established itself. Mammalian scavengers (raccoons, opossums, skunks) feed on dead birds, contract the virus, and die. Their carcasses are then consumed by other scavengers or birds (vultures, eagles), perpetuating the cycle independent of the initial waterfowl introduction.¹⁵

4.3 Environmental Persistence

The spread potential in the wild is amplified by the environment itself. Influenza viruses are stable in cool, moist conditions. A wetland contaminated by the feces of a migrating flock in November can remain infectious to local non-migratory birds or mammals well into January. This environmental persistence decouples the presence of the virus from the presence of the host, making "wild spread" difficult to predict and impossible to contain.

5. The Poultry Crisis: Urban and Agricultural Spread

5.1 The Scale of Devastation

The U.S. poultry industry has absorbed a historic blow. From the start of the outbreak in February 2022 through January 2026, over 166 million birds have been depopulated.¹ This figure encompasses commercial broilers (meat chickens), turkeys, and egg-laying hens.

• Recent Losses (Jan 2026): The first week of 2026 alone saw 76,210 birds affected, including large outbreaks in California game bird farms and North Carolina turkey plants.¹⁴

5.2 Biosecurity and "Fortress Farming"

Commercial poultry farming in the U.S. operates on a model of "bio-exclusion." Farms are designed as fortresses to keep pathogens out. Measures include shower-in/shower-out protocols for staff, air filtration, and vehicle disinfection.

• The Breach: H5N1 exposes the tiny cracks in this fortress. The virus enters via microscopic dust particles carried on the wind (aerosolization from nearby wetlands) or via "fomites"—minute amounts of contaminated mud on a truck tire or a worker's boot. The sheer density of animals in commercial houses (often 20,000 to 50,000 birds per barn) means that once the virus breaches the perimeter, R0 (the reproduction number) skyrockets, leading to 100% infection or culling within days.

5.3 The Urban/Peri-Urban Interface: Backyard Flocks

A distinct epidemiological category is the "backyard flock." Often located in peri-urban or rural residential areas, these small holdings bridge the gap between the wild and the human.

• The "Canary in the Coal Mine": Data indicates that infections in backyard flocks often precede commercial outbreaks in the same county by approximately 9 days.¹⁶ They serve as sentinels for local environmental contamination.

• The Biosecurity Gap: Unlike commercial farms, backyard flocks often have outdoor access, allowing direct contact with wild birds. The owners rarely have access to commercial-grade PPE. The H5N5 human case in Washington was directly linked to a backyard flock, illustrating that while the economic impact of backyard outbreaks is low, the public health risk is disproportionately high due to intimate human-animal contact.³

5.4 Economic and Food Security Implications

The relentless culling of flocks has had tangible economic ripples. The egg layer industry, which accounts for 78% of total affected birds, has struggled to recover fully, leading to sustained high egg prices.¹⁷ The "urban agriculture" spread potential is thus not just a viral metric but an economic one; the high connectivity of the food system means an outbreak in Iowa impacts grocery prices in New York.

6. The Marine Mammal Outbreak

6.1 West Coast Strandings (2025-2026)

While H5N1 had previously ravaged pinniped populations in South America, the U.S. West Coast had largely been spared mass mortality events until late 2025. The confirmation of H5N1 in three harbor seals in Puget Sound, Washington, marked a critical expansion of the virus's marine range.¹⁸

• Significance: These detections bring the virus into the intricate ecosystem of the Salish Sea, threatening not just seals but potentially endangered populations of Southern Resident Killer Whales that might interact with infected seals or carcasses.

6.2 Transmission Mechanisms in Marine Environments

Transmission among marine mammals is facilitated by their social biology. Seals and sea lions "haul out" in dense colonies, lying in close contact.

• The "Colony Effect": This density mimics intensive agriculture. If a seal contracts the virus (likely by scavenging a dead seabird), it can transmit it to neighbors via respiratory droplets or mucosal contact. The South American outbreaks provided strong genomic evidence of mammal-to-mammal transmission, with the virus acquiring specific mutations to sustain this spread.¹⁹ The U.S. outbreaks are currently being monitored to see if similar seal-adapted clades are emerging in American waters.

7. The Human Interface: Clinical and Occupational Reality

7.1 Case Count and Demographics

As of January 2026, the official U.S. case count stands at 71.

• Dairy Exposure: 41 cases.

• Poultry Exposure: 24 cases.

• Unknown/Other: 6 cases.20This distribution confirms that H5N1 in the U.S. remains primarily an occupational disease of agriculture.

7.2 The Fatalities

The outbreak has resulted in two confirmed deaths in the U.S., challenging the narrative that the current clade causes only mild disease in humans.

1. Washington (Nov 2025): An adult with underlying conditions died after infection with the H5N5 reassortant. Exposure was linked to a backyard flock. This highlights the risk of novel reassortants emerging from the "mixing bowl" of backyard poultry.⁷

2. Louisiana (Jan 2026/Dec 2025): A fatality associated with the D1.1 genotype. This case was alarming because the patient had no known exposure to dairy cattle (the primary reservoir of mammalian virus) but did have poultry exposure. Genomic analysis of the patient's virus revealed mutations not present in the poultry, suggesting intra-host evolution during the course of the fatal infection.²¹

7.3 Clinical Presentation

The clinical spectrum is bifurcated.

• Mild Disease (B3.13): Most dairy workers infected with the cattle-adapted B3.13 strain present with conjunctivitis (pink eye) and mild respiratory symptoms. This is likely due to the route of exposure (splashes of contaminated milk) and the virus's receptor preference (the human eye contains alpha-2,3 receptors similar to birds).

• Severe Disease (D1.1 / H5N5): The fatalities associated with wild-origin genotypes suggest these viruses may possess intrinsic virulence factors that, once established in the lower respiratory tract, lead to severe viral pneumonia and acute respiratory distress syndrome (ARDS).

8. Comparative Spread Potential: Urban/Ag vs. Wild

8.1 Urban (Agriculture) Based Spread

Mechanism: The primary driver is anthropogenic connectivity.

• Fomites: The virus moves on truck tires, feed delivery vehicles, and shared farm equipment. In the dairy sector, the movement of asymptomatic cattle between states for breeding or grazing has been the super-spreader event of the epizootic.

• Density: The "monoculture" of modern farming provides an endless supply of genetically identical hosts. Once introduced, the virus faces no immunological firebreaks.

• Spread Potential: HIGH INTENSITY / CONTROLLED EXTENT. An outbreak in a poultry barn is explosive (high R0 locally) but can be contained to that premise via quarantine and depopulation ("stamping out"). However, the interconnectedness of the industry means that if biosecurity fails at a systemic level (e.g., a contaminated feed mill), the spread can become regional or national very quickly.

8.2 Wild Spread

Mechanism: The primary driver is ecological connectivity.

• Migration: The virus moves with the seasons. Spring and Fall migrations guarantee the re-seeding of viral diversity across the continent.

• Trophic Cascades: The virus moves up the food chain (duck -> eagle) and down (carcass -> scavenger).

• Spread Potential: VARIABLE INTENSITY / UNLIMITED EXTENT. Wild outbreaks are rarely as explosive as those in a chicken house because wild populations are less dense and more genetically diverse (herd immunity exists in wild ducks). However, the extent is limitless. The virus can reach the most remote wetland in Alaska or the most isolated seal colony in Maine. It cannot be contained, only monitored.

8.3 The Intersection: The Danger Zone

The highest spread potential exists at the Urban-Wild Interface.

• The Scenario: A dairy farm with an open lagoon attracts wild waterfowl. The waterfowl introduce the D1.1 genotype. The cows get infected (asymptomatic). The farm ships heifers to another state. The virus moves 1,000 miles in 24 hours.

• The Risk: This interface combines the unlimited extent of wild spread (constant introduction) with the high intensity of agricultural spread (amplification in cattle/poultry). It is this intersection that has sustained the outbreak from 2022 through 2026.

9. Conclusion

The H5N1 outbreak in the United States has evolved from an agricultural emergency into a persistent, multi-species panzootic. By 2026, the virus has successfully demonstrated its ability to navigate the complex landscape of North American biology, establishing reservoirs in wild birds, dairy cattle, and marine mammals.

The emergence of the D1.1 genotype and the H5N5 reassortant underscores the dynamic nature of this threat. The virus is not static; it is actively exploring the evolutionary space, acquiring mutations like PB2 D701N and M631L that lower the barrier to mammalian infection. While the lack of human-to-human transmission provides a continued (though fragile) safety margin for the general public, the agricultural workforce remains on the frontline of a high-stakes biological conflict.

The "spread potential" of H5N1 is no longer a theoretical projection but an observed reality. In the wild, it is ubiquitous and uncontrollable. In urban agriculture, it is manageable but prone to catastrophic breaches due to human error and systemic connectivity. The future of this outbreak depends on the rigorous application of "One Health" principles—recognizing that the health of the dairy cow, the migratory goose, and the farm worker are inextricably linked in the viral web of H5N1.

Data Tables

Table 1: Comparative Profile of H5N1 Genotypes in the U.S. (Jan 2026)

Feature	Genotype B3.13 (The Bovine Strain)	Genotype D1.1 (The Wild Strain)	H5N5 Reassortant
Origin	Spillover from wild birds (late 2023)	Recent spillover (late 2025)	Pacific Flyway Reassortment
Primary Reservoir	Dairy Cattle	Wild Birds	Wild Birds / Backyard Poultry
Key Mutation	PB2 M631L (Adaptation to mammalian ANP32A)	PB2 D701N (Enhanced nuclear import)	Variable / Under Analysis
Clinical Signs (Cattle)	High Morbidity: Drop in milk, thick milk, lethargy	Asymptomatic / Subclinical (in early detections)	Not established in cattle
Human Impact	Multiple non-fatal cases (conjunctivitis)	1 Fatal Case (Louisiana)	1 Fatal Case (Washington)
Detection Method	Clinical observation & Testing	Silo/Bulk Tank Surveillance (NMTS)	Clinical testing of patient

Table 2: Confirmed Human Cases of H5 Bird Flu in the U.S. (2024–2026)

State	Case Count	Primary Exposure Context
California	High (>20)	Dairy Cattle & Poultry Workers
Colorado	High (>10)	Poultry Cullers (Cluster Event)
Michigan	Moderate	Dairy Cattle
Washington	Moderate	Poultry / Backyard Flocks (Inc. 1 Death)
Louisiana	Low (1)	Poultry / Unknown (1 Death)
Missouri	Low (1)	No known animal exposure (Sentinel case)
Texas	Low	Dairy Cattle (Index cases)
TOTAL	71	Predominantly Occupational

Source Data: CDC Situation Summary, Jan 2026.²

Detailed Biological Mechanisms (Descriptive)

To further elucidate the mechanisms discussed in Section 2, we provide a descriptive breakdown of the viral replication cycle and how specific mutations alter it.

The Polymerase Complex:

Imagine the viral polymerase as a photocopy machine. Its job is to copy the viral RNA genome inside the nucleus of the host cell.

• Avian Polymerase: In bird cells, this machine runs hot (41°C) and relies on a specific "power source" provided by the bird cell, a protein called ANP32A.

• The Mammalian Problem: In mammal cells, the temperature is cooler (33-37°C) and the "power source" (Mammalian ANP32A) is shaped differently—it is missing a specific segment that the avian polymerase grabs onto. Consequently, a standard bird flu virus is like a photocopier unplugged; it works very poorly in humans.

• The M631L Solution (Genotype B3.13): The virus acquires a mutation (M631L) that changes the shape of the polymerase. This allows it to "plug in" to the shorter mammalian ANP32A protein. The photocopier turns on, and the virus replicates efficiently in the cow's udder or the human eye.

• The D701N Solution (Genotype D1.1): This mutation affects a different part of the process—getting the photocopier into the office (the nucleus). The D701N mutation acts like a VIP pass, allowing the viral polymerase to interact more strongly with the cellular "doorman" (importin-alpha), ensuring that more polymerase molecules enter the nucleus to start copying the genome.

Hemagglutinin Binding:

• Avian Receptors (Alpha-2,3): Think of these as a specific shape of door handle found on cells. In birds, these handles are everywhere (gut, lungs). In humans, these handles are rare in the nose but present deep in the lungs and on the surface of the eye. This explains why humans get eye infections (conjunctivitis) or deep pneumonia, but don't easily spread the virus via sneezing (which requires infection of the nose).

• Human Receptors (Alpha-2,6): These are the door handles found in the human nose and throat. For H5N1 to become a pandemic, it must mutate its HA protein to grab these handles. As of 2026, despite the other adaptations, H5N1 has not yet made this critical switch.

10. Spread Potential Analysis: A Theoretical Framework

The spread of H5N1 can be analyzed through the concept of the Basic Reproduction Number (R0), which represents the average number of new infections generated by one infected individual.

In the Wild:

• R0 varies seasonally. During migration, when birds congregate in millions at stopover sites, R0 > 1 (epidemic spread). In the summer, when birds disperse to breed, R0 drops (endemic maintenance). The persistence of the virus in the environment (water) creates a "reservoir effect," meaning R0 doesn't need to stay above 1 for the virus to survive; it can wait in the mud for the next host.

In Urban Agriculture (Dairy/Poultry):

• R0 is artificially amplified. In a poultry barn with 50,000 birds, density is maximum. Once introduced, R0 is extremely high (often >10).

• In Dairy: The "effective R0" depends on human intervention. Without sanitation, the milking machine ensures R0 > 1. With strict sanitation, R0 < 1. The persistence of the outbreak suggests that biosecurity execution is imperfect.

• The Network Effect: The U.S. agriculture system is a "small-world network." Farms are connected by feed trucks, veterinarians, and livestock haulers. This high connectivity means that a localized outbreak has a high potential to become systemic if movement restrictions are not immediate.

In Humans:

• Current R0 < 1. The virus spills over (R > 0) but cannot sustain a chain of transmission. The goal of public health is to ensure R0 remains below 1 by preventing the specific mutations (like the HA receptor switch) that would increase transmissibility.

This framework explains why the "Urban/Ag" spread is characterized by explosive clusters that require drastic intervention (culling), while "Wild" spread is a slow-burning, unstoppable continental wave. The current strategy in the U.S. is to build a "firewall" between these two systems—a firewall that, in 2026, is under severe strain.

Works cited

1. USDA announces additional $1B toward H5N1 efforts, accessed January 8, 2026, https://www.avma.org/news/usda-announces-additional-1b-toward-h5n1-efforts

2. Novel H5N1 Bird Flu Outbreak - American Academy of Ophthalmology, accessed January 8, 2026, https://www.aao.org/education/bird-flu

3. 11/20/25 Provider Alert: Case of H5N5 Influenza Confirmed in Washington - Whatcom, accessed January 8, 2026, https://providers.whatcomcounty.org/2025/11/11-19-25-provider-alert-case-of-h5n5-influenza-confirmed-in-washington/

4. Polymerase mutations underlie early adaptation of H5N1 influenza virus to dairy cattle and other mammals | bioRxiv, accessed January 8, 2026, https://www.biorxiv.org/content/10.1101/2025.01.06.631435v2.full-text

5. The Occurrence of Another Highly Pathogenic Avian Influenza (HPAI) Spillover from Wild Birds into Dairy Cattle - Animal and Plant Health Inspection Service - USDA, accessed January 8, 2026, https://www.aphis.usda.gov/sites/default/files/dairy-cattle-hpai-tech-brief.pdf

6. Timing and molecular characterisation of the transmission to cattle of H5N1 influenza A virus genotype D1.1, clade 2.3.4.4b - Virological, accessed January 8, 2026, https://virological.org/t/timing-and-molecular-characterisation-of-the-transmission-to-cattle-of-h5n1-influenza-a-virus-genotype-d1-1-clade-2-3-4-4b/991

7. Avian Influenza A(H5N5)- United States of America - World Health Organization (WHO), accessed January 8, 2026, https://www.who.int/emergencies/disease-outbreak-news/item/2025-DON590

8. Avian influenza virus type A (H5N1) in U.S. dairy cattle | American Veterinary Medical Association, accessed January 8, 2026, https://www.avma.org/resources-tools/animal-health-and-welfare/animal-health/avian-influenza/avian-influenza-virus-type-h5n1-us-dairy-cattle

9. H5N1 dairy cow study finds sustained milk production drop, extensive transmission across herd | CIDRAP, accessed January 8, 2026, https://www.cidrap.umn.edu/avian-influenza-bird-flu/h5n1-dairy-cow-study-finds-sustained-milk-production-drop-extensive

10. USDA Confirms Highly Pathogenic Avian Influenza in a Dairy Herd in Wisconsin, accessed January 8, 2026, https://www.aphis.usda.gov/news/agency-announcements/usda-confirms-highly-pathogenic-avian-influenza-dairy-herd-wisconsin

11. Wildlife linked to H5N1 spread in Wisconsin dairy farm, accessed January 8, 2026, https://www.dvm360.com/view/wildlife-linked-to-h5n1-spread-in-wisconsin-dairy-farm

12. Rapid Review: Survivability of Influenza A(H5N1) in Milk - Public Health Ontario, accessed January 8, 2026, https://www.publichealthontario.ca/-/media/Documents/A/24/ah5n1-survivability-influenza-milk.pdf?rev=69786e6f11fd402c8aba52b35f998e9f&sc_lang=en

13. Emergence of D1.1 reassortant H5N1 avian influenza viruses in North America | bioRxiv, accessed January 8, 2026, https://www.biorxiv.org/content/10.64898/2025.12.19.695329v1.full

14. Over 76K birds infected by bird flu since start of 2026, accessed January 8, 2026, https://www.ktvb.com/article/news/nation-world/bird-flu-infects-thousands-since-start-of-2026/507-693deda2-81ee-46e0-9725-791e63f26a16

15. Risk of avian influenza to animals that scavenge on infected carcasses | Wildlife Research, accessed January 8, 2026, https://connectsci.au/wr/article/52/12/WR25052/266096/Risk-of-avian-influenza-to-animals-that-scavenge

16. Intensive transmission in wild, migratory birds drove rapid geographic dissemination and repeated spillovers of H5N1 into agriculture in North America - PubMed Central, accessed January 8, 2026, https://pmc.ncbi.nlm.nih.gov/articles/PMC11702765/

17. Update on Highly Pathogenic Avian Influenza - Farm Credit Administration, accessed January 8, 2026, https://www.fca.gov/template-fca/about/2025MarchUpdateonHPAI.pdf

18. Tests confirm H5N1 avian flu in Washington seals | CIDRAP, accessed January 8, 2026, https://www.cidrap.umn.edu/avian-influenza-bird-flu/tests-confirm-h5n1-avian-flu-washington-seals

19. Bird flu is increasingly adapting to mammals - University of California, accessed January 8, 2026, https://www.universityofcalifornia.edu/news/bird-flu-increasingly-adapting-mammals

20. H5 Bird Flu: Current Situation - CDC, accessed January 8, 2026, https://www.cdc.gov/bird-flu/situation-summary/index.html

21. Genetic Sequences of Highly Pathogenic Avian Influenza A(H5N1) Viruses Identified in a Person in Louisiana | Bird Flu | CDC, accessed January 8, 2026, https://www.cdc.gov/bird-flu/spotlights/h5n1-response-12232024.html