ArticleAdvanced genetics (Hoboken, N.J.)2026
Evolution of H5N1 Cross-Species Transmission: Adaptive Mutations Driving Avian-to-Human Infection.
Article in Advanced genetics (Hoboken, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Experimental Highly Pathogenic Avian Influenza A(H5N1) Clade 2.3.4.4b Virus Infection in Alpacas, 2026.Emerging infectious diseases · 2026Article
- Novel Reassortant H5N2 Highly Pathogenic Avian Influenza Viruses from Backyard Poultry in Mexico.Viruses · 2026Article
- Evolution of H5N1 Cross-Species Transmission: Adaptive Mutations Driving Avian-to-Human Infection.Advanced genetics (Hoboken, N.J.) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
First detected in poultry in China in 1996, the H5N1 avian influenza virus has evolved into a significant global public health hazard, primarily owing to its high pathogenicity and potential for interspecies transmission. While primarily affecting avian species, H5N1 has repeatedly breached species barriers, infecting mammals including humans, minks, seals, and cattle. This review synthesizes current knowledge on the molecular mechanisms underpinning H5N1's host adaptation, focusing on key mutations in viral proteins-such as hemagglutinin (HA), neuraminidase (NA), and polymerase subunits (PB2)-which boost binding affinity to human-type receptors, increase replicative efficiency in mammalian cells, and facilitate immune evasion. Critical mutations, including HA-Q226L, HA-T199I, PB2-E627K, and NA-H274Y, are discussed in detail, highlighting their roles in altering receptor specificity, promoting antiviral resistance, and expanding viral tropism. The paper also outlines epidemiological trends, global dissemination patterns driven by migratory birds and trade, and current strategies for prevention and control, including antiviral therapeutics and vaccine development. Ultimately, this comprehensive analysis underscores the urgent need for continued surveillance, broad-spectrum countermeasures, and international collaboration to reduce the pandemic risk posed by H5N1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.