An influenza A virus containing influenza B virus 5' and 3' noncoding regions on the neuraminidase gene is attenuated in mice.

Muster, Thomas; Subbarao, E K; Enami, Masayoshi; Murphy, Brian R.; Palese, Peter

doi:10.1073/pnas.88.12.5177

Cited by 89 publications

(81 citation statements)

References 21 publications

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“…The influenza B virus polymerase complex has been shown previously to replicate and transcribe RNA transcripts containing influenza A virus 5' and 3' UTRs (Crescenzo-Chaigne et al, 1999;Jackson et al, 2002;Jambrina et al, 1997;Muster et al, 1991), but in all cases the level of reporter gene expression was significantly reduced. Our results show even lower levels of VIRGS activity in response to influenza B virus infection.…”

Section: Discussionmentioning

confidence: 99%

Virus-inducible reporter genes as a tool for detecting and quantifying influenza A virus replication

Lutz

Dyall

Olivo

et al. 2005

Journal of Virological Methods

103

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SummaryThe use of influenza A virus-inducible reporter gene segments in detecting influenza A virus replication was investigated. The RNA polymerase I promoter/terminator cassette was used to express RNA transcripts encoding green fluorescence protein or firefly luciferase flanked by the untranslated regions of the influenza A/WSN/33 NP segment. Reporter gene activity was detected after reconstitution of the influenza A virus polymerase complex from cDNA or after virus infection, and was influenza A virus-specific. Reporter gene activity could be detected as early as 6 hours post infection and was virus dose-dependent. Inhibitory effects of antibodies or amantadine could be detected a nd quantified rapidly, providing a means of not only identifying influenza A virus -specific replication, but of determining the antigenic subtype as well as antiviral drug susceptibility. Induction of virus-specific reporter genes provides a rapid, sensitive method for detecting virus replication, quantifying virus titers and assessing antiviral sensitivity as well as antigenic subtype.

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Section: Discussionmentioning

confidence: 99%

Virus-inducible reporter genes as a tool for detecting and quantifying influenza A virus replication

Lutz

Dyall

Olivo

et al. 2005

Journal of Virological Methods

103

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“…Amino acid at position 473 (in the peptide of 473-481) in the nucleoprotein was relatively conserved in subtype H1N1 and H3N2 IAVs, and was reported to stimulate the host to produce IFN-c (Wahl et al, 2009). These findings are of interest because the non-coding regions and some coding regions of genome segments affect viral RNA synthesis and packing (Liang et al, 2005;Muster et al, 1991;Ng et al, 2008;Sun et al, 2015;Watanabe et al, 2003;Zheng et al, 1996). Further experiments are needed to validate the roles of sequence changes in the discrepancy seen in patterns of virus shedding and antibody response dynamics between the swine in the treatment and sentinel groups.…”

Section: Evaluation Of Current Protocols For Using An Ai Multis-screementioning

confidence: 82%

Dynamics of virus shedding and antibody responses in influenza A virus-infected feral swine

Sun

Cunningham

Harris

et al. 2015

Journal of General Virology

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Given their free-ranging habits, feral swine could serve as reservoirs or spatially dynamic 'mixing vessels' for influenza A virus (IAV). To better understand virus shedding patterns and antibody response dynamics in the context of IAV surveillance amongst feral swine, we used IAV of feral swine origin to perform infection experiments. The virus was highly infectious and transmissible in feral swine, and virus shedding patterns and antibody response dynamics were similar to those in domestic swine. In the virus-inoculated and sentinel groups, virus shedding lasted #6 and #9 days, respectively. Antibody titres in inoculated swine peaked at 1 : 840 on day 11 post-inoculation (p.i.), remained there until 21 days p.i. and dropped to ,1 : 220 at 42 days p.i. Genomic sequencing identified changes in wildtype (WT) viruses and isolates from sentinel swine, most notably an amino acid divergence in nucleoprotein position 473. Using data from cell culture as a benchmark, sensitivity and specificity of a matrix gene-based quantitative reverse transcription-PCR method using nasal swab samples for detection of IAV in feral swine were 78.9 and 78.1 %, respectively. Using data from haemagglutination inhibition assays as a benchmark, sensitivity and specificity of an ELISA for detection of IAV-specific antibody were 95.4 and 95.0 %, respectively. Serological surveillance from 2009 to 2014 showed that ,7.58 % of feral swine in the USA were positive for IAV. Our findings confirm the susceptibility of IAV infection and the high transmission ability of IAV amongst feral swine, and also suggest the need for continued surveillance of IAVs in feral swine populations.

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“…These observations may be surprising because, although terminal sequences at both ends of the NCRs containing the promoter sequences needed for RNA transcription and replication are conserved among viruses of the same type, they differ between type A and B RNA segments. By contrast, Muster et al (1991) were unable to generate a mutant virus in which the NCRs for the type A NA segment were replaced with those of the type B NA segment. These data together suggest that functional compatibility between the type A and B NCRs depends on the specific RNA segment.…”

Section: Introductionmentioning

confidence: 99%

“…By contrast, several artificial A/B chimeric viruses have been made by reverse genetics. Muster et al (1991) produced a mutant type A virus whose non-coding regions (NCRs) of the neuraminidase (NA) segment were replaced with those of the type B NS segment, suggesting that at least the NCRs of type B NS are compatible with type A components with respect to RNA transcription, replication, and packaging. In addition, we have shown that the type A polymerase machinery can express type B HA from the type B HA segment (Horimoto et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Limited compatibility between the RNA polymerase components of influenza virus type A and B

Iwatsuki‐Horimoto

Hatta

et al. 2008

Virus Research

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Reassortants between type A and B influenza viruses have not been detected in nature, although both viruses co-circulate in human populations. One explanation for this may be functional incompatibility of RNA transcription and replication between type A and B viruses. To test this possibility, we constructed type A/B mosaic polymerase machinery, containing PB2, PB1, PA and nucleoprotein from each of the two virus types, and assessed their polymerase activities with a type A promoter in a reporter assay. Type B polymerase machinery containing homologous components was functional with the type A promoter albeit to various extents depending on the segments from which the regions downstream of the promoter sequence were derived, indicating functional compatibility between the type A promoter and B polymerase machinery. However, all of the A/B mosaic polymerase machinery, except that containing PA from a type A and the others from a type B virus strain, did not function with the type A promoter, indicating limited compatibility among polymerase components of both types. Taken together, these data suggest that incompatibility among components of the polymerase machinery for RNA transcription and replication alone is not responsible for the lack of heterotypic reassortants.

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An influenza A virus containing influenza B virus 5' and 3' noncoding regions on the neuraminidase gene is attenuated in mice.

Cited by 89 publications

References 21 publications

Virus-inducible reporter genes as a tool for detecting and quantifying influenza A virus replication

Virus-inducible reporter genes as a tool for detecting and quantifying influenza A virus replication

Dynamics of virus shedding and antibody responses in influenza A virus-infected feral swine

Limited compatibility between the RNA polymerase components of influenza virus type A and B

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