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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-helicalsegment?-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-Str?ussler-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
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