2022
SARS-CoV-2 accessory proteins ORF7a and ORF3a use distinct mechanisms to down-regulate MHC-I surface expression
Arshad N, Laurent-Rolle M, Ahmed W, Hsu J, Mitchell S, Pawlak J, Sengupta D, Biswas K, Cresswell P. SARS-CoV-2 accessory proteins ORF7a and ORF3a use distinct mechanisms to down-regulate MHC-I surface expression. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 120: e2208525120. PMID: 36574644, PMCID: PMC9910621, DOI: 10.1073/pnas.2208525120.Peer-Reviewed Original ResearchConceptsMHC-I expressionSARS-CoV-2Major histocompatibility complex (MHC) class I moleculesT cell recognitionVirus-infected cellsClass I moleculesAntigen presentationOngoing COVID-19 pandemicHeavy chainImmune evasionViral peptidesSecretory pathwayDistinct mechanismsMHCI moleculesPeptide-MHCInfected cellsCausative agentCell recognitionCD8COVID-19 pandemicViral proteinsEndoplasmic reticulumHuman MHCORF7a
2021
Translational shutdown and evasion of the innate immune response by SARS-CoV-2 NSP14 protein
Hsu JC, Laurent-Rolle M, Pawlak JB, Wilen CB, Cresswell P. Translational shutdown and evasion of the innate immune response by SARS-CoV-2 NSP14 protein. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2101161118. PMID: 34045361, PMCID: PMC8214666, DOI: 10.1073/pnas.2101161118.Peer-Reviewed Original ResearchConceptsSARS-CoV-2Interferon-stimulated genesImmune responseSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Host protein synthesisRespiratory syndrome coronavirus 2Syndrome coronavirus 2Innate immune responseUnprecedented global health crisisCoronavirus 2N7-methyltransferase activityOngoing COVID-19 pandemicHuman coronavirusesTranslational shutdownVirus replicationNsp14 proteinGlobal health crisisProtein synthesisInhibition activityCausative agentCOVID-19COVID-19 pandemicSARS-CoV-2 nsp14Dependent inductionSARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2
Lu Q, Liu J, Zhao S, Gomez Castro MF, Laurent-Rolle M, Dong J, Ran X, Damani-Yokota P, Tang H, Karakousi T, Son J, Kaczmarek ME, Zhang Z, Yeung ST, McCune BT, Chen RE, Tang F, Ren X, Chen X, Hsu JCC, Teplova M, Huang B, Deng H, Long Z, Mudianto T, Jin S, Lin P, Du J, Zang R, Su TT, Herrera A, Zhou M, Yan R, Cui J, Zhu J, Zhou Q, Wang T, Ma J, Koralov SB, Zhang Z, Aifantis I, Segal LN, Diamond MS, Khanna KM, Stapleford KA, Cresswell P, Liu Y, Ding S, Xie Q, Wang J. SARS-CoV-2 exacerbates proinflammatory responses in myeloid cells through C-type lectin receptors and Tweety family member 2. Immunity 2021, 54: 1304-1319.e9. PMID: 34048708, PMCID: PMC8106883, DOI: 10.1016/j.immuni.2021.05.006.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme 2Binding SitesCell LineCOVID-19CytokinesGene Expression RegulationHost-Pathogen InteractionsHumansInflammation MediatorsLectins, C-TypeMembrane ProteinsModels, MolecularMyeloid CellsNeoplasm ProteinsProtein BindingProtein ConformationSARS-CoV-2Single-Domain AntibodiesSpike Glycoprotein, CoronavirusStructure-Activity RelationshipConceptsSARS-CoV-2Proinflammatory responseMyeloid cellsFamily member 2Robust proinflammatory responseC-type lectin receptorsCOVID-19 therapyCOVID-19 severityMember 2SARS-CoV-2 spikeCoronavirus disease 2019Single-cell RNA sequencing analysisReceptor-binding domainImmune hyperactivationImmune cellsDisease 2019Enzyme 2Pulmonary cellsC-type lectinRNA sequencing analysisCanonical receptorLectin receptorsPotential targetPredominant expressionReceptor interaction