Cocirculation of Genetically Distinct Highly Pathogenic Avian Influenza H5N5 and H5N1 Viruses in Crows, Hokkaido, Japan.

We isolated highly pathogenic avian influenza (HPAI) H5N5 and H5N1 viruses from crows in Hokkaido, Japan, during winter 2023-24. They shared genetic similarity with HPAI H5N5 viruses from northern Europe but differed from those in Asia. Continuous monitoring and rapid information sharing between countries are needed to prevent HPAI virus transmission.

Novel Genotype of HA Clade 2.3.4.4b H5N8 Subtype High Pathogenicity Avian Influenza Virus Emerged at a Wintering Site of Migratory Birds in Japan, 2021/22 Winter.

Surveillance of avian influenza virus (AIV) was conducted in the 2021-2022 winter season at a wintering site of migratory in Japan. An H5N8 subtype high pathogenicity AIV (HPAIV) with a unique gene constellation and four low pathogenicity AIVs (LPAIVs) were isolated from environmental samples. The genetic origin of the HPAIV (NK1201) was determined with whole-genome sequencing and phylogenetic analyses.

Genetic and antigenic analyses of H5N8 and H5N1 subtypes high pathogenicity avian influenza viruses isolated from wild birds and poultry farms in Japan in the winter of 2021-2022.

In the winter of 2021-2022, multiple subtypes (H5N8 and H5N1) of high pathogenicity avian influenza viruses (HPAIVs) were confirmed to be circulating simultaneously in Japan. Here, we phylogenetically and antigenically analyzed HPAIVs that were isolated from infected wild birds, an epidemiological investigation of affected poultry farms, and our own active surveillance study. H5 subtype hemagglutinin (HA) genes of 32 representative HPAIV isolates were classified into clade 2.

Detection of H5N1 High Pathogenicity Avian Influenza Viruses in Four Raptors and Two Geese in Japan in the Fall of 2022.

In the fall of 2022, high pathogenicity avian influenza viruses (HPAIVs) were detected from raptors and geese in Japan, a month earlier than in past years, indicating a shift in detection patterns. In this study, we conducted a phylogenetic analysis on H5N1 HPAIVs detected from six wild birds during the 2022/2023 season to determine their genetic origins. Our findings revealed that these HPAIVs belong to the G2 group within clade 2.

Susceptibility of common dabbling and diving duck species to clade 2.3.2.1 H5N1 high pathogenicity avian influenza virus: an experimental infection study.

In the winter of 2010-2011, Japan experienced a large outbreak of infections caused by clade 2.3.2.

Multiple infections with H5N8 subtype high pathogenicity avian influenza viruses in a feral mallard.

During the 2020-2021 winter, Eurasian countries experienced large outbreaks caused by the clade 2.3.4.

Susceptibility of common family Anatidae bird species to clade 2.3.4.4e H5N6 high pathogenicity avian influenza virus: an experimental infection study.

Background: There were large outbreaks of high pathogenicity avian influenza (HPAI) caused by clade 2.3.4.

Susceptibility of herons (family: ) to clade 2.3.2.1 H5N1 subtype high pathogenicity avian influenza virus.

The pathogenicity of the H5 subtype high pathogenicity avian influenza viruses (HPAIVs) in bird species has not been investigated yet despite the increasing infections reported. Therefore, the present study aimed to examine the susceptibility of the species, which had already been reported to be susceptible to HPAIVs, to a clade 2.3.

Contribution of mutation I142M in fusion protein and Q44R in matrix protein of Newcastle disease virus to virulence in ducks.

Although verogenic Newcastle disease viruses (NDVs) generally cause subclinical infection in waterfowls such as ducks, NDVs with high virulence in waterfowl have been sporadically reported. We previously reported that the NDV d5a20b strain, which is obtained by serial passaging of the velogenic 9a5b strain in domestic ducks, showed increased virulence in ducks (Hidaka et al., 2021).

Prior infection with antigenically heterologous low pathogenic avian influenza viruses interferes with the lethality of the H5 highly pathogenic strain in domestic ducks.

Low and highly pathogenic avian influenza viruses (LPAIVs and HPAIVs, respectively) have been co-circulating in poultry populations in Asian, Middle Eastern, and African countries. In our avian-flu surveillance in Vietnamese domestic ducks, viral genes of LPAIV and HPAIV have been frequently detected in the same individual. To assess the influence of LPAIV on the pathogenicity of H5 HPAIV in domestic ducks, an experimental co-infection study was performed.

Dynamics of invasion and dissemination of H5N6 highly pathogenic avian influenza viruses in 2016-2017 winter in Japan.

Large highly pathogenic avian influenza (HPAI) outbreaks caused by clade 2.3.4.

The chicken-derived velogenic Newcastle disease virus can acquire high pathogenicity in domestic ducks via serial passaging.

Velogenic Newcastle disease virus (NDV) strains, which show high mortality in chickens, generally do not cause severe disease in waterfowl such as ducks. To elucidate the difference in the pathogenic mechanisms of NDV between chickens and ducks, a chicken-derived velogenic strain (9a5b) was passaged in domestic ducks five times in their air sacs, followed by 20 times in their brains. Eventually, 9a5b acquired higher intracerebral and intranasal pathogenicity in ducks.

Characterization of H3 subtype avian influenza viruses isolated from poultry in Vietnam.

To date, avian influenza viruses (AIVs) have persisted in domestic poultry in wet markets in East Asian countries. We have performed ongoing virus surveillance in poultry populations in Vietnam since 2011, with the goal of controlling avian influenza. Throughout this study, 110 H3 AIVs were isolated from 2760 swab samples of poultry in markets and duck farms.

Pathogenicity of clade 2.3.2.1 H5N1 highly pathogenic avian influenza virus in American kestrel ().

Birds of prey, including endangered species, have been infected with H5 highly pathogenic avian influenza viruses (HPAIVs) in several countries. In this present study, we assessed the pathogenicity of the clade 2.3.

Pathogenicity of H5 highly pathogenic avian influenza virus in rooks ().

Rooks () are considered migratory crows in Japan. Some rooks share a wintering site in the Izumi plain in Kagoshima Prefecture with hooded cranes () and white-necked cranes (), which are designated as "endangered" in the International Union for Conservation of Nature (IUCN) Red List of Threatened Species. Highly pathogenic avian influenza (HPAI), caused by H5 subtype viruses, has recently been reported in these crane species in Japan, in conjunction with a massive decrease in their population.

Outbreaks of highly pathogenic avian influenza in zoo birds caused by HA clade 2.3.4.4 H5N6 subtype viruses in Japan in winter 2016.

In late 2016, two zoos, one in northern Japan and the other in central Japan, experienced highly pathogenic avian influenza (HPAI) outbreaks, in which multiple zoo birds were infected with H5N6 subtype HPAI virus (HPAIV). Here, we report an overview of these HPAI outbreaks. HPAIV infections were confirmed by virus isolation in three black swans (Cygnus atratus) and three snowy owls (Bubo scandiacus) kept in the Omoriyama Zoo hospital.

H5N8 avian influenza virus acquires enhanced pathogenicity after a single passage in chicken.

The H5N8 highly pathogenic avian influenza viruses (HPAIVs) isolated in Japan during the 2014-2015 winter differed in their pathogenicity in chickens. In the present study, we examined the possibility that a comparatively less pathogenic strain was first brought into the country by migratory birds, and then acquired enhanced pathogenicity by infecting chicken flocks. We showed that the A/tundra swan/Tottori/C6nk/2014 (H5N8) (Tottori P0) strain required 10 days to kill all chickens via the intranasal route.

Multiple polymerase gene mutations for human adaptation occurring in Asian H5N1 influenza virus clinical isolates.

The role of the influenza virus polymerase complex in host range restriction has been well-studied and several host range determinants, such as the polymerase PB2-E627K and PB2-D701N mutations, have been identified. However, there may be additional, currently unknown, human adaptation polymerase mutations. Here, we used a database search of influenza virus H5N1 clade 1.

Five distinct reassortants of H5N6 highly pathogenic avian influenza A viruses affected Japan during the winter of 2016-2017.

To elucidate the evolutionary pathway, we sequenced the entire genomes of 89 H5N6 highly pathogenic avian influenza viruses (HPAIVs) isolated in Japan during winter 2016-2017 and 117 AIV/HPAIVs isolated in Japan and Russia. Phylogenetic analysis showed that at least 5 distinct genotypes of H5N6 HPAIVs affected poultry and wild birds during that period. Japanese H5N6 isolates shared a common genetic ancestor in 6 of 8 genomic segments, and the PA and NS genes demonstrated 4 and 2 genetic origins, respectively.

Characterization of Highly Pathogenic Avian Influenza Virus A(H5N6), Japan, November 2016.

Highly pathogenic avian influenza viruses (HPAIVs) A(H5N6) were concurrently introduced into several distant regions of Japan in November 2016. These viruses were classified into the genetic clade 2.3.

Therapeutic efficacy of peramivir against H5N1 highly pathogenic avian influenza viruses harboring the neuraminidase H275Y mutation.

High morbidity and mortality associated with human cases of highly pathogenic avian influenza (HPAI) viruses, including H5N1 influenza virus, have been reported. The purpose of the present study was to evaluate the antiviral effects of peramivir against HPAI viruses. In neuraminidase (NA) inhibition and virus replication inhibition assays, peramivir showed strong inhibitory activity against H5N1, H7N1 and H7N7 HPAI viruses with sub-nanomolar activity in enzyme assays.

Vaccination against H9N2 avian influenza virus reduces bronchus-associated lymphoid tissue formation in cynomolgus macaques after intranasal virus challenge infection.

H9N2 avian influenza virus causes sporadic human infection. Since humans do not possess acquired immunity specific to this virus, we examined the pathogenicity of an H9N2 virus isolated from a human and then analyzed protective effects of a vaccine in cynomolgus macaques. After intranasal challenge with A/Hong Kong/1073/1999 (H9N2) (HK1073) isolated from a human patient, viruses were isolated from nasal and tracheal swabs in unvaccinated macaques with mild fever and body weight loss.

Characterization of clade 2.3.4.4 H5N8 highly pathogenic avian influenza viruses from wild birds possessing atypical hemagglutinin polybasic cleavage sites.

Since 2014, clade 2.3.4.

Comparison of pathogenicities of H7 avian influenza viruses via intranasal and conjunctival inoculation in cynomolgus macaques.

The outbreak of H7N9 low pathogenic avian influenza viruses in China has attracted attention to H7 influenza virus infection in humans. Since we have shown that the pathogenicity of H1N1 and H5N1 influenza viruses in macaques was almost the same as that in humans, we compared the pathogenicities of H7 avian influenza viruses in cynomolgus macaques via intranasal and conjunctival inoculation, which mimics natural infection in humans. H7N9 virus, as well as H7N7 highly pathogenic avian influenza virus, showed more efficient replication and higher pathogenicity in macaques than did H7N1 and H7N3 highly pathogenic avian influenza viruses.

A novel immunochromatographic system for easy-to-use detection of group 1 avian influenza viruses with acquired human-type receptor binding specificity.

A switch of viral hemagglutinin receptor binding specificity from bird-type α2,3- to human-type α2,6-linked sialic acid is necessary for an avian influenza virus to become a pandemic virus. In this study, an easy-to-use strip test to detect receptor binding specificity of influenza virus was developed. A biotinylated anti-hemagglutinin antibody that bound a broad range of group 1 influenza A viruses and latex-conjugated α2,3 (blue) and α2,6 (red) sialylglycopolymers were used in an immunochromatographic strip test, with avidin and lectin immobilized on a nitrocellulose membrane at test and control lines, respectively.