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1、VIRALIMMUNOLOGYVolume23,Number4,2010aMaryAnnLiebert,Inc.Pp.437–442DOI:10.1089/vim.2010.0008CharacterizationofaVariantVirusfromAsciticFluidofSubacuteGranulomatousSerositisinInterferon-g-De?cientC57BL/6MicePersistentlyInfectedwithMurineCoronavirusStrainJHM
2、1123ShigeruKyuwa,SatoshiTakagaki,ShutokuMatsuyama,FumihiroTaguchi,4561JunzoSaegusa,YoichirohIwakura,Yoh-IchiTagawa,andYasuhiroYoshikawaAbstractPreviously,weshowedthatintraperitonealinfectionwithmurinecoronavirusstrainJHM(JHMV)establishedapersistentinfect
3、ionwithsubacutegranulomatousserositisininterferon-g-de?cientC57BL/6(B6-GKO)mice.Herein,wecharacterizeavariantvirusfromB6-GKOmicepersistentlyinfectedwithJHMV.Viruseswereisolatedfromascitesat25dpost-infectionandclonedbylimitingdilutiononDBTcells;onevariant
4、wasnamed25V16G.Tocomparepathogenicityinvivo,weinoculated25V16GandJHMVintraperitoneallyinto8-to12-week-oldB6-GKOmice.WhereasnearlyalloftheB6-GKOmiceinfectedwithJHMVsurvivedover14d,allofthoseinfectedwith25V16Gdiedby9dpost-infection.Histopathologicalexamina
5、tionrevealedthat25V16GinducedacutefulminanthepatitisinB6-GKOmice,whereasJHMVcausedseverebutfocalhepatitis.Thevirustiterof25V16Gintheliverwas50-and250-foldhigherthanthatofJHMVat5and7dpost-infection,respec-tively.However,therewasnosigni?cantdifferenceinvir
6、algrowthbetween25V16GandJHMVincelllinesculturedinvitro.NucleotidesequencingoftheSgeneof25V16GandJHMVrevealedadeletionof29aminoacidsencompassingS511–539,whichcoversamajorcytotoxicTlymphocyte(CTL)epitopeinC57BL/6mice,andtwopointmutationsresultinginaminoaci
7、dchangesintheSproteinof25V16G.Oneexplanationforthegreaterpathogenicityof25V16Gisthat25V16GescapesCTL-mediatedprotectioninB6-GKOmice.ThisexperimentalmodelmaybeusedtoassesstheroleofIFN-ginviralpersistenceinvivo.Introductionantiviralimmuneresponses,allowing
8、themtoreplicateandpersistsuccessfullyinthehost(8,17,18).Althoughresearch-Hostsequipthemselveswithelaborateimmuneers’understandingofpersistentviralinfectionshasbeenad-systemstodefendthemselvesfromviruses.Theanti-vancedbyuse
