Molecular studies of influenza B virus in the reverse genetics era

Jackson, David J.; Elderfield, Ruth A.; Barclay, William

doi:10.1099/vir.0.026187-0

Cited by 68 publications

(62 citation statements)

References 142 publications

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“…Indeed, IAV and IBV possess eight vRNA segments, which have been shown to encode up to 17 and 11 proteins, respectively. ICV has seven vRNA segments that encode nine viral proteins (10, 11). In the case of IAV, segment 2 encodes the polymerase basic (PB) proteins PB1, PB1-F2, and PB1-N40 by using alternative translation initiation sites (12, 13); segment 3 encodes the polymerase acidic (PA) proteins PA and PA-X by a ribosomal frameshift, as well as two additional N-terminally truncated forms (PA-N155 and PA-N182) by using alternative translation initiation sites (14, 15); and finally, segment 7 encodes the matrix (M) protein M1 and ion channel proteins M2 and M42 and segment 8 encodes the nonstructural (NS) protein NS1, nuclear export protein NS2/NEP, and NS3 by alternative mRNA splicing.…”

Section: Introductionmentioning

confidence: 99%

Influenza Viruses and mRNA Splicing: Doing More with Less

Dubois

Terrier

Rosa‐Calatrava

2014

mBio

130

132

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During their nuclear replication stage, influenza viruses hijack the host splicing machinery to process some of their RNA segments, the M and NS segments. In this review, we provide an overview of the current knowledge gathered on this interplay between influenza viruses and the cellular spliceosome, with a particular focus on influenza A viruses (IAV). These viruses have developed accurate regulation mechanisms to reassign the host spliceosome to alter host cellular expression and enable an optimal expression of specific spliced viral products throughout infection. Moreover, IAV segments undergoing splicing display high levels of similarity with human consensus splice sites and their viral transcripts show noteworthy secondary structures. Sequence alignments and consensus analyses, along with recently published studies, suggest both conservation and evolution of viral splice site sequences and structure for improved adaptation to the host. Altogether, these results emphasize the ability of IAV to be well adapted to the host’s splicing machinery, and further investigations may contribute to a better understanding of splicing regulation with regard to viral replication, host range, and pathogenesis.

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Section: Introductionmentioning

confidence: 99%

Influenza Viruses and mRNA Splicing: Doing More with Less

Dubois

Terrier

Rosa‐Calatrava

2014

mBio

130

132

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“…Influenza B viruses, similarly to influenza A viruses, are members of the family Orthomyxoviridae, and each contains a single-stranded, negative sense, segmented RNA genome [1]. Unlike influenza A viruses, which can be divided into several antigenic subtypes and infect a variety of host species [2][3][4], influenza B viruses cannot be divided into distinct subtypes and infect mainly humans (except for a strain isolated from a Seal in the Netherlands) [5].…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization of influenza B viruses isolated in east-central China in 2009–2010

Zhu

Zhao

et al. 2012

Virus Genes

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The current circulating influenza B viruses can be divided into two major phylogenetic lineages: the Victoria and Yamagata lineages. We conducted a survey of influenza B viruses in Hubei and Zhejiang provinces during 2009-2010. Out of 341 throat swabs, 18 influenza B viruses were isolated. Five isolates were selected for genetic and phylogenetic analysis. The molecular analyses revealed that all the isolates had similar antigenic characteristics to B/Brisbane/60/2008. However, in the three viruses isolated from Zhejiang, a single asparagine to aspartic acid substitution in position 197 was observed, thereby eliminating the glycosylation at that site and possibly causing an antigenic change. None of the viruses had amino acid mutations at positions 116, 149, 152, 198, 222, 250, 291, and 402 of the neuraminidase (NA) gene, predicting that the viruses would still be sensitive to NA inhibitors. Phylogenetic analyses revealed that all five isolates were closely related to B/Brisbane/60/2008-the 2010 vaccine strain-and contained Victoria-like hemagglutinin and Yamagata-like NA genes, suggesting that reassortment may had occurred. In addition, similar phylogenetic patterns among the acidic polymerase, nucleoprotein and matrix protein genes, as well as between the basic polymerase 1 and basic polymerase 2 genes, were observed, suggesting possible functional interactions among these proteins. All the results highlighted the importance of molecular monitoring of influenza B viruses for reassortment and antigenic drift.

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“…They are also distinguished by accessory proteins encoded from overlapping open reading frames (ORFs) and by the antigenic differences of internal proteins (5). For instance, influenza A and B viruses both encode ion channel proteins, M2 and BM2, respectively, whereas influenza A virus expresses the PB1-F2 pathogenicity factor and influenza B virus expresses the NB ion channel, which are absent in the converse virus (1).…”

mentioning

confidence: 99%

Influenza A and B Virus Intertypic Reassortment through Compatible Viral Packaging Signals

Baker

Nogales

Finch

et al. 2014

J Virol

104

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Influenza A and B viruses cocirculate in humans and together cause disease and seasonal epidemics. These two types of influenza viruses are evolutionarily divergent, and exchange of genetic segments inside coinfected cells occurs frequently within types but never between influenza A and B viruses. Possible mechanisms inhibiting the intertypic reassortment of genetic segments could be due to incompatible protein functions of segment homologs, a lack of processing of heterotypic segments by influenza virus RNA-dependent RNA polymerase, an inhibitory effect of viral proteins on heterotypic virus function, or an inability to specifically incorporate heterotypic segments into budding virions. Here, we demonstrate that the full-length hemagglutinin (HA) of prototype influenza B viruses can complement the function of multiple influenza A viruses. We show that viral noncoding regions were sufficient to drive gene expression for either type A or B influenza virus with its cognate or heterotypic polymerase. The native influenza B virus HA segment could not be incorporated into influenza A virus virions. However, by adding the influenza A virus packaging signals to full-length influenza B virus glycoproteins, we rescued influenza A viruses that possessed HA, NA, or both HA and NA of influenza B virus. Furthermore, we show that, similar to single-cycle infectious influenza A virus, influenza B virus cannot incorporate heterotypic transgenes due to packaging signal incompatibilities. Altogether, these results demonstrate that the lack of influenza A and B virus reassortants can be attributed at least in part to incompatibilities in the virus-specific packaging signals required for effective segment incorporation into nascent virions. IMPORTANCEReassortment of influenza A or B viruses provides an evolutionary strategy leading to unique genotypes, which can spawn influenza A viruses with pandemic potential. However, the mechanism preventing intertypic reassortment or gene exchange between influenza A and B viruses is not well understood. Nucleotides comprising the coding termini of each influenza A virus gene segment are required for specific segment incorporation during budding. Whether influenza B virus shares a similar selective packaging strategy or if packaging signals prevent intertypic reassortment remains unknown. Here, we provide evidence suggesting a similar mechanism of influenza B virus genome packaging. Furthermore, by appending influenza A virus packaging signals onto influenza B virus segments, we rescued recombinant influenza A/B viruses that could reassort in vitro with another influenza A virus. These findings suggest that the divergent evolution of packaging signals aids with the speciation of influenza A and B viruses and is in part responsible for the lack of intertypic viral reassortment.

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Molecular studies of influenza B virus in the reverse genetics era

Cited by 68 publications

References 142 publications

Influenza Viruses and mRNA Splicing: Doing More with Less

Influenza Viruses and mRNA Splicing: Doing More with Less

Molecular characterization of influenza B viruses isolated in east-central China in 2009–2010

Influenza A and B Virus Intertypic Reassortment through Compatible Viral Packaging Signals

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