2016
CJD and Scrapie Require Agent‐Associated Nucleic Acids for Infection
Botsios S, Manuelidis L. CJD and Scrapie Require Agent‐Associated Nucleic Acids for Infection. Journal Of Cellular Biochemistry 2016, 117: 1947-1958. PMID: 26773845, DOI: 10.1002/jcb.25495.Peer-Reviewed Original ResearchConceptsTSE agentsTransmissible spongiform encephalopathiesAdaptive immune responsesDegenerative brain changesInfectious particlesHost prion proteinGT1 neuronal cellsForms of PrPLymphoreticular tissuesBrain changesImmune responseTSE strainsNeuronal cellsNeurodegenerative diseasesLatent virusInfectivity assaysSpongiform encephalopathiesNucleic acid genomeTitersEpidemic spreadViral structuresPrion proteinHost proteinsVirusHost components
2014
Highly Infectious CJD Particles Lack Prion Protein but Contain Many Viral‐Linked Peptides by LC‐MS/MS
Kipkorir T, Tittman S, Botsios S, Manuelidis L. Highly Infectious CJD Particles Lack Prion Protein but Contain Many Viral‐Linked Peptides by LC‐MS/MS. Journal Of Cellular Biochemistry 2014, 115: 2012-2021. PMID: 24933657, PMCID: PMC7166504, DOI: 10.1002/jcb.24873.Peer-Reviewed Original ResearchConceptsSporadic CJDMouse brainTransmissible encephalopathiesNormal human brain samplesHost prion proteinHuman brain samplesSCJD brainsPrion proteinAmyloid pathologyAPP processingNew therapiesUninfected controlsBrain homogenatesBrain samplesCellular findingsDetectable PrPNeurodegenerative diseasesSheep scrapieInfectious titerBrainProteinase KCJDLC-MS/MSViral motifsInfectious form
2012
Continuous Production of Prions after Infectious Particles Are Eliminated: Implications for Alzheimer’s Disease
Miyazawa K, Kipkorir T, Tittman S, Manuelidis L. Continuous Production of Prions after Infectious Particles Are Eliminated: Implications for Alzheimer’s Disease. PLOS ONE 2012, 7: e35471. PMID: 22509412, PMCID: PMC3324552, DOI: 10.1371/journal.pone.0035471.Peer-Reviewed Original Research
2011
High CJD infectivity remains after prion protein is destroyed
Miyazawa K, Emmerling K, Manuelidis L. High CJD infectivity remains after prion protein is destroyed. Journal Of Cellular Biochemistry 2011, 112: 3630-3637. PMID: 21793041, PMCID: PMC3202053, DOI: 10.1002/jcb.23286.Peer-Reviewed Original ResearchConceptsTransmissible spongiform encephalopathy agentsSpongiform encephalopathy agentInfectious particlesHost prion proteinPK digestionTotal PrPCJD infectivityInfectious homogenatesPrion proteinBrain resultsHigh titersTitersCell infectivityCell-based assaysCell culture assaysInfectivityProteinase K treatmentInfectious formPrPBrainCulture assaysAssaysProteinSensitive formK treatment
2001
Blood borne transit of CJD from brain to gut at early stages of infection
Radebold K, Chernyak M, Martin D, Manuelidis L. Blood borne transit of CJD from brain to gut at early stages of infection. BMC Infectious Diseases 2001, 1: 20. PMID: 11716790, PMCID: PMC59894, DOI: 10.1186/1471-2334-1-20.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainCreutzfeldt-Jakob SyndromeDigestive SystemDisease Models, AnimalMicePrPSc ProteinsConceptsCreutzfeldt-Jakob diseaseIC inoculationAbnormal PrPCJD agentTransmissible spongiform encephalopathiesLymphoreticular tissuesEnteric infectionsIp inoculationPrP accumulationSpinal cordPeripheral tissuesGastrointestinal tractInfectious inoculumLymphatic drainageInfectious agentsVascular routeCell infectivityInfectionTerminal stageDiseaseSpongiform encephalopathiesDifferent organsBrainDaysProgressive appearance