Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence 英文参考文献.docVIP

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Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence 英文参考文献.doc

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Different Domains of the RNA Polymerase of Infectious Bursal Disease Virus Contribute to Virulence 英文参考文献

DifferentDomainsoftheRNAPolymeraseofInfectious BursalDiseaseVirusContributetoVirulence CyrilLeNoue¨n1¤a,DidierToquin1,HermannMu¨ller2,Ru¨digerRaue2¤b,KatherineM.Kean3 ,Patrick Langlois4,MartineCherbonnel1,NicolasEterradossi1* 1Avian and Rabbit Virology, Immunologyand Parasitology Unit, OIE Reference Laboratory for Infectious Bursal Disease, French Agency for Food, Environmental and OccupationalHealthSafety(Anses),Ploufragan,France,2InstituteforVirology,FacultyofVeterinaryMedicine,UniversityofLeipzig,Leipzig,Germany,3CNRSURA3015, InstitutPasteur,Paris,France,4VirusGeneticsandBiosecurityUnit,FrenchAgencyforFood,EnvironmentalandOccupationalHealthSafety(ANSES),Ploufragan,France Abstract Background:Infectiousbursaldiseasevirus(IBDV)isapathogenofworldwidesignificancetothepoultryindustry.IBDVhas abi-segmenteddouble-strandedRNAgenome.SegmentsAandBencodethecapsid,ribonucleoproteinandnon-structural proteins,ortheviruspolymerase(RdRp),respectively.Sincethelateeighties,veryvirulent(vv)IBDVstrainshaveemergedin Europeinducingupto60%mortality.Althoughsomeprogresshasbeenmadeinunderstandingthemolecularbiologyof IBDV,themolecularbasisforthepathogenicityofvvIBDVisstillnotfullyunderstood. Methodology,PrincipalFindings:Strain88180belongstoalineageofpathogenicIBDVphylogeneticallyrelatedtovvIBDV. Byreversegenetics,werescuedamolecularclone(mc88180),aspathogenicasitsparentstrain.Tostudythemolecular basisfor88180pathogenicity,weconstructedandcharacterizedinvivoreassortantormosaicrecombinantvirusesderived fromthe88180andtheattenuatedCu-1IBDVstrains.ThereassortantvirusrescuedfromsegmentsAof88180(A88)andB ofCu-1(BCU1)wasmilderthanmc88180showingthatsegmentBisinvolvedin88180pathogenicity.Next,theexchangeof differentregionsofBCU1withtheircounterpartsinB88inassociationwithA88didnotfullyrestoreavirulenceequivalent tomc88180.ThisdemonstratedthatseveralregionsifnotthewholeB88areessentialfortheinvivopathogenicityof88180. Conclusion, Significance: The present results show that different domains of the