2020
CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses
Lin T, Geng T, Harrison AG, Yang D, Vella AT, Fikrig E, Wang P. CXCL10 Signaling Contributes to the Pathogenesis of Arthritogenic Alphaviruses. Viruses 2020, 12: 1252. PMID: 33147869, PMCID: PMC7692144, DOI: 10.3390/v12111252.Peer-Reviewed Original ResearchConceptsChikungunya virusAlphaviral arthritisArthritogenic alphavirusesLargest immune cell populationMacrophages/T cellsImmune cell populationsInflammatory immune responseLow viral loadWild-type miceO'nyong-nyong virusWild-type animalsRheumatic manifestationsImmune infiltratesViral loadT cellsImmune responseAlphaviral diseaseArthritic diseasesTherapeutic targetCXCL10PathogenesisViral RNACell populationsArthritisFootpadMechanisms of SARS-CoV-2 Transmission and Pathogenesis
Harrison AG, Lin T, Wang P. Mechanisms of SARS-CoV-2 Transmission and Pathogenesis. Trends In Immunology 2020, 41: 1100-1115. PMID: 33132005, PMCID: PMC7556779, DOI: 10.1016/j.it.2020.10.004.Peer-Reviewed Original ResearchConceptsSARS-CoV-2Severe acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Coronavirus infectious disease 2019Respiratory syndrome coronavirus 2SARS-CoV-2 transmissionTissue tropismSyndrome coronavirus 2SARS-CoV-2 researchBroad tissue tropismCoronavirus 2Pathogenic coronavirusesDisease 2019Immune antagonismTherapeutic testingAnimal modelsViral pathogenesisVaccine developmentPathogenesisTropismFuture investigationsHuman population
2016
Exploration of West Nile Virus Infection in Mouse Models
Wang P. Exploration of West Nile Virus Infection in Mouse Models. Methods In Molecular Biology 2016, 1435: 71-81. PMID: 27188551, DOI: 10.1007/978-1-4939-3670-0_7.Peer-Reviewed Original ResearchConceptsWest Nile virusMouse modelWest Nile virus infectionExperimental mouse modelAntiviral immune responseCentral nervous systemWNV pathogenesisLeukocyte numbersVirus infectionImmune responseBlood leukocytesWNV infectionNervous systemNeurological diseasesMouse brainViral titersResidential cellsLeukocytesNile virusVirus spreadInfectionImmunopathologyPathogenesisCNSDisease
2007
Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis
Pal U, Wang P, Bao F, Yang X, Samanta S, Schoen R, Wormser GP, Schwartz I, Fikrig E. Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis. Journal Of Experimental Medicine 2007, 205: 133-141. PMID: 18166585, PMCID: PMC2234379, DOI: 10.1084/jem.20070962.Peer-Reviewed Original ResearchConceptsLyme arthritisMouse jointsB. burgdorferi antigensBurgdorferi-infected miceSevere arthritisSpirochete numbersArthritisHost responseLyme diseaseAffinity-purified antibodiesBorrelia burgdorferiChain reactionMiceOriginal phenotypeBasic membrane proteinMutant spirochetesGene expressionJointsInflammationPathogenesisAntigenDiseaseB. burgdorferi gene expression