An NA-deficient 2009 pandemic H1N1 influenza virus mutant can efficiently replicate in cultured cells

We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to...

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Published inArchives of virology Vol. 159; no. 4; pp. 797 - 800
Main Authors Inoue, Emi, Ieko, Masahiro, Takahashi, Nobuhiko, Osawa, Yoshiaki, Okazaki, Katsunori
Format Journal Article
LanguageEnglish
Published Vienna Springer Vienna 01.04.2014
Springer Nature B.V
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Abstract We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 °C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.
AbstractList We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 °C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.
We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 °C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.
We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 degree C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.
We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 °C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in the NA gene and lacked an enzymatic domain. Although the yield of the NA-deficient virus was limited, it formed large plaques when applied to MDCK cell cultures, indicating that the virus was able to spread to adjacent cells. Furthermore, the NA-deficient virus was eluted from chicken erythrocytes at 37 °C, even in the presence of the antiviral drug peramivir. Spread of this NA-deficient virus may pose a potential threat to anti-influenza therapies.
Author Takahashi, Nobuhiko
Inoue, Emi
Osawa, Yoshiaki
Okazaki, Katsunori
Ieko, Masahiro
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CitedBy_id crossref_primary_10_1016_j_chom_2024_05_018
crossref_primary_10_1016_j_vaccine_2015_09_106
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  publication-title: PLos One
  doi: 10.1371/journal.pone.0028178
– volume: 79
  start-page: 2814
  year: 2005
  ident: 1887_CR2
  publication-title: J Virol
  doi: 10.1128/JVI.79.5.2814-2822.2005
– volume: 141
  start-page: 1091
  year: 1996
  ident: 1887_CR16
  publication-title: Arch Virol
  doi: 10.1007/BF01718612
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Snippet We identified a novel neuraminidase (NA)-deficient virus that was a 2009 pandemic influenza H1N1 virus mutant. The mutant virus had a deletion of 1,009 nt in...
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SubjectTerms Animals
Biomedical and Life Sciences
Biomedicine
Brief Report
cell culture
Cell Line
Chickens
cultured cells
deficiency
Dogs
drugs
Enzymes
erythrocytes
Genes
genetics
Genomes
Health sciences
Humans
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influenza
Influenza A virus
Influenza A Virus, H1N1 Subtype
Influenza A Virus, H1N1 Subtype - genetics
Influenza A Virus, H1N1 Subtype - isolation & purification
Influenza A Virus, H1N1 Subtype - physiology
Influenza virus
Influenza, Human
Influenza, Human - virology
isolation & purification
Medical Microbiology
Molecular Sequence Data
mutants
Mutation
Neuraminidase
Neuraminidase - deficiency
pandemic
Pandemics
Phylogenetics
physiology
Proteins
RNA, Viral
RNA, Viral - genetics
Sequence Analysis, DNA
Sequence Deletion
sialidase
Swine flu
Viral Plaque Assay
Viral Proteins
Virology
Virus Replication
Viruses
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Title An NA-deficient 2009 pandemic H1N1 influenza virus mutant can efficiently replicate in cultured cells
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