Transboundary and Emerging Diseases, Volume: 2026, Issue: 1,
First published: 18 August 2026, DOI: (10.1155/tbed/2623621)
#19,308
Yesterday, in Conservation Bio: Emerging threat of avian influenza to the world's vultures, we looked - in broad terms - at the current and potential future impact of HPAI H5N1 on raptors and other scavenger birds.
Today we've a study - published last week in Transboundary and Emerging Diseases - which looks at one specific investigation into an H5N1-infected endangered Cinereous Vulture recovered in South Korea earlier this year.
While hardly a new finding (see Cell: The Neuropathogenesis of HPAI H5Nx Viruses in Mammalian Species Including Humans), once again we see strong evidence of neurological involvement in this recovered vulture; in clinical presentation, histopathological findings, and in high titers of the virus found in brain tissue.
This is a topic we've looked at often, most recently last month in Viruses: First Ecuadorian Pediatric Case of Multisystem and Neurological Involvement Associated with Influenza A—H5N1 Virus—Case Report, and before that, in last May's QJM: Avian Influenza in Humans: Virology, Transmission, and Clinical Priorities.
This study also found that the HPAI H5N1 virus recovered from the vulture was a reassortant (see graphic at top of blog). Its HA, NA, and M gene segments closely resembled a G10-like East Asian H5N1 virus which circulated circa 2022–2023, while its internal genes appear derived from multiple regional and flyway HPAI and LPAI viruses.
While much of this study is fairly technical, and will be primarily of interest to researchers, it is an excellent reminder of just how much hidden diversity there is in HPAI H5Nx in the wild, and that their evolution never stops.
I've only posted some excerpts. Those wishing a deeper dive will want to follow the link to read it in its entirety.
Chang-Gi Jeong, Seongwon Hwang, Taeyeong Jung, Su-Beom Chae, Tae-Nam Kim, Nchimunya Siamulonga, Serin Sim, Geonwoo Baek … See all authors
First published: 18 August 2026 https://doi.org/10.1155/tbed/2623621Digital Object Identifier (DOI)Academic Editor: Fabian Lean
Abstract
Clade 2.3.4.4b highly pathogenic avian influenza viruses (HPAIVs) continue to circulate widely in East Asia and undergo frequent reassortment in wild birds. Raptors are regarded as spillover hosts that may be exposed through predation or scavenging, yet integrated clinicopathologic and genomic investigations in cinereous vultures remain limited.
Here, we describe a fatal H5N1 HPAIV infection in a cinereous vulture (Aegypius monachus) found in South Korea on January 17, 2026. On presentation, the cinereous vulture showed severe neurologic dysfunction, including inability to stand, right-sided head tilt with pathologic nystagmus, reduced oculocephalic and palpebral reflexes, and intermittent bilateral leg tremors. The cinereous vulture died within 2 days after rescue, and a complete necropsy was performed.
Hematologic and biochemical testing revealed marked heterophil predominance, severe lymphopenia, mild monocytosis, and globulin values near the upper end of the reference interval. An oropharyngeal swab tested positive for influenza A virus, and a virus isolate, designated A/Cinereous_Vulture/Korea/26-JBN47/2026(H5N1), was recovered in embryonated chicken eggs. Histopathology showed nonsuppurative encephalitis and necrotizing myocarditis, and influenza A nucleoprotein was detected immunohistochemically in neurons and cardiomyocytes.
Tissue real-time RT-PCR showed the lowest cycle threshold value in the brain. Whole-genome sequencing demonstrated that 26-JBN47 belonged to clade 2.3.4.4b and contained a polybasic HA cleavage site (PLREKRRKR/GLF). Segment-level phylogenetic analysis revealed a reassortant genome constellation comprising a maintained H5N1 backbone in HA, NA, and M; low PAIV (LPAIV)-associated but H5N1-incorporated PA and NP segments; flyway-associated PB2 and NS segments; and a PB1 segment phylogenetically linked to regional LPAIV lineages.
Molecular marker analysis identified multiple substitutions previously reported to be associated with receptor-binding properties, polymerase-related fitness, virulence, and host-response modulation, whereas canonical PB2 mammalian-adaptive markers were absent. These findings show that 26-JBN47 was a reassortant clade 2.3.4.4b H5N1 HPAIV associated with systemic disease and clinicopathological findings consistent with neurotropic and cardiotropic infection in a cinereous vulture. They also support the potential value of scavenging raptors as sentinels of local or regional HPAIV circulation involving reassortant viruses in East Asia.
(SNIP)
5. Conclusion
This study documents a fatal clade 2.3.4.4b H5N1 HPAIV infection in a cinereous vulture in South Korea and links severe clinicopathologic disease with a reassortant viral genome. The affected cinereous vulture developed marked neurologic dysfunction and showed nonsuppurative encephalitis, necrotizing myocarditis, and viral antigen distribution in the brain and heart, with the highest viral RNA burden detected in the brain.
Together, these findings are consistent with neurotropic and cardiotropic infections in this case. Genomic analyses showed that 26-JBN47 retained an East Asian H5N1 backbone in the HA, NA, and M segments, which clustered with G10-like viruses, whereas the internal genes reflected multiple reassortment histories involving regional AIV gene pools. The molecular marker profile was broadly consistent with contemporary avian-origin clade 2.3.4.4b H5N1 viruses and did not indicate advanced mammalian adaptation.
These findings show that cinereous vultures can develop severe fatal diseases after HPAIV infection and support their potential utility as sentinels of local or regional HPAIV circulation involving reassortant viruses near wildlife interfaces in East Asia.
(Continue . . . )
