Novel H5 clade 2.3.4.6 viruses with both α-2,3 and α-2,6 receptor binding properties may pose a pandemic threat

Li, Qunhui; Wang, Xuan; Gu, Minghong; Jun, Zhu; Hao, Xiaoli; Zhao, Guimin; Sun, Zhongtao; Hu, Jiao; Hu, Shunlin; Wang, Xiaoquan; Liu, Xiaowen; Liu, Xiufan

doi:10.1186/s13567-014-0127-2

Cited by 29 publications

(23 citation statements)

References 18 publications

(23 reference statements)

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“…Others have reported similar transmission results for clade 2.3.4.4 HPAI H5N8 viruses in ferrets (4) and guinea pigs (47). However, an H5N2 virus isolated in China (A/duck/Eastern China/1112/2011) that had high nucleotide identity with H5N8 viruses circulating in South Korea was able to efficiently transmit between cohoused guinea pigs (47).…”

Section: Figmentioning

confidence: 88%

“…The removal of this glycosylation site has previously been shown to be critical for H5 subtype influenza viruses to gain enhanced receptor binding affinity to humanlike receptors and transmission in mammalian hosts (45,46). The weak binding of the H5Nx viruses to human-like receptors (30,47) along with reduced replication efficiency at temperatures found in the upper respiratory tract of humans likely contribute to the poor transmission of the H5Nx viruses. Others have reported similar transmission results for clade 2.3.4.4 HPAI H5N8 viruses in ferrets (4) and guinea pigs (47).…”

Section: Figmentioning

confidence: 99%

“…The weak binding of the H5Nx viruses to human-like receptors (30,47) along with reduced replication efficiency at temperatures found in the upper respiratory tract of humans likely contribute to the poor transmission of the H5Nx viruses. Others have reported similar transmission results for clade 2.3.4.4 HPAI H5N8 viruses in ferrets (4) and guinea pigs (47). However, an H5N2 virus isolated in China (A/duck/Eastern China/1112/2011) that had high nucleotide identity with H5N8 viruses circulating in South Korea was able to efficiently transmit between cohoused guinea pigs (47).…”

Section: Figmentioning

confidence: 99%

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Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

Pulit-Penaloza

Sun

Creager

et al. 2015

J Virol

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A novel highly pathogenic avian influenza (HPAI) H5N8 virus, first detected in January 2014 in poultry and wild birds in South Korea, has spread throughout Asia and Europe and caused outbreaks in Canada and the United States by the end of the year. The spread of H5N8 and the novel reassortant viruses, H5N2 and H5N1 (H5Nx), in domestic poultry across multiple states in the United States pose a potential public health risk. To evaluate the potential of cross-species infection, we determined the pathogenicity and transmissibility of two Asian-origin H5Nx viruses in mammalian animal models. The newly isolated H5N2 and H5N8 viruses were able to cause severe disease in mice only at high doses. Both viruses replicated efficiently in the upper and lower respiratory tracts of ferrets; however, the clinical symptoms were generally mild, and there was no evidence of systemic dissemination of virus to multiple organs. Moreover, these influenza H5Nx viruses lacked the ability to transmit between ferrets in a direct contact setting. We further assessed viral replication kinetics of the novel H5Nx viruses in a human bronchial epithelium cell line, Calu-3. Both H5Nx viruses replicated to a level comparable to a human seasonal H1N1 virus, but significantly lower than a virulent Asian-lineage H5N1 HPAI virus. Although the recently isolated H5N2 and H5N8 viruses displayed moderate pathogenicity in mammalian models, their ability to rapidly spread among avian species, reassort, and generate novel strains underscores the need for continued risk assessment in mammals. O n 16 December 2014, the U.S. Department of Agriculture (USDA) confirmed the presence of a novel highly pathogenic avian influenza (HPAI) H5N8 virus in a captive gyrfalcon and H5N2 virus in a northern pintail duck from Whatcom County, Washington (1). This represented the first appearance of HPAI H5 virus in the United States since 2004 when H5N2 subtype virus was confirmed on a poultry farm in Texas (2). HPAI H5N8 viruses were first reported in duck farms in eastern China in 2010, and in early 2014 a novel reassortant H5N8 virus was detected in poultry in South Korea (3-5). The novel virus, belonging to Eurasian lineage clade 2.3.4.4 (formerly clade 2.3.4.6), subsequently spread to China, Japan, and five countries in Europe (6, 7). In November 2014, the virus was detected on chicken and turkey farms in British Columbia, Canada, followed by Washington State, USA, the following month (8). The novel H5N8 viruses continue to spread to multiple regions and have been found in three North America flyways (Pacific, Central, and Mississippi), where wild-bird migrations occur (USDA, Animal and Plant Health Inspection Service [http://www.aphis.usda.gov]). In addition, genetic reassortment with circulating North American avian influenza viruses has resulted in novel HPAI viruses, including H5N2 and H5N1 subtypes. These novel reassortant viruses carry a Eurasian-origin hemagglutinin (HA) gene genetically related to H5N8 viruses detected in South Korea in 2014 and the neura...

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Section: Figmentioning

confidence: 88%

Section: Figmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

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Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

Pulit-Penaloza

Sun

Creager

et al. 2015

J Virol

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“…Other researchers have reported that clade 2.3.4.4 HPAI H5N8 viruses lack the contact transmissi- bility in ferrets (34,36) and guinea pigs (35). An H5N2 virus isolated in China (A/duck/Eastern China/1112/2011), however, was able to efficiently transmit between cohoused guinea pigs (35).…”

Section: Discussionmentioning

confidence: 99%

“…Yen et al found that combined deglycosylation at residue 158 and S227N substitution could substantially increase the affinity of HA for SA␣2,6Gal-linked receptor (33). The four emergent H5N6 viruses possess mutations in the RBS of HA and lack the N-linked glycosylation site at HA residue 158, which are characteristic of most clade 2.3.4.4 H5 viruses, including H5N2 and H5N8, indicating that these viruses have acquired other features, as yet not understood, for human-type receptor-binding affinity (34,35).…”

Section: Discussionmentioning

confidence: 99%

Highly Pathogenic Avian Influenza H5N6 Viruses Exhibit Enhanced Affinity for Human Type Sialic Acid Receptor and In-Contact Transmission in Model Ferrets

Sun

Wei

et al. 2016

J Virol

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Since May 2014, highly pathogenic avian influenza H5N6 virus has been reported to cause six severe human infections three of which were fatal. The biological properties of this subtype, in particular its relative pathogenicity and transmissibility in mammals, are not known. We characterized the virus receptor-binding affinity, pathogenicity, and transmissibility in mice and ferrets of four H5N6 isolates derived from waterfowl in China from 2013-2014. All four H5N6 viruses have acquired a binding affinity for human-like SA␣2,6Gal-linked receptor to be able to attach to human tracheal epithelial and alveolar cells. The emergent H5N6 viruses, which share high sequence similarity with the human isolate A/Guangzhou/39715/2014 (H5N6), were fully infective and highly transmissible by direct contact in ferrets but showed less-severe pathogenicity than the parental H5N1 virus. The present results highlight the threat of emergent H5N6 viruses to poultry and human health and the need to closely track their continual adaptation in humans. O n 7 May 2014, the Chinese National Health and Family Planning Commission (NHFPC) announced the first human case of avian H5N6 influenza virus infection (1). Subsequently, three more human infections with H5N6 virus cases were reported in the winter of 2014-2015 (2, 3). Between 30 December 2015 and 2 January 2016, the NHFPC notified the World Health Organization of two additional human cases of avian H5N6 virus infection. All six human infections were presented as acute respiratory distress syndrome (ARDS) of which three were fatal. Five cases had a common history of contact with or exposure to poultry or livebird markets before disease onset (1-3), suggesting zoonotic transmission. Sequence analyses of the human H5N6 isolates indicated that the virus was derived from clade 2.3.4.4 avian H5N6 viruses that are circulating in poultry in China (1, 2, 4). Avian H5N6 influenza virus was first isolated from mallards in North America in 1975 (5). In China, H5N6 virus first emerged in 2010 and has since been extensively circulating in both domestic and wild birds (6-9). Recent surveillance data from the Ministry of Agriculture of China indicate that H5N6 viruses have become enzootic in domestic poultry. Unlike the worldwide distribution H5N2 and H5N8 viruses (10-12), prevailing H5N6 viruses appear to be largely confined to China and Laos (13). We recently characterized the novel H5N6 viruses in poultry (14); however, their zoonotic capability and characteristics are poorly understood. In the present study, we examined the emergent H5N6 virus for its genetic characteristics, receptor binding properties, pathogenicity, and transmissibility in mice and ferrets. MATERIALS AND METHODS Ethical

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Pandemic potential of highly pathogenic avian influenza clade 2.3.4.4 A(H5) viruses

Yamaji

Saad

Davis

et al. 2020

Reviews in Medical Virology

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Summary The panzootic caused by A/goose/Guangdong/1/96‐lineage highly pathogenic avian influenza (HPAI) A(H5) viruses has occurred in multiple waves since 1996. From 2013 onwards, clade 2.3.4.4 viruses of subtypes A(H5N2), A(H5N6), and A(H5N8) emerged to cause panzootic waves of unprecedented magnitude among avian species accompanied by severe losses to the poultry industry around the world. Clade 2.3.4.4 A(H5) viruses have expanded in distinct geographical and evolutionary pathways likely via long distance migratory bird dispersal onto several continents and by poultry trade among neighboring countries. Coupled with regional circulation, the viruses have evolved further by reassorting with local viruses. As of February 2019, there have been 23 cases of humans infected with clade 2.3.4.4 H5N6 viruses, 16 (70%) of which had fatal outcomes. To date, no HPAI A(H5) virus has caused sustainable human‐to‐human transmission. However, due to the lack of population immunity in humans and ongoing evolution of the virus, there is a continuing risk that clade 2.3.4.4 A(H5) viruses could cause an influenza pandemic if the ability to transmit efficiently among humans was gained. Therefore, multisectoral collaborations among the animal, environmental, and public health sectors are essential to conduct risk assessments and develop countermeasures to prevent disease and to control spread. In this article, we describe an assessment of the likelihood of clade 2.3.4.4 A(H5) viruses gaining human‐to‐human transmissibility and impact on human health should such human‐to‐human transmission occur. This structured analysis assessed properties of the virus, attributes of the human population, and ecology and epidemiology of these viruses in animal hosts.

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Novel H5 clade 2.3.4.6 viruses with both α-2,3 and α-2,6 receptor binding properties may pose a pandemic threat

Cited by 29 publications

References 18 publications

Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

Pathogenesis and Transmission of Novel Highly Pathogenic Avian Influenza H5N2 and H5N8 Viruses in Ferrets and Mice

Highly Pathogenic Avian Influenza H5N6 Viruses Exhibit Enhanced Affinity for Human Type Sialic Acid Receptor and In-Contact Transmission in Model Ferrets

Pandemic potential of highly pathogenic avian influenza clade 2.3.4.4 A(H5) viruses

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