Maudry Laurent-Rolle, MD, PhD, BS
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Appointments
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About
Titles
Assistant Professor
Biography
Dr. Maudry Laurent-Rolle received her B.S. from Long Island University, Brooklyn Campus in Biology in 2001. She then obtained her MD and PhD from Icahn School of Medicine at Mount Sinai. Her dissertation research was funded by an NIH pre-doctoral fellowship, which allowed her to examine the molecular mechanisms by which flaviviruses inhibit host innate immune responses. She completed residency training in Internal Medicine at Albert Einstein/Montefiore Medical Center in 2016 then joined the Infectious Diseases Fellowship program here at Yale University. Her research focus is on vaccine design and development of antivirals. She is originally from the beautiful Caribbean island of Dominica, known for its many rivers, tropical rainforests, and natural hot springs.
Appointments
Infectious Diseases
Assistant ProfessorPrimaryMicrobial Pathogenesis
Assistant ProfessorSecondary
Other Departments & Organizations
Education & Training
- Research Fellow in Infectious Diseases
- Section of Infectious Diseases (2020)
- Fellow
- Yale University (2019)
- Resident
- Albert Einstein/Montefiore Medical Center (2016)
- MD
- Icahn School of Medicine at Mount Sinai (2013)
- PhD
- Icahn School of Medicine at Mount Sinai, Microbiology (2011)
- Non Degree Program
- Icahn School of Medicine at Mount Sinai, Postbaccalaureate Research Education Program (2004)
- BS
- Long Island University, Biology (2001)
Research
Overview
I spent the last 16 years studying the molecular mechanisms utilized by pathogenic viruses, specifically flaviviruses, to antagonize host immune responses. During my training in the Post Baccalaureate Research Education Program (PREP) at the Icahn School of Medicine at Mount Sinai I helped developed a reporter assay system that was used to screen dengue virus-encoded proteins’ ability to inhibit the type I interferon response. During my graduate school years, I was awarded a competitive NIH F31 grant based on my doctoral studies focused on understanding how West Nile virus (WNV), dengue virus (DENV) and yellow fever virus (YFV) inhibit the host innate immune response. I characterized the molecular mechanisms by which these viruses use the nonstructural protein 5 (NS5) to inhibit interferon signaling albeit through distinct mechanisms. My thesis project as well as several collaborations resulted in a provisional vaccine patent, a book chapter, and several articles that have been published in high impact journals.
After completing my Internal Medicine residency, I joined the Infectious Diseases Fellowship program here at Yale University. After the first intensive clinical year, I transitioned to basic science research where I focus on characterizing the molecular mechanism(s) by which the antiviral protein, CMPK2 restricts viral replication. The results of this work may lead to the development of new drug targets. In addition to my research, I am also a lecturer in the department of Molecular Biophysics and Biochemistry here at Yale School of Medicine. My clinical experiences and research training in virology as well as biochemical and immunological methods place me in a position to answer the fundamental questions that will contribute to my overall long term goal of vaccine design and development of antivirals.
Research at a Glance
Yale Co-Authors
Publications Timeline
Joanna Pawlak, PhD, MSc
Peter Cresswell, PhD, FRS
Craig B. Wilen, MD, PhD
Fangyong Li, MS, MPH
Jeanne Hendrickson, MD
Mahalia S. Desruisseaux, MD
Publications
2024
Comprehensive Assessment of Inactivation Methods for Madariaga Virus
Boytz R, Keita K, Pawlak J, Laurent-Rolle M. Comprehensive Assessment of Inactivation Methods for Madariaga Virus. Viruses 2024, 16: 206. PMID: 38399982, PMCID: PMC10892135, DOI: 10.3390/v16020206.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsEastern equine encephalitis virusMadariaga virusMethod of inactivationInactivation methodSelective agentNorth American strainsEEEV strainsEquine encephalitis virusTRIzol LSAmino acid levelsAmerican strainsEncephalitis virusAcid levelsTRIzolInfected cellsVirusFormalinInactivationPathogensPublic health threatInfected supernatantStrain
2023
CMPK2 restricts Zika virus replication by inhibiting viral translation
Pawlak J, Hsu J, Xia H, Han P, Suh H, Grove T, Morrison J, Shi P, Cresswell P, Laurent-Rolle M. CMPK2 restricts Zika virus replication by inhibiting viral translation. PLOS Pathogens 2023, 19: e1011286. PMID: 37075076, PMCID: PMC10150978, DOI: 10.1371/journal.ppat.1011286.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCytidine/uridine monophosphate kinase 2I interferon-stimulated genesZika virus replicationYellow fever virusAntiviral activityAntiviral effectVirus replicationKunjin virusType I interferon-stimulated genesFirst lineOverall antiviral responseHost's first lineEffective therapeutic interventionsViral translationBroad antiviral activityInterferon-stimulated genesGlobal health threatAntiviral treatmentFlaviviral infectionsPathogenic flavivirusesAntiviral functionDrug AdministrationTherapeutic interventionsAntiviral responseDengue virus
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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMHC-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 MHCORF7aProtocol for assessing translational regulation in mammalian cell lines by OP-Puro labeling
Hsu JC, Pawlak JB, Laurent-Rolle M, Cresswell P. Protocol for assessing translational regulation in mammalian cell lines by OP-Puro labeling. STAR Protocols 2022, 3: 101654. PMID: 36072758, PMCID: PMC9442383, DOI: 10.1016/j.xpro.2022.101654.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsTranslational regulationMammalian cell linesDifferent cell typesDifferent growth conditionsMammalian cellsTranslation activityGene expressionBiological processesCell typesComplete detailsConfocal microscopyCell linesGrowth conditionsPuromycin analoguesCritical roleRegulationCellsProteinLabelingFundamental stepExpressionClick chemistry reactionActivityCytometryViperin triggers ribosome collision-dependent translation inhibition to restrict viral replication
Hsu JC, Laurent-Rolle M, Pawlak JB, Xia H, Kunte A, Hee JS, Lim J, Harris LD, Wood JM, Evans GB, Shi PY, Grove TL, Almo SC, Cresswell P. Viperin triggers ribosome collision-dependent translation inhibition to restrict viral replication. Molecular Cell 2022, 82: 1631-1642.e6. PMID: 35316659, PMCID: PMC9081181, DOI: 10.1016/j.molcel.2022.02.031.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsInterferon-stimulated genesS-adenosyl methionineTranslation inhibitionRadical S-adenosyl methionineInnate immune responseIntegrated stress response pathwayStress response pathwaysViral RNA translationImmune responseAntiviral responseInnate immunityAntiviral mechanismTranslation regulatorsTranslational repressionViral replicationEnzymatic productDidehydro-CTPResponse pathwaysRNA translationViperinSAM activityPathwayInhibitionBroad spectrumReplication
2021
Early but not late convalescent plasma is associated with better survival in moderate-to-severe COVID-19
Briggs N, Gormally MV, Li F, Browning SL, Treggiari MM, Morrison A, Laurent-Rolle M, Deng Y, Hendrickson JE, Tormey CA, Desruisseaux MS. Early but not late convalescent plasma is associated with better survival in moderate-to-severe COVID-19. PLOS ONE 2021, 16: e0254453. PMID: 34320004, PMCID: PMC8318280, DOI: 10.1371/journal.pone.0254453.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCOVID-19 convalescent plasmaSevere COVID-19Convalescent plasmaPlasma recipientsHospital mortalityUnexposed cohortCCP administrationSevere COVID-19 infectionPropensity score-matched analysisCOVID-19Limited therapeutic optionsCOVID-19 infectionCoronavirus disease 2019CCP recipientsHospital stayPrimary endpointSecondary endpointsHospital daysHospital dischargeEarly administrationComplete followMechanical ventilationTherapeutic optionsClinical differencesSevere diseaseTranslational 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 ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSARS-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 ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH 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
2020
Prolonged incubation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in a patient on rituximab therapy
Koff A, Laurent-Rolle M, Hsu JC, Malinis M. Prolonged incubation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in a patient on rituximab therapy. Infection Control And Hospital Epidemiology 2020, 42: 1286-1288. PMID: 33023685, PMCID: PMC7578652, DOI: 10.1017/ice.2020.1239.Peer-Reviewed Case Reports and Technical NotesCitationsAltmetricMeSH Keywords and ConceptsConceptsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Respiratory syndrome coronavirus 2Syndrome coronavirus 2Coronavirus 2Coronavirus disease 2019Rituximab therapyPatient populationDisease 2019Longer quarantine durationQuarantine durationPatientsIncubation periodDaysHypogammaglobulinemiaTherapyProlonged incubation
2019
The Role of NS5 Protein in Determination of Host Cell Range for Yellow Fever Virus
Laurent-Rolle M, Morrison J. The Role of NS5 Protein in Determination of Host Cell Range for Yellow Fever Virus. DNA And Cell Biology 2019, 38: 1414-1417. PMID: 31633391, DOI: 10.1089/dna.2019.5115.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsCitationsAltmetricMeSH Keywords and Concepts
Academic Achievements and Community Involvement
activity Reviewer
Peer Review Groups and Grant Study Sections Early Career Reviewer Program at the Center for Scientific Review (CSR), National Institutes of HealthDetails2023 - PresentDescription Early Career Reviewer Program at the Center for Scientific Review (CSR), National Institutes of Health.activity Member
Professional OrganizationsInfectious Disease Society of AmericaDetails2016 - Presentactivity Member
Professional OrganizationsAmerican Society for VirologyDetails2020 - Presentactivity Member
Professional OrganizationsAmerican Medical AssociationDetails2021 - Presentactivity Member
Professional OrganizationsAmerican College of PhysiciansDetails2022 - Present
Links & Media
News
- April 02, 2024
Yale Department of Internal Medicine Promotions and Appointments (April 2024)
- July 25, 2023Source: Stamford Advocate
Yale researchers are working on a whole new type of vaccine, targeting the insects that carry pathogens
- July 06, 2023
4 Things to Know About Zika Virus
- June 28, 2023
“Coolest Protein” Restricts Zika Virus Replication
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