传染病学 狂犬病病毒、朊粒(英文)

RABIESVIRUSChapter31BIOLOGICALCHARACTERISTICS1.Bulletshaped2.–ssRNA,helicalsymmetry,enveloped.3.Cytoplasmicinclusions(NegriBody)4.Fiveserotypes.5.Resistance:weak2CYTOPLASMICINCLUSIONS

(NegriBody)34

PATHOGENESISCause:BitefromaRabidAnimalIncubationPeriod:average3-8weeks.(dependingontheseverityandsiteofwound)Viruses:(inthesalivaofRabidAnimals)woundNervefiberCNSFatalencephalitis56HYDROPHOBIA78

CONTROLTreatthewoundPassiveImmunization:anti-rabiesimmunoglobulinVACCINE:InactivatedVaccine9

VACCINATIONPost-exposureprophylaxis0,3,7,14,28dayPre-exposureprophylaxis

0,7,21/28day10

Humanpapillomavirus(HPV)1.DsDNA,icosahadralcapsid,non-envelopedEarlygene(E1-E7),Lategene(L1,L2),VLP

3.Cannotculture4.Transmittedbyskin-toskincontactorbygenitalcontact.

2.Morethan100typeshavebeenidentified.12LIFECYCLEOFHUMANPAPILLOMAVIRUS135.Pathogenesis:HPV16,18(high-risktype)---cervicalcarcinomaHPV6,11(low-risktype)---condylomaacuminatum

E6protein---inactivateP53protein,E7protein---inactivateRBprotein,InactivatinoftheP53andRBproteinsisanimportantstepintheprocessbywhichanormalcellbecomesacancercell.

6.Vaccine:HPVL1VLP(virus-likeparticle)vaccine14PRIONChapter3215Prion:proteinaceousinfectiousparticleNobelPrizeinPhysiologyorMedicineStanleyB.PrusinerCarletonGajdusek16Definition

prions

areinfectiousparticlesencodedbygeneofnormalhostcellswhichhaveabnormalconformation;theyarecomposedsolelyofproteinandcausetransmissiblespongiformencephalopathy(TSE)

inanimalsandhuman.171.Aproteinparticlethatiscapableofcausinganinfectiousdisease.2.Priondoesnotcontaingeneticmaterial(DNAorRNA).3.Aproteinencodedbyanormalgenewhichhasanabnormalconformation.

BIOLOGICALPROPERTIES18PrionproteinPrP

PrPc

(cellularprionprotein):isthoughttobethebenignformoftheproteinandisfoundinnormal,healthycells.PrPsc

(scrapieprionprotein):isthoughttobetheinfectious"scrapie"formwhichcausesneurodegenerativediseasessuchasbovinespongiformencephalopathy(BSE),Creutzfeldt-Jakobdisease(CJD),kuru,andGerstmann-Strausslersyndrome.19PrPc(cellularprionprotein):ThenormalproteinAlphahelicesissensitivetodigestionbyproteaseKPrPsc(scrapieprionprotein)Thedisease-producingproteinBetaconformation,AlphahelicesishighlyresistanttodigestionbyproteaseK20PrPc

PrPsc21PrPcPrPscsoluble+-enzymedigesting+-polypeptidechainɑ-helicalsegmentß-sheetpathogenecity-+22

Resistancetophysicalorchemicalreagents:verystrongInactivationofprion:1mol/LNaOHor5.2%NaClOfor1houratroomtemperature,followingby134℃formorethan2hours.23

PATHOGENESISPriondiseaseortransmissiblespongiformencephalopathy(TSE)isafamilyofrareprogressiveneurodegenerativedisordersthataffectbothhumansandanimals.Theyaredistinguishedbylongincubationperiods,characteristicspongiformchangesassociatedwithneuronloss,andafailuretoinduceinflammatoryresponse.24Pathologicalchanges25Routeoftransmission:

AlimentarytractBloodNerveClassificationofhumanpriondisease:InfectiousHereditarySporadic26HumanPrionDiseasesForm

Phenotype(Clinicalfeatures)SporadicCreutzfeldt-Jakobdisease(CJD)FamilialCreutzfeldt-Jakobdisease(CJD),FatalFamilialInsomnia(FFI),Gerstmann-Sträussler-ScheinkerSyndrome(GSS)AcquiredCreutzfeldt-Jakobdisease(CJD),Kuru,variantCreutzfeldt-Jakobdisease(v-CJD)27AnimalPrionDiseases*Scrapieofsheepandgoat*Bovinespongiformencephalopathy(BSE)*Chronicwastingdisease(CWD)*Transmissibleminkencephalopathy(TME)*Felinespongiformencephalopathy(FSE)28MICROBIALDETECTIONImmunohistochemistrymethod:PrPantibodyWesternblotting:themostfrequentlyusedmethodGeneanalysis:familialpriondisease29PREVENTION1.Inactivationofprion:1mol/LNaOHor5.2%NaClOfor