Full-length genome sequences of the first H9N2 avian influenza viruses isolated in the Northeast of Algeria

Barberis, A.; Boudaoud, Amine; Gorrill, Angelina; Loupias, Josianne; Ghram, Abdeljelil; Lachheb, Jihene; Alloui, N.; Ducatez, Mariette

doi:10.1186/s12985-020-01377-z

Cited by 15 publications

(10 citation statements)

References 91 publications

(152 reference statements)

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“…Therefore, the mutations at positions 372, 380, and 432 are likely more crucial. The S372A and R403W substitutions in NA enhance the ability of the virus to cross the species barrier and adapt to a mammalian host ( 55 ). These substitutions have also been detected in H9N2, H2N2, and H3N2 subtypes ( 56 ).…”

Section: Discussionmentioning

confidence: 99%

Host-Adaptive Signatures of H3N2 Influenza Virus in Canine

Liu

Qiu

et al. 2021

Front. Vet. Sci.

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Wild aquatic birds are the primary natural reservoir of influenza A viruses (IAVs), although a small number of viruses can spill over to mammals and circulate. The focus of IAV infection in mammals was largely limited to humans and swine variants, until the emergence of H3N2 canine influenza viruses (CIVs), which provides new perspective for interspecies transmission of the virus. In this study, we captured 54 canine-adaptive signatures in H3N2 CIVs through entropy computation, which were largely concentrated in the interaction region of polymerase proteins on ribonucleoprotein complex. The receiver operating characteristic curves of these sites showed >95% accuracy in distinguishing between the hosts. Nine of the 54 canine-adaptive signatures were shared in avian–human/equine or equine–canine (PB2-82; PB1-361; PA-277; HA-81, 111, 172, 196, 222, 489), suggesting their involvement in canine adaptation. Furthermore, we found that IAVs can establish persistent transmission in lower mammals with greater ease compared to higher mammals, and 25 common adaptation signatures of H3 IAVs were observed in diverse avian–mammals comparison. There were few human-like residues in H3N2 CIVs, which suggested a low risk of human infection. Our study highlights the necessity of identifying and monitoring the emerging adaptive mutations in companion animals by enhanced surveillance and provides a basis for mammal adaptation of avian influenza viruses.

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Section: Discussionmentioning

confidence: 99%

Host-Adaptive Signatures of H3N2 Influenza Virus in Canine

Liu

Qiu

et al. 2021

Front. Vet. Sci.

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“…Worldwide, the avian influenza virus (AIV) is an economically significant pathogen in the poultry industry that causes infectious viral diseases that can potentially cause zoonotic and pandemic outbreaks [ 1 ]. AIV is an enveloped virus from the Orthomyxoviridae family with a single-stranded, negative-sense RNA characterized by a segmented genome fragmented into eight segments to code for more than 11 viral proteins [ 2 ]. These proteins are either inside the lipid envelope (PB1, PB2, PA, NP, M1, NS1, and NEP) or embedded in the envelope (M2, HA, and NA), and each protein functions individually or forms complexes with a structural, nonstructural, or regulatory function during the virus’ life cycle [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Genetic Characterization and Phylogeographic Analysis of the First H13N6 Avian Influenza Virus Isolated from Vega Gull in South Korea

Flores,

Cammayo-Fletcher,

Nguyen

et al. 2024

Viruses

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Avian influenza virus (AIV) is a pathogen with zoonotic and pandemic potential. Migratory birds are natural reservoirs of all known subtypes of AIVs, except for H17N10 and H18N11, and they have been implicated in previous highly pathogenic avian influenza outbreaks worldwide. This study identified and characterized the first isolate of the H13N6 subtype from a Vega gull (Larus vegae mongolicus) in South Korea. The amino acid sequence of hemagglutinin gene showed a low pathogenic AIV subtype and various amino acid substitutions were found in the sequence compared to the reference sequence and known H13 isolates. High sequence homology with other H13N6 isolates was found in HA, NA, PB1, and PA genes, but not for PB2, NP, M, and NS genes. Interestingly, various point amino acid mutations were found on all gene segments, and some are linked to an increased binding to human-type receptors, resistance to antivirals, and virulence. Evolutionary and phylogenetic analyses showed that all gene segments are gull-adapted, with a phylogeographic origin of mostly Eurasian, except for PB2, PA, and M. Findings from this study support the evidence that reassortment of AIVs continuously occurs in nature, and migratory birds are vital in the intercontinental spread of avian influenza viruses.

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“…H9N2 avian influenza virus (AIV), one of the primary subtypes of influenza virus circulating in poultry, has been widely distributed around the world ( 1 – 4 ). Since the H9N2 AIV was first isolated from turkeys in the US in 1966, it has been rapidly transmitted in all continents ( 5 – 7 ).…”

Section: Introductionmentioning

confidence: 99%

Real-Time Visualization of the Infection and Replication of a Mouse-Lethal Recombinant H9N2 Avian Influenza Virus

Lao

Qiu

et al. 2022

Front. Vet. Sci.

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H9N2 avian influenza viruses (AIVs) continuously cross the species barrier to infect mammalians and are repeatedly transmitted to humans, posing a significant threat to public health. Importantly, some H9N2 AIVs were found to cause lethal infection in mice, but little is known about the viral infection dynamics in vivo. To analyze the real-time infection dynamics, we described the generation of a mouse-lethal recombinant H9N2 AIV, an influenza reporter virus (VK627-NanoLuc virus) carrying a NanoLuc gene in the non-structural (NS) segment, which was available for in vivo imaging. Although attenuated for replication in MDCK cells, VK627-NanoLuc virus showed similar pathogenicity and replicative capacity in mice to its parental virus. Bioluminescent imaging of the VK627-NanoLuc virus permitted successive observations of viral infection and replication in infected mice, even following the viral clearance of a sublethal infection. Moreover, VK627-NanoLuc virus was severely restricted by the K627E mutation in PB2, as infected mice showed little weight loss and a low level of bioluminescence. In summary, we have preliminarily established a visualized tool that enables real-time observation of the infection and replication dynamics of H9N2 AIV in mice, which contributes to further understanding the mechanisms underlying the pathogenic enhancement of H9N2 AIV to mice.

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Full-length genome sequences of the first H9N2 avian influenza viruses isolated in the Northeast of Algeria

Cited by 15 publications

References 91 publications

Host-Adaptive Signatures of H3N2 Influenza Virus in Canine

Host-Adaptive Signatures of H3N2 Influenza Virus in Canine

Genetic Characterization and Phylogeographic Analysis of the First H13N6 Avian Influenza Virus Isolated from Vega Gull in South Korea

Real-Time Visualization of the Infection and Replication of a Mouse-Lethal Recombinant H9N2 Avian Influenza Virus

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