カナダ初のヒト鳥インフルエンザ感染例、新たなパンデミック監視の手掛かり(Canada’s first human bird flu case offers new clues for monitoring pandemic threats)

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2026-09-28 カナダ・ブリティッシュコロンビア大学(UBC)

カナダで初めて確認されたヒトH5N1鳥インフルエンザ症例について、ブリティッシュコロンビア大学(UBC)の研究チームが、患者由来ウイルスに生じていた2つの特徴的な変異の機能を解析した。クライオ電子顕微鏡でウイルス表面タンパク質の構造を原子レベルに近い解像度で調べ、ヒト・鳥の細胞受容体への結合性を評価した結果、これらの変異は予想に反してヒト細胞への結合能力を弱めていた。一方、細胞への侵入に必要な膜融合は可能で、肺細胞では効率が低下しながらも融合能力が維持されていた。研究は、遺伝子配列の変化だけではウイルスのヒト感染性を判断できず、変異が実際にタンパク質機能へ及ぼす影響を実験的に検証する必要性を示している。遺伝子監視と機能解析を組み合わせることが、新興感染症リスクの評価に重要だとする。

カナダ初のヒト鳥インフルエンザ感染例、新たなパンデミック監視の手掛かり(Canada’s first human bird flu case offers new clues for monitoring pandemic threats)
UBC researchers mapped the atomic structure of the H5N1 surface protein from the B.C. case to study the two mutations (yellow). Image credit: Subramaniam lab.

<関連情報>

ヒト患者で同定された新規H5N1インフルエンザヘマグルチニン変異株におけるシアロシド結合能の低下 Diminished sialoside binding in novel H5N1 influenza hemagglutinin variants identified in a human patient

John H. Ni, Saeid Malek Zadeh, Alison M. Berezuk, Ryan Lynam, Peter Axerio-Cilies, Xing Zhu, Katharine S. Tuttle, Gethin Rh. Owen, Maria Tokuyama & Sriram Subramaniam
Nature Communications  Published:28 September 2026
DOI:https://doi.org/10.1038/s41467-026-77829-x

Abstract

In 2024, an adolescent female in British Columbia was hospitalised presenting with severe symptoms including respiratory failure due to infection with a novel H5N1 influenza strain (BC24). Using cryogenic electron microscopy, we show here that the N169 α2,3-linked auto-glycan that is found in the sialic acid binding site of previously studied H5 hemagglutinin (HA) proteins is absent in purified BC24 HA protein, suggesting greatly reduced affinity for α2,3-linked sialosides. Glycan microarray and enzyme-linked immunosorbent assay analyses show that HA variants identified in the BC24 case display severely reduced or no binding to both α2,3-linked sialosides and α2,6-linked sialosides. Full-length BC24 HA expressed in A549 alveolar carcinoma cells drives membrane fusion, albeit at lower levels than previous H5 HA proteins, and post-infection sera from the patient display strong binding to BC24 HA and HA proteins from other influenza subtypes. As each of the two mutations of interest, independently and in conjunction, severely reduce sialoside binding, there appears to have been in this case multiple populations of virus with the diminished receptor binding phenotype. The substantial minority prevalence of weakly binding HA variants in this BC24 case reveals further complexity in the factors that may be present in severe avian influenza infection.

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