Reassortment of NS Segments Modifies Highly Pathogenic Avian Influenza Virus Interaction with Avian Hosts and Host Cells

Petersen, Henning; Wang, Zhongfang; Lenz, Eva; Pleschka, Stephan; Rautenschlein, Silke

doi:10.1128/jvi.02969-12

Cited by 11 publications

(18 citation statements)

References 54 publications

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“…The tubes were placed upside down in the glycine buffer for 3 h and were subsequently retransferred for 12 h into a freshly prepared glycine buffer at 4°C. Finally, supernatants were neutralized with PBS (pH 7.4) for 3 h and placed again in fresh PBS for an additional 1 h at 4°C (Petersen et al, 2013).…”

Section: Methodsmentioning

confidence: 99%

“…Primers and probes for chicken and turkey IFN-α were used as previously described (Petersen et al, 2013). For detection of iNOS mRNA expression, the following primers and probes were used: chicken: forward primer 5′-CAA CAG GAA CCT ACC ATC TGA C-3′, reverse primer 5′-GAC CAC TGG ATT CTC CCA ATA C-3′, probe 5′-(FAM)-ACT GAT CTT TGC TGC CAA ACA GGC-(TAMRA)-3′ (Genbank accession number NM_204961) and turkey: forward primer 5′-CTC TCC CAG GCT TTG ACA TAT T-3′, reverse primer 5′-GTT TGT CTC CTT CCG CTG TTA-3′, probe 5′-(FAM)-TCA CTA CTC CAC CCT CCC AAC AAT-(TAMRA)-3′ (Genbank accession number NM_001303213).…”

Section: Methodsmentioning

confidence: 99%

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Avian metapneumovirus infection of chicken and turkey tracheal organ cultures: comparison of virus–host interactions

Hartmann¹,

Sid²,

Rautenschlein³

2015

Avian Pathology

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Avian metapneumovirus (aMPV) is a pathogen with worldwide distribution, which can cause high economic losses in infected poultry. aMPV mainly causes infection of the upper respiratory tract in both chickens and turkeys, although turkeys seem to be more susceptible. Little is known about virus-host interactions at epithelial surfaces after aMPV infection. Tracheal organ cultures (TOC) are a suitable model to investigate virus-host interaction in the respiratory epithelium. Therefore, we investigated virus replication rates and lesion development in chicken and turkey TOC after infection with a virulent aMPV subtype A strain. Aspects of the innate immune response, such as interferon-α and inducible nitric oxide synthase mRNA expression, as well as virus-induced apoptosis were determined. The aMPV-replication rate was higher in turkey (TTOC) compared to chicken TOC (CTOC) (P < 0.05), providing circumstantial evidence that indeed turkeys may be more susceptible. The interferon-α response was down-regulated from 2 to 144 hours post infection in both species compared to virus-free controls (P < 0.05); this was more significant for CTOC than TTOC. Inducible nitric oxide synthase expression was significantly up-regulated in aMPV-A-infected TTOC and CTOC compared to virus-free controls (P < 0.05). However, the results suggest that NO may play a different role in aMPV pathogenesis between turkeys and chickens as indicated by differences in apoptosis rate and lesion development between species. Overall, our study reveals differences in innate immune response regulation and therefore may explain differences in aMPV -A replication rates between infected TTOC and CTOC, which subsequently lead to more severe clinical signs and a higher rate of secondary infections in turkeys.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Avian metapneumovirus infection of chicken and turkey tracheal organ cultures: comparison of virus–host interactions

Hartmann¹,

Sid²,

Rautenschlein³

2015

Avian Pathology

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“…This alteration results in HA cleavage-activation not only by tissue-restricted trypsin-like proteases that cleave LPAIV in the respiratory and digestive tracts, but also by ubiquitous furin-like proteases found throughout the host resulting in systemic infection6. Nevertheless, several H5 and H7 viruses with pCS exhibited relatively low virulence in chickens and further mutations within or beyond the HA were required for high virulence and/or efficient transmissibility in birds891011121314. To date little is known about the impact of different pCS sequences on virulence of AIV in chickens and modulation of virulence by the reassortment of different gene segments.…”

mentioning

confidence: 99%

Composition of the Hemagglutinin Polybasic Proteolytic Cleavage Motif Mediates Variable Virulence of H7N7 Avian Influenza Viruses

Mostafa

Veits

Ulrich

et al. 2016

Sci Rep

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Acquisition of a polybasic cleavage site (pCS) in the hemagglutinin (HA) is a prerequisite for the shift of low pathogenic (LP) avian influenza virus (AIV) to the highly pathogenic (HP) form in chickens. Whereas presence of a pCS is required for high pathogenicity, less is known about the effect of composition of pCS on virulence of AIV particularly H7N7. Here, we investigated the virulence of four avian H7N7 viruses after insertion of different naturally occurring pCS from two HPAIV H7N7 (designated pCSGE and pCSUK) or from H7N1 (pCSIT). In vitro, the different pCS motifs modulated viral replication and the HA cleavability independent on the HA background. However, in vivo, the level of virulence conferred by the different pCS varied significantly. Within the respective viral backgrounds viruses with pCSIT and pCSGE were more virulent than those coding for pCSUK. The latter showed also the most restricted spread in inoculated birds. Besides the pCS, other gene segments modulated virulence of these H7N7 viruses. Together, the specific composition of the pCS significantly influences virulence of H7N7 viruses. Eurasian LPAIV H7N7 may shift to high pathogenicity after acquisition of “specific” pCS motifs and/or other gene segments from HPAIV.

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“…Mutations at residues 103 and 106 of NS1 increased virus replication in tissue culture, 33 , 36 and deletion of amino acids 191 to 195 reduced the ability of the virus to antagonize IFN production in chicken embryo fibroblast cells 37 . Introduction of NS1 from an H5N1 into H7N1 altered host range and tissue tropism, increased suppression of the host immune response and influenced virus replication in cell culture 35 , 38 , 39 . In contrast, NS1 reassortant viruses of H5N1 subtypes did not result in alteration of replication, tropism or pathogenicity of the viruses in experimentally infected ducks 40 .…”

Section: Ns1: Enhancement Of Virus Replicationmentioning

confidence: 99%

“…Deletion of amino acids 191 to 195, corresponding to the CPSF30 binding domain, attenuated swine-origin H5N1 virus in chickens 37 . Introduction of NS1 from an H5N1 into H7N1 increased virulence in mice and chicken embryos 35 , 38 , 39 . Moreover, a sequence motif at the C-terminal end of NS1, “ESEV” or “EPEV” in AIV or “RSKV” or “RSEV”, in human H5N1 influenza viruses, in addition to interaction with PDZ-domain (postsynaptic density protein 95, Drosophila disc large tumor suppressor, and zonula occludens 1 protein) involved in cellular signal transduction pathways, was considered a species-specific virulence marker 43 - 45 .…”

Section: Ns1: a Virulence Markermentioning

confidence: 99%

Avian influenza virus NS1

2013

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Reassortment of NS Segments Modifies Highly Pathogenic Avian Influenza Virus Interaction with Avian Hosts and Host Cells

Cited by 11 publications

References 54 publications

Avian metapneumovirus infection of chicken and turkey tracheal organ cultures: comparison of virus–host interactions

Avian metapneumovirus infection of chicken and turkey tracheal organ cultures: comparison of virus–host interactions

Composition of the Hemagglutinin Polybasic Proteolytic Cleavage Motif Mediates Variable Virulence of H7N7 Avian Influenza Viruses

Avian influenza virus NS1

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