Will the Wolf Ever Show Up? Pandemic Influenza Outlook for 2026

USDA-APHIS-VS senior leaders retire, adding a bit more uncertainty to the public health and pandemic preparedness dumpster fire at HHS-CDC plus mid-January HPAI case counts are here

I retired from APHIS-Veterinary Services in December 2023 with a large cadre of really remarkable scientists in place within the institution’s policy, program, and laboratory positions in animal and zoonotic disease diagnostics and management. Several of these outstanding public servants-scientists remain, but massive disruptive staffing losses have occurred. USDA announced the retirement of 2 more top leaders this week: USDA names new APHIS leadership.

Administrator Dr. Michael Watson (left) and Chief Veterinary Officer Dr. Rosemary Sifford (right) are retiring from the U.S. Department of Agriculture’s Animal & Plant Health Inspection Service.

The U.S. Department of Agriculture has announced important leadership changes within the Animal & Plant Health Inspection Service. Dr. Michael Watson, APHIS administrator, will retire at the end of January after decades of distinguished service, and Dr. Rosemary Sifford, deputy administrator for Veterinary Services (VS) and U.S. chief veterinary officer, has recently retired from federal service after a similarly notable career.

Beginning Feb. 1, 2026, Kelly Moore will serve as acting administrator, and effective immediately, Dr. Alan Huddleston will serve as the acting U.S. chief veterinary officer. Additionally, to ensure continuity during this transition, APHIS VS Associate Deputy Administrator Dr. Adis Dijab will continue to provide operational oversight of VS.

Losing professional enterprise is always costly; technical skills can be replaced via training of qualified new hires. However, institutional awareness and political savvy is critical in federal service and much more challenging to cultivate and quickly replace. Adis and Alan are good friends to me, possessing loads of astute experience that will continue to serve them well as they take the reins at VS.

The far larger leadership threat faced by the federal animal and one health mission is the hollowing out of the large core of the agency’s staffing via the accumulation of ill-advised staff reductions / early retirements / mandatory relocations / budget cutting policies rained down by the “Department” of Government Efficiency and Office of Management and Budget (OMB) butchers in early-mid 2025. Upper leadership continuity within federal service requires a “farm system” for talent development. When minor league rosters are needlessly decimated by short-sighted and vindictive measures to run up illusory budget savings, the resulting replacement bench is really thin as veterans step down. Moving to SES leadership is even less attractive to potential candidates when considering demoralized staffs saddled with 100% back-to-office mandates in arbitrary new regional “red state” centers, combined with new expectations that ALL policies and procedures must align with dogmatic politicized administration priorities.

Actually, this administrative demoralization is not a “bug, but a feature” of the entire process in the eyes of the current Administration and OMB. This is an openly stated plan to greatly shrink the federal workforce of autonomous professionals, to be replaced with political at will hires answerable to the White House through OMB and the White House Policy Director’s Office. The concept is that the entire administrative branch should operate as all levels as an extension of the president’s political and policy goals

For all the complaints about an arrogant federal bureaucracy that answers to no one, I suspect we are quickly learning via the CDC-FDA carnage (and a multitude of other examples) that excessive adherence to selective political pressure (e.g. RFK Jr and MAHA) in executive branch policies and decision-making fairly quickly literally leads to mortal danger (e.g. measles, Hepatitis B).

The U.S. Civil Service, guarded by an independent, protected Senior Executive Service with independent Inspectors General in each agency serves vital functions in a free society. Additionally, the entire democratic system fails when political parties abdicate their critical Legislative oversight in subservience to political calculations. 2026 is a pivotal year in our nation’s history regarding whether we choose to return to checks and balances that maintain our freedoms and safety. When our political leadership fails to meet its responsibilities for good governance over political opportunism, the voters must replace them.

To wrap up this mini-rant I’d hasten to add that in my opinion the USDA under Secretary Rollins has to date avoided the worst of the excesses in administrative mismanagement rained down in HHS. I have absolutely no inside track to “life on the inside” at USDA; however, the interim appointments announced this week for the leadership positions seem reasonable. I hope the reality of the upcoming elections will help to restore more needed funding and reverse some of the more egregious cutting and reorganization excesses hastily laid out in 2025. The resources the U.S. spends in animal and human health research, detection, response, and recovery are miniscule compared to the real future costs of inaction and mal governance.

The Regulatory Medicine Response Ecology

U.S. government and USDA ag policy development and execution related to animal health, food safety, and zoonotic disease management are fascinating topics, well beyond the scope of a paragraph, a column, and really beyond my depth of knowledge. The institutional and financial interests with a stake in setting policies are both rich and powerful. We’ve all seen estimates for calamitous losses expected in the event of a foreign animal disease outbreak, with a big share of the pain due to export market dependency for meat in particular. Any unexpected new threat to our animal food production-supply system sets off texts to multitudes of producers, processing companies, commodity organizations, public and private scientists, plus international, federal, state, and local government agencies.

We’d like to think that in an ideal world our seasoned federal, state, and local outbreak decision-makers, in collaboration with industry leadership, would utilize pre-ordained plans, best practices, and diagnostic protocols to develop a unified response to the threat. In fact, we faithfully practice those events repeatedly for named foreign animal disease agents via tabletop exercises and declare ourselves ready for the challenge.

So how did our responses work for the last real world highly contagious animal disease outbreaks: 1) PEDV in pigs; 2) SARS-CoV-II in minks, big cats, pets, etc.; and 3) H5N1 2.3.4.4b B3.13 in TX dairy cattle? In all those examples, concerns over trade disruptions and interstate commerce, lack of “validated tests”, response capacity concerns, and/or fears over lack of authority aborted chances for effective action to stop spread of infectious agents beyond early containment or effectively manage worker zoonotic risk. We are not wired as a society as reflected in our governmental restraints, to take effective collective action to prevent spread of highly infectious disease agents! The COVID pandemic has only made our prospects more remote. Private interests with extreme financial risk, deep pockets and competent lawyers will likely legally prevent or at least delay the widespread testing needed to make early detection and response possible for elimination of highly infectious novel or FAD agents.

H5N1 B3.13 in cattle may have been the ultimate test of whether the government had the wherewithal to use “extraordinary emergency” rules to enforce testing and movement controls. They declined to do so under pressure from powerful lobbying interests, despite H5N1 being a known zoonotic reportable animal disease in poultry and a listed Select Agent. It’s certainly doubtful whether we had the knowledge and capacity to get ahead of that virus, especially with a long-delayed diagnosis and widespread interstate movements. My point is that we will likely be forced into “fallback positions” short of immediate elimination, no matter what the agent (including FAD’s) with a detection system reliant only on visible clinical signs in industries moving so many animals across multiple states daily.

APHIS-VS is a science-based agency! It does the very best it can to meet scientifically rigorous standards within the constraints of the real world where it operates. “Political science” is an unfortunate reality in the imperfect world where the federal-state-industry animal health collaboration operates.

HPAI and Regulatory Medicine

I hope VS can maintain and enhance its science-based approach to HPAI by leading stakeholders in re-examining the assumptions upon which the H5/H7 NPIP Program was established. It’s become apparent that the current HPAI outbreak is “not your father’s” regulatory H5, in any shape or form! We have a state-federal-industry NPIP Program that aligns with inflexible international trade and vaccine policies built for rare H5/H7 viral incursions into the world poultry production stage, manageable with reasonable biosecurity and exclusion protocols and fallbacks through zoning and compartmentalization.

Now we have agents (H5N1 2.3.4.4b genotypes) that don’t respect those assumptions! Wildlife vectors are entirely too widespread, and zoning / compartmentalization does not counteract intense area spread pressures. We cannot offer the industry proven protocols that reliably assure negative production locations or processes! Intense bio-security protocols are certainly of great assistance; however, breakthroughs are inevitable and expensive. We still lack good case-control studies showing relative efficacy results for various biosecurity recommendations. Recently a new review was released arguing that human downtime restrictions are not scientifically proven to be effective in preventing disease transmission: Are Visitor and Personnel Downtime Restrictions an Effective Biosecurity Measure to Prevent the Indirect Transmission of Pathogens to Livestock? The same questions could be asked of truck traffic, visitors, air and dust, etc.

What we DO know is that we now have lots of H5N1 2.3.4.4b outbreaks across North America, all of Europe, and much of the rest of the world with all reporting difficult control options. Wildlife viral isolation is increasingly widespread, extending to mammals, and on all continents, except Australia.

H5N1 2.3.4.4b is a world-wide highly transmissible endemic virus with documented aerosol transmission risk harbored in migrating wildlife reservoirs with nearly 100% lethality in domesticated poultry populations. The ecological viral reservoir risk for the world’s poultry population has completely transformed from low level and sporadic 10 years ago to increasingly intense today. Additionally, this virus has now acquired increased mammalian adaptations, with multiple documented spillovers and mutational adaptations in its genomes, adding additional mammalian reservoirs and zoonotic risk with this pathogen.

However, we still attempt manage HPAI risk with regulatory and trade rules assuming that we can consistently exclude HPAI from larger populations solely with biosecurity exclusion measures, a program designed for a historical HPAI viral profile of very limited and transient risk for wildlife carriage of a less transmissible virus. Our exclusion and trade assurance strategies have not changed to keep pace with the changes in the HPAI virus.

I don’t know when the dam will burst, but the current situation is unsustainable.

HPAI as of mid-January 2026

On January 14th we crossed 300 cases for the fall-winter 2025026 HPAI season in U.S. Poultry by my summary of USDA reporting:

We’ve been collectively fortunate on the egg front, in that the earlier large layer outbreak took place in an area with groups of smaller layer buildings, rather than the larger complexes hit in 2024-25. The national impact on the egg supply has been nonexistent. Additionally, the U.S. has had relatively more backyard flock outbreaks recently, since the northern Indiana area commercial flocks outbreak burned out.

After November and December averaged nearly 3 detections per day, January may be moving closer to 2 per day, as backyard flocks tend to be “one offs”. That could deteriorate if another poultry-dense area should become widely infected where multiple sites break concurrently.

Here is a look at the most recent January 2026 outbreak list:

20 of the 35 reported cases have been in backyard flocks (17) or live markets (3). Recent broiler outbreaks in GA and DE and turkey outbreaks in MN and NC bear watching, since both are in poultry dense areas. Hopefully, those outbreaks will remain contained on affected sites. (Note near release time: 3 large Minnesota turkey sites (over 370,000 birds) were reported Monday by NVSL in Meeker and Stearns Counties)

Zoonotic Outlook

I came across 2 articles for your review recently:

NYTimes011026-Bird Flu Viruses Raise Mounting Concerns Among Scientists

‘It’s completely out of control’: Scientists warn bird flu could spark a human pandemic in 2026 | BBC Science Focus Magazine

I didn’t really spot anything totally new or revelatory in the interviews, but we need to keep reading them as reminders of the overriding zoonotic threats we face. I’m more interested in some less publicized research summarized this week by Michael Coston in his Avian Flu Diary posting regarding a recent bioRx release from Switzerland: Avian Flu Diary: Preprint: Bovine-derived Influenza A virus (H5N1) Shows Efficient Replication in Well-differentiated Human Nasal Epithelial Cells Without Requiring Genetic Adaptation

Based on limited surveillance and reporting systems (see NAS : Diagnostic Tools, Gaps, and Collaborative Pathways in Human H5N1 Detection (Rapid Expert Consultation), the available evidence suggests that HPAI H5N1 viruses are not currently transmitting efficiently (or often) among humans.

While somewhat reassuring, we’ve also seen evidence to suggest that mild, or asymptomatic cases are likely being missed (see MMWR: Serologic Evidence of Recent Infection with HPAI A(H5) Virus Among Dairy Workers and JAMA Open: Asymptomatic Human Infections With Avian Influenza A(H5N1) Virus Confirmed by Molecular and Serologic Testing).

While the WHO, PAHO, and the ECDC (see ECDC Pre-pandemic Guidance: Strategies to Fight Avian and Swine flu in Humans) have all called for increased vigilance, there appears to be some reluctance among many member countries - and their agricultural interests - to comply.

Meanwhile, we continue to see studies and preprints that suggest that HPAI H5Nx viruses are continuing to accrue mammalian adaptations (see here, here, here, here, and here).

To this rapidly expanding list we can add a new preprint from researchers in Switzerland who conducted experiments to test the replication of the bovine (B3.13) H5N1 virus in human nasal epithelial cells - and found they replicated remarkably well - even at low temperatures.

That said, after 24-hours, the human innate immune system was able to substantially reduce replication via IFN-λ (`lambda interferons’), which may explain its relatively mild presentation.

Here is the link to the entire release: Bovine-derived influenza A virus (H5N1) shows efficient replication in well-differentiated human nasal epithelial cells without requiring genetic adaptation | bioRxiv

I found the concluding section of the Discussion related to why B3.13 had not yet spread well in the humans to be quite interesting:

Overall, our results show that bovine-derived H5N1Tex/24 replicates at high titers in primary human nasal epithelial cells even though it lacks many canonical markers of adaptation to mammals. This observation contrasts with the currently low number of confirmed human infections. There are several possible explanations for this discrepancy. First, the sensitivity of H5N1Tex/24 to the antiviral effects of MxA may limit virus dissemination to the lower respiratory tract and thus disease severity. Second, human infections may go undetected because they are completely asymptomatic or because they are associated with only mild symptoms. Third, efficient airborne transmission of H5N1 requires that HA induces membrane fusion at pH values significantly lower than pH 6.0. However, the HA protein of bovine H5N1 retains typical avian characteristics, with fusion triggered at approximately pH 6.0. Finally, preexisting immunity to influenza viruses may provide some partial protection against bovine H5N1. Cross-reactive antibodies against the NA protein of human H1N1 viruses can particularly inhibit avian N1 sialidase activity, thereby potentially limiting replication of clade-2.3.4.4b viruses. The recent fatal human case caused by a H5N5 HPAI virus in the United States is alarming, as there is probably no pre-existing immunity to the N5 antigen in the human population. Overall, our results show that H5N1Tex/24 has a remarkable ability to replicate in primary human nasal epithelial cells. Since well-differentiated nasal epithelial cells represent a relevant model for the human upper respiratory tract, it is not unlikely that the virus can also replicate efficiently in vivo in humans.

Finally, the Avian Flu Diary blog references a paper released on November 24th by researchers from the University of Hong Kong-China:

Avian Influenza Virus A(H5N1) Genotype D1.1 Is Better Adapted to Human Nasal and Airway Organoids Than Genotype B3.13 | The Journal of Infectious Diseases | Oxford Academic

The Abstract of this paper states:

Three critically ill or fatal avian influenza A(H5N1) human infections have been reported in North America since November 2024. Notably, all were infected with genotype D1.1 instead of B3.13, the dominant genotype before November 2024. Here, we demonstrated that D1.1 could replicate to higher titers in human nasal and airway organoid–derived transwell monolayers from 6 donors. D1.1 exhibited a better binding to α2,3- and α2,6-linked sialic acid than B3.13. No significant differences in most inflammatory or antiviral cytokines/chemokines were observed. These observations suggest that D1.1 is better adapted to both the upper and lower human respiratory tract epithelium than B3.13.

Further, the paper later makes the following statement: “As D1.1 is now widespread among dairy cows in the United States…”

I believe we need to keep a few cautions in mind in possibly overinterpreting the conclusions of this paper. The discussion states:

The reverse genetically derived D1.1 strain we used in this experiment was constructed based on the D1.1 from a critically ill patient and contained 3 markers of human adaptation, including HA E186D, HA Q222H, and PB2 E627K [2]. HA Q222L and PB2 E627K have been associated with airborne transmission of H5N1 virus [15]. Further studies are required to delineate whether the difference in replication between D1.1 and B3.13 is related to these markers.

Thus, the D1.1 strain utilized in the Chinese study was reverse engineered with adaptation markers which are not universally found in all D1.1 isolates in poultry or mammals in the U.S. The paper by Alvin Crespo-Bellido and Martha I. Nelson discussed in my last blog (Peace on Earth in Solstice Darkness as Wisconsin Dairy Case is Sequenced as a Separate H5N1 2.3.4.4b D1.1 Spillover) states that:

“Most spillovers from D1.1 into humans, domestic cats, and terrestrial and marine carnivores involve direct exposure to wild birds, and key PB2 mutations that improve replication efficiency in mammals (e.g., E627K and D701N) are frequently selected for. Of the nine D1.1 infections in humans, three viruses acquired PB2 mammalian adaptations: D701N in A/Nevada/10/2025 and E627K in A/Wyoming/01/2025 and A/British Columbia/PHL-2032/2024 (Figure 1B).”

While D1.1 PB2 mammalian adaptations are certainly selected for in spillovers, they have not to our knowledge been universally incorporated into a stable replicating mammalian strain circulating in cattle or other mammalian species in the U.S. (only 3 of nine had known adaptations).

Additionally, we can certainly discuss to what degree our surveillance could be missing D1.1 infections in dairy herds, but no one could credibly consider our dairy cattle D1.1 infection status to be “widespread” at this point, with or without a fixed PB2 E627K enhanced mammalian transmission mutation.

The take home points from all the papers to me remains that H5N1 2.3.4.4b zoonotic potential remains and is likely increasing as this virus continues to roll the dice with mammals, given its ubiquity in birds. We have 2 huge tasks at hand, neither of which we are accomplishing very well at this point:

1. Increase viral detection and sequencing breadth, speed, and transparency in wild birds, domestic poultry, wild mammals, and domestic livestock and pets in an integrated fashion.

2. Open up the information to the national and international research community for accelerated research progress. Refer to the comments in the Discussion section of the Crespo-Bellido-Nelson paper regarding the effects of severe data deficiencies on analyses for D1.1 and H5N5, both urgent topics of current concern.

I’m actually quite pessimistic that we will make much progress in any of these areas…We can’t even report sporadic human ILI in poultry, dairy, or swine contacts for testing at this point! We may repeat sporadic severe H5 illnesses yet this winter related to backyard flock or commercial outbreak exposures.

Not to be excessively morbid, but we have a 0.88% mortality rate to date (1 of 113 infected flocks) for owners of infected backyard poultry flocks. We lost a producer in Washington to H5N5 due to a very delayed human influenza diagnosis; I assume that flock was only diagnosed after the owner was positively diagnosed. The poultry industry does a wonderful job of outreach to small producers, but it’s an overwhelming task to reach so many life-style producers across the country.

Also, consider the challenge for the medical community. Here is King County WA Public Health’s Updated guidance for clinical consideration of Avian Influenza (where the unfortunate fatality occurred). In reading through the underlined and highlighted sections, it’s pretty clear that local hospitals and emergency personnel are not yet fully cognizant on the H5N1 risks and clues for people exposed to birds or mammals at risk for influenza infections. Given what was disclosed publicly regarding the deceased patient’s illness timeline, delayed human diagnostics and treatment for zoonotic influenza likely remain a big challenge, especially in resource challenged smaller medical facilities. Any assistance we can provide on the veterinary side in client education and diagnostic diligence on the farm may be critical in pointing human clinicians towards earlier influenza diagnostic differential testing for exposed workers or their families.

B3.13-D1.1 Cross Exposure Dairy Cattle

I had promised in the last blog to return to the ARS-ISU paper: Inoculation with highly pathogenic avian influenza H5N1 genotype D1.1 in naïve dairy cows and dairy cows previously exposed to genotype B3.13 | Research Square. Briefly, the results raise a lot more questions, which I’m sure are on the docket:

1. Will D1.1 transmit in BSL-3 via aerosol/respiratory any better than B3.13?

2. Is D1.1 more prominent in the blood stream (as evidenced by movement to other quarters)?

3. Does it tend to accumulate further mutations upon replication in cattle? Are these mutations stable (fixed) and transferable on to new species?

4. What about D1.1 or B3.13 reinfection of D1.1 infected cattle?

5. Are cattle isolates still fully infectious back to poultry/other avian species?

Hopefully, research and field diagnostics for D1.1 will accelerate now as some of the fear fades among producers over potential governmental response.

Wrapping Up

I think it’s worth repeating my earlier thoughts related to HPAI and Regulatory Medicine:

H5N1 2.3.4.4b is a world-wide highly transmissible endemic virus with documented aerosol transmission risk harbored in migrating wildlife reservoirs with nearly 100% lethality in domesticated poultry populations. The ecological viral reservoir risk for the world’s poultry population has completely transformed from low level and sporadic 10 years ago to increasingly intense today. Additionally, this virus has now acquired increased mammalian adaptations, with multiple documented spillovers and mutational adaptations in its genomes, adding additional reservoirs and zoonotic risk with this pathogen.

However, we still attempt manage HPAI risk with regulatory and trade rules that assume we can consistently exclude HPAI from larger populations solely with biosecurity exclusion measures, a program designed for a historical HPAI viral profile with very limited and transient risk for wildlife carriage of a less transmissible virus. Our exclusion and trade assurance strategies have not changed to keep pace with the changes in the HPAI virus.

I don’t know when the dam will burst, but the current situation is unsustainable. Another 600,000 turkeys and broilers bit the dust this past week in MN, GA, and DE as of this evening, none of them layers, yet…

Every day is an adventure - stay strong…

John