12 October 2026
Researchers at the Taiwan Centers for Disease Control identified the first human case of low-pathogenicity avian influenza A(H7N7) carrying the mammalian-adaptive PB2 E627K mutation in a duck-farm worker, highlighting potential gaps in wild bird–poultry surveillance.
In early 2026, a 50-year-old duck-farm worker in central Taiwan with underlying chronic medical conditions developed mild respiratory symptoms that progressed to high fever and severe pneumonia within two days. Following hospitalization and antiviral treatment with oral oseltamivir, his condition gradually improved, and he was discharged on day 14.
Epidemiological investigations revealed that the patient primarily worked in duck catching and maintained open-air paddocks across several farms. Comprehensive surveillance and virological sampling at the farms he had visited detected neither clinical signs of disease nor avian influenza virus in the poultry flocks.
Following negative initial rapid antigen tests, investigators conducted extensive molecular and serological testing. Reverse-transcription quantitative PCR (RT-qPCR) of respiratory specimens detected influenza A(H7) viral RNA. Close human contacts tested negative. Hemagglutination inhibition (HI) assays and ELISA confirmed an eightfold increase in H7N7-specific antibody titers. Whole-genome sequencing using Nanopore technology characterized the viral strain, designated A/Taiwan/1/2026(H7N7).
The hemagglutinin (HA) cleavage site lacked polybasic amino acid motifs and contained the dibasic sequence PEIPKGR|G, consistent with low-pathogenicity avian influenza strains that can circulate without causing overt disease or mortality in poultry. Crucially, the PB2 polymerase subunit carried the E627K substitution, a well-established mammalian-adaptive marker associated with enhanced viral ribonucleoprotein (vRNP) replication at the lower temperatures of the mammalian upper respiratory tract. The HA protein retained an avian-type receptor-binding preference for α2,3-linked sialic acids and lacked typical human-adaptive receptor-binding substitutions, such as G186V or Q226L.
This case highlights a potential shift in the epidemiology of zoonotic avian influenza. Unlike previous European A(H7N7) outbreaks, including those in the Netherlands in 2003 and Italy in 2013, which were associated with poultry outbreaks, the Taiwanese case appears to have occurred without detectable infection in the sampled domestic duck flocks. This raises the possibility of transmission at the wild bird–domestic duck interface without conspicuous poultry disease or mortality.
Low-pathogenicity avian influenza (LPAI) viruses can cause few or no clinical signs in domestic waterfowl, allowing them to evade conventional passive surveillance systems that rely on increased flock mortality. A comparable surveillance challenge emerged with avian influenza A(H7N9) in eastern China in 2013. The original H7N9 lineage circulated as an LPAI virus in poultry, spreading widely through live poultry markets without causing apparent disease or mortality in chickens. Despite its low pathogenicity in birds, the virus caused severe human disease, including viral pneumonia and acute respiratory distress syndrome (ARDS), with a case-fatality proportion of approximately 40% among reported cases (The H7N9 comparison also requires care: the approximately 40% figure refers to the case-fatality proportion among reported human cases, not the infection-fatality rate). The virus frequently acquired the PB2 E627K substitution during replication in humans. The absence of obvious clinical signs in poultry complicated early detection and containment, while subsequent evolution of some H7N9 viruses resulted in highly pathogenic avian influenza (HPAI) variants.
Reference: Li et al. (2026). Human Infection with Avian Influenza A(H7N7) Virus, Taiwan, 2026. medRxiv preprint.
