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During the 2022-23 winter season, >1,500 endangered cranes, including hooded cranes (Grus monacha) and white-naped cranes (Grus vipio), were found debilitated or dead in the Izumi Plain, Japan. Most of the cranes, particularly those collected in November, were infected with highly pathogenic avian influenza (HPAI) H5N1 viruses; virus shedding was higher from the trachea than from the cloaca. The isolation rate from the cranes' roost water was not markedly higher than that of previous seasons, suggesting that the viruses might be more effectively transmitted among cranes via the respiratory route than through feces. Most wild bird-derived H5N1 isolates were phylogenetically distinct from viruses isolated on nearby chicken farms, indicating limited relationship between the wild bird and chicken isolates. Serologic analyses suggested that herd immunity had little effect on outbreak subsidence. This study deepens our understanding of the circumstances surrounding the unexpected HPAI outbreaks among these endangered cranes.

Genetic analyses of highly pathogenic avian influenza H5 subtype viruses isolated from the Izumi Plain, Japan, revealed cocirculation of 2 genetic groups of clade 2.3.4.4b viruses among migratory waterfowl. Our findings demonstrate that both continuous surveillance and timely information sharing of avian influenza viruses are valuable for rapid risk assessment.

Background: The accurate determination of bird sex is crucial in various biological fields, including ecology, behavioral research, and conservation. However, this task remains challenging in species in which males and females exhibit similar external morphologies, such as owls. Although polymerase chain reaction (PCR)-based molecular sexing techniques that target the chromodomain helicase DNA-binding protein 1 gene found on sex chromosomes Z (CHD1-Z gene) and W (CHD1-W gene) are widely used, we encountered atypical banding patterns when applying the previously reported primers 2550F and 2718R to four wild owls of unknown sex. This study aims to reveal the owl-specific genetic structure of the CHD1 gene. Methods: We developed a new primer set and determined the nucleotide sequences—including the binding sites for the primers 2550F and 2718R—within both the CHD1-Z and CHD1-W genes. Results: Sequencing analysis, conducted using a newly developed primer set that successfully amplified both Z- and W-derived CHD1 products across various owl species, revealed a unique genetic insertion of approximately 600 bp in intron 17 of the CHD1-W gene. This insertion reversed the usual length relationship between PCR products from the chromosomes Z and W. Additionally, mutations identified in the 2550F primer binding site of the CHD1-Z gene in certain owl species may explain the failure to amplify CHD1-Z-derived PCR products. Conclusion: These findings provide valuable insights for improving molecular sexing in owls.

Inclusion body disease of cranes (IBDCs) is fatal in many cases and reportedly caused by a herpes‐like virus labeled as gruid herpesvirus 1 (GrHV‐1). Although GrHV‐1 has been isolated from IBDC‐affected cranes, it has not been genetically classified because its genome has not been partially or fully sequenced. In this study, we isolated an alphaherpesvirus from hooded cranes ( Grus monacha ) diagnosed with IBDC in Japan. Next‐generation sequencing revealed that this virus isolate was GrHV‐1, based on the 99.98% sequence homology with a previously isolated GrHV‐1 strain. Furthermore, phylogenetic analysis of eight conserved herpesvirus genes supported the taxonomic assignment of GrHV‐1 to the genus Mardivirus of the Alphaherpesvirinae subfamily. Based on these results, GrHV‐1 can be more accurately classified and diagnostic tools to investigate suspected cases of IBDC can be developed. Furthermore, GrHV‐1 showed effective replication in primary cultured cells derived from duck and chicken embryos and embryo tissues, highlighting the importance of further studies to evaluate its interspecies transmission.

Background: The accurate determination of bird sex is crucial in various biological fields, including ecology, behavioral research, and conservation. However, this task remains challenging in species in which males and females exhibit similar external morphologies, such as owls. Although polymerase chain reaction (PCR)-based molecular sexing techniques that target the chromodomain helicase DNA-binding protein 1 gene found on sex chromosomes Z (CHD1-Z gene) and W (CHD1-W gene) are widely used, we encountered atypical banding patterns when applying the previously reported primers 2550F and 2718R to four wild owls of unknown sex. This study aims to reveal the owl-specific genetic structure of the CHD1 gene. Methods: We developed a new primer set and determined the nucleotide sequences—including the binding sites for the primers 2550F and 2718R—within both the CHD1-Z and CHD1-W genes. Results: Sequencing analysis, conducted using a newly developed primer set that successfully amplified both Z- and W-derived CHD1 products across various owl species, revealed a unique genetic insertion of approximately 600 bp in intron 17 of the CHD1-W gene. This insertion reversed the usual length relationship between PCR products from the chromosomes Z and W. Additionally, mutations identified in the 2550F primer binding site of the CHD1-Z gene in certain owl species may explain the failure to amplify CHD1-Z-derived PCR products. Conclusion: These findings provide valuable insights for improving molecular sexing in owls.