Abrupt Shift in H5N1 Genotypes in Wild Birds in US/Canada
#19,120
After its arrival in eastern Canada in late 2021, HPAI H5N1 spread quickly to the U.S. - reassorting with local LPAI avian flu viruses as it traveled - producing more than 100 new genotypes.While most of these reassortants were unremarkable, in early 2024 a B3.13 genotype emerged that was particularly well-suited for infecting dairy cattle. Six months later, another new genotype appeared in North American birds; D1.1.
In short order (see chart above), this upstart D1.1 genotype went from zero detections to dominating in wild birds, spilling over into poultry farms, infecting poultry workers, and sometimes displaying signs of antiviral resistance (see Emerg. Microbes & Inf: Oseltamivir Resistant H5N1 (Genotype D1.1) found On 8 Canadian Poultry Farms).
Unlike the `bovine' strain - which typically produced mild (primarily conjunctival) symptoms in humans, D1.1 produced more serious illness in a number of cases.
- In November of 2024, we learned of a severe case involving a teenage girl in British Columbia (see NEJM: Critical Illness in an Adolescent with Influenza A(H5N1) Virus Infection)
- The following January the Louisiana Department of Health Announced the 1st U.S. H5N1-related Fatality
- And a Fatal case was reported in Mexico (see WHO DON Update On Mexico's Fatal H5N1 Infection) in April.
Recent studies suggest it may also be better adapted to human physiology (see J.I.D.: Avian influenza virus A(H5N1) genotype D1.1 is better adapted to human nasal and airway organoids than genotype B3.13).
All of which brings us to a Brief Communications - published in Nature Medicine - which details the origins, and rapid spread, of D1.1 in North American birds. I've only posted some brief excerpts, so follow the link to read it in its entirety.
I'll return with more after the break.
Published: 15 April 2026
Walter N. Harrington, Anthony Signore, Lisa Kercher, Jolene A. Giacinti, Ahmed Kandeil, Christina A. Ahlstrom, Sarah Bevins, Beate Crossley, Karlie Eure, Thomas P. Fabrizio, Trushar Jeevan, Julianna Lenoch, Jacqueline M. Nolting, Daniel Rejmanek, David Stallknecht, Trent Bollinger, Evan J. Buck, Deborah Carter, Bradley S. Cohen, Krista E. Dilione, Jamie C. Feddersen, John Franks, Dayna Goldsmith, Cory J. Highway, …Richard J. Webby
Nature Medicine (2026)Cite this article
Abstract
In late 2021, high pathogenicity avian influenza A(H5N1) clade 2.3.4.4b viruses entered North America and reassorted rapidly with local avian influenza viruses. In September 2024, we detected a new reassortant later classified as genotype D1.1. Using active and passive avian influenza surveillance across Canada and the USA, we tracked the emergence and rapid spread of D1.1 viruses in wild birds during the 2024 fall migration.
Phylodynamic analysis showed that D1.1 viruses formed a monophyletic group and displaced earlier A(H5) genotypes across several flyways. Their expansion coincided with detections in other hosts, including 17 human cases, 4 of which were severe or fatal. None of the mammalian-adaptive markers detected in human cases were found in wild bird viruses, and candidate vaccine viruses retained antigenic cross-reactivity with D1.1 strains.
(SNIP)
Conclusion
The emergence and rapid spread of HPAI A(H5N1) genotype D1.1 viruses across North American migratory flyways during the 2024 migration season represents a notable shift in clade 2.3.4.4b epidemiology. Several factors may explain the unusually efficient transmission of D1.1. Genomic analyses show that this genotype includes a distinct North American–derived neuraminidase (NA) segment, which may provide antigenic advantages because population immunity to this NA is probably lower than to NA segments circulating widely before 2024.
Although principal mammalian adaptation markers were absent in the wild bird samples, some D1.1 viruses carried several mutations with reported phenotypic effects (Supplementary Table 2), which may have contributed to their dominance. Increased densities of immunologically naive juvenile birds during southbound migration may have facilitated rapid viral amplification at staging areas14.
Environmental conditions also probably played some role in the dissemination of genotype D1.1 viruses. Persistent drought and altered habitat use at important breeding and staging areas may have led to increased mixing and density of wild birds, facilitating interspecies viral transmission15. These ecological factors, combined with the novelty of the genotype in wild populations, may have enabled the rapid geographic spread observed.
Although D1.1 viruses circulating in wild birds currently lack principal mammalian adaptation markers, their sustained replication in mammalian hosts, such as US dairy cattle16, increases the evolutionary potential for zoonotic transmission. D1.1 viruses detected in poultry in British Columbia were found to carry the NA-H275Y mutation—a known marker for resistance to oseltamivir17, demonstrating that resistance and adaptation markers can emerge stochastically, even without selection pressure.
(SNIP)
In conclusion, the emergence of the D1.1 viruses coincided temporally with the southward autumn migration of North American waterfowl, favoring their dissemination. Their spread highlights the need for an integrated One Health response18 that aligns wildlife surveillance, agricultural biosecurity and public health preparedness.
D1.1 likely remains a key player in North American birds, but the lack of genomic specificity in recent reporting makes it difficult to quantify how prevalent it remains in 2026. The USDA's dashboard of wildbird detections does not specify genotype, and instead classifies viruses as:
- EA = Eurasian; AM = North American; the EA H5 (2.3.4.4) viruses are highly pathogenic to poultry.
- EA/AM: reassortant of H5 goose/Guangdong and North American wild bird lineage
While D1.1 has demonstrated remarkable ecological success - and a concerning ability to spillover into mammals - it doesn't appear to be ready for prime time.
It does, however, remind us how abruptly the novel fluscape can change.
Whatever critical zoonotic traits D1.1 (and other genotypes) currently lack could easily be rectified by some future untoward reassortment event.
But without substantially improved wildlife and agricultural surveillance under a One Health framework - and the rapid and open sharing of data - we'll likely never see it coming.
