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1、VIRALIMMUNOLOGYVolume20,Number4,2007©MaryAnnLiebert,Inc.Pp.599–608DOI:10.1089/vim.2007.0056CCR1DeficiencyIncreasesSusceptibilitytoFatalCoronavirusInfectionoftheCentralNervousSystemMICHELLEJ.HICKEY,1KATHERINES.HELD,1ELIZABETHBAUM,1JI-LIANGGAO,2PHILIPM.MURPHY,2andTHOMASE.LANE1ABSTRACTTheroleofCCc
2、hemokinereceptor1(CCR1)inhostdefenseanddiseasedevelopmentwasdeter-minedinamodelofviral-inducedneurologicdisease.Intracerebral(IC)infectionofmicewithmousehepatitisvirus(MHV)resultsinanacuteencephalitisfollowedbyachronicdemyelinatingdiseasesimilarinpathologytothediseasemultiplesclerosis(MS).Noinc
3、reaseinmortalitywasobservedduringtheacutephaseofdiseasefollowingMHVinfectionofmicelackingCCR1(CCR1/)ascomparedtowild-type(CCR1/)mice.However,by21dpost-infection,74%ofCCR1/micehadsuccumbedtodeathcomparedtoonly32%mortalityofCCR1/mice,indicatingthatchemokinesignalingthroughCCR1significantl
4、y(p0.04)enhancedsurvivalfollowingICinfec-tionwithMHV.IncreasedmortalityinCCR1/micewasnotassociatedwithincreasedviralre-coveryfromtheCNS,althoughCCR1deficiencycorrelatedwithreducedT-cellaccumulationwithintheCNSduringacute,butnotchronic,disease.DespitethereductioninT-celltraffickingintotheCNSo
5、fCCR1/miceduringacutedisease,componentsofhostdefenseremainedunaltered;T-celleffectorfunctionsincludingcytolyticactivityandproliferationandtheexpressionofIFN-withintheCNSwerenotsignificantlydifferentbetweenCCR1/andCCR1/infectedmice.Inaddi-tion,macrophageinfiltrationintotheCNSwasunaffected
6、inMHV-infectedCCR1/micewhencomparedtoCCR1/mice.Furthermore,assessmentofneuropathologyrevealednodifferenceintheseverityofdemyelinationbetweenCCR1-deficientandwild-typemice.Together,thesefindingsrevealthatT-cellandmacrophagetraffickingarenotdependentonCCR1andhighlightanim-portantroleforCCR1si
7、gnalinginpromotingsurvivalduringchronicMHVinfection.INTRODUCTIONtheseevents.InsupportofthisarestudiesdemonstratingrobustchemokinegeneexpressionfollowingCNSinfec-IRALINFECTIONOFTHEcentralnervoussystem(CNS)tionwithawidevarietyofviru
