Albert C Shaw, MD, PhD
Professor of Medicine (Infectious Diseases)DownloadHi-Res Photo
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Professor of Medicine (Infectious Diseases)
Biography
Dr. Shaw is a graduate of Harvard College who completed his M.D. training at Harvard Medical School and his Ph.D. in the laboratory of Philip Leder. After completing his clinical training in Internal Medicine and Infectious Diseases at Massachusetts General Hospital, he was a postdoctoral fellow in the laboratory of Fred Alt. Dr. Shaw joined the faculty at Yale in 2001, and is currently Professor of Medicine in the Section of Infectious Diseases. His research focuses on the immunology of aging, and his laboratory has interests in age-associated alterations in innate immune function and vaccine response in humans, as well as circadian regulation of immune response and mechanisms of inflammatory dysregulation in medication-associated treatment of opioid use disorder. He was a Howard Hughes Postdoctoral Physician Research Fellow, Brookdale National Fellow, and T. Franklin Williams Scholar, and he is a Fellow of the Infectious Disease Society of America and member of the Interurban Clinical Club.
Last Updated on April 07, 2025.
Appointments
Infectious Diseases
ProfessorPrimary
Other Departments & Organizations
- Center for Infection and Immunity
- Claude D. Pepper Older Americans Independence Center
- CPIRT - Center for Pulmonary Injury, Inflammation, Repair and Therapeutics
- Human and Translational Immunology Program
- Infectious Diseases
- Internal Medicine
- Rheumatic Diseases Research Core
- Yale Center for Research on Aging (Y-Age)
- Yale Medicine
- Yale Ventures
- Yale-UPR Integrated HIV Basic and Clinical Sciences Initiative
Education & Training
- Fellow
- Massachusetts General Hospital (1997)
- Intern and Resident
- Massachusetts General Hospital (1994)
- PhD
- Harvard University (1991)
- MD
- Harvard Medical School (1991)
- AB
- Harvard College (1983)
Research
Overview
Medical Research Interests
Aging; DNA Repair; Immune System; Immunity, Innate; Infectious Disease Medicine; Influenza Vaccines; Toll-Like Receptors
ORCID
0000-0003-4970-7640
Research at a Glance
Yale Co-Authors
Frequent collaborators of Albert C Shaw's published research.
Publications Timeline
A big-picture view of Albert C Shaw's research output by year.
Research Interests
Research topics Albert C Shaw is interested in exploring.
Ruth R Montgomery, PhD
Steven Kleinstein, PhD
David A. Hafler, MD, FANA
Akiko Iwasaki, PhD
Albert Ko, MD
Nathan Grubaugh, PhD
70Publications
8,415Citations
Aging
Immunity, Innate
Influenza Vaccines
Toll-Like Receptors
Immune System
Publications
2025
A multi-omics recovery factor predicts long COVID in the IMPACC study
Gabernet G, Maciuch J, Gygi J, Moore J, Hoch A, Syphurs C, Chu T, Jayavelu N, Corry D, Kheradmand F, Baden L, Sekaly R, McComsey G, Haddad E, Cairns C, Rouphael N, Fernandez-Sesma A, Simon V, Metcalf J, Higuita N, Hough C, Messer W, Davis M, Nadeau K, Pulendran B, Kraft M, Bime C, Reed E, Schaenman J, Erle D, Calfee C, Atkinson M, Brakenridge S, Melamed E, Shaw A, Hafler D, Augustine A, Becker P, Ozonoff A, Bosinger S, Eckalbar W, Maecker H, Kim-Schulze S, Steen H, Krammer F, Westendorf K, Network I, Peters B, Fourati S, Altman M, Levy O, Smolen K, Montgomery R, Diray-Arce J, Kleinstein S, Guan L, Ehrlich L. A multi-omics recovery factor predicts long COVID in the IMPACC study. Journal Of Clinical Investigation 2025 PMID: 40924481, DOI: 10.1172/jci193698.Peer-Reviewed Original ResearchAltmetricConceptsSARS-CoV-2 infectionCOVID-19 patientsMulti-OmicsSARS-CoV-2Risk of LCAcute COVID-19 severityImmune profiling dataSubset frequenciesBiomarkers of LCPlasma metabolomeCOVID-19 severityPotential treatment targetPBMC transcriptomesClinical parametersBiological underpinningsStress erythropoiesisCell frequencyInflammatory mediatorsLC biomarkersTherapeutic opportunitiesHospital dischargeAndrogenic steroidsDisease severityTreatment targetPatientsExoproteome of calorie-restricted humans identifies complement deactivation as an immunometabolic checkpoint reducing inflammaging.
Mishra M, Kim HH, Youm YH, Gonzalez-Hurtado E, Zaitsev K, Dlugos T, Shchukina I, Gliniak C, Ravussin E, Mohanty S, Shaw AC, Scherer PE, Artyomov MN, Dixit VD. Exoproteome of calorie-restricted humans identifies complement deactivation as an immunometabolic checkpoint reducing inflammaging. BioRxiv 2025 PMID: 40799539, DOI: 10.1101/2025.08.04.668533.Publications for non-academic audiencesBaseline predictors for 28-day COVID-19 severity and mortality among hospitalized patients: results from the IMPACC study
Hou J, Haslund-Gourley B, Diray-Arce J, Hoch A, Rouphael N, Becker P, Augustine A, Ozonoff A, Guan L, Kleinstein S, Peters B, Reed E, Altman M, Langelier C, Maecker H, Kim S, Montgomery R, Krammer F, Wilson M, Eckalbar W, Bosinger S, Levy O, Steen H, Rosen L, Baden L, Melamed E, Ehrlich L, McComsey G, Sekaly R, Schaenman J, Shaw A, Hafler D, Corry D, Kheradmand F, Atkinson M, Brakenridge S, Agudelo Higuita N, Metcalf J, Hough C, Messer W, Pulendran B, Nadeau K, Davis M, Fernandez Sesma A, Simon V, Kraft M, Bime C, Calfee C, Erle D, Impacc Network, Robinson L, Cairns C, Haddad E, Comunale M. Baseline predictors for 28-day COVID-19 severity and mortality among hospitalized patients: results from the IMPACC study. Frontiers In Medicine 2025, 12: 1604388. PMID: 40687705, PMCID: PMC12271175, DOI: 10.3389/fmed.2025.1604388.Peer-Reviewed Original ResearchAltmetricConceptsSequential Organ Failure AssessmentPeripheral blood mononuclear cellsLaboratory biomarkersSequential Organ Failure Assessment scoreAntibody titersNasal viral loadOrgan Failure AssessmentBlood mononuclear cellsSARS-CoV-2 antibody titersSARS-CoV-2 infectionCOVID-19 patientsCOVID-19 cohortMortality prediction modelCOVID-19 severityPatient ageViral loadBlood cytometryImmunophenotypic assessmentMononuclear cellsClinical dataBaseline biomarkersFailure AssessmentBiomarkers of COVID-19Hospitalized patientsIL-6MICBG406A polymorphism reduces risk of mechanical ventilation and death during viral acute lung injury
Pickering H, Alipanah-Lechner N, Chen E, Duchen D, Maecker H, Kim-Schulze S, Montgomery R, Cotsapas C, Steen H, Krammer F, Langelier C, Levy O, Baden L, Melamed E, Ehrlich L, McComsey G, Sekaly R, Cairns C, Haddad E, Shaw A, Hafler D, Corry D, Kheradmand F, Atkinson M, Brakenridge S, Higuita N, Metcalf J, Hough C, Messer W, Pulendran B, Nadeau K, Davis M, Fernandez-Sesma A, Simon V, Kraft M, Bime C, Erle D, Schaenman J, Ozonoff A, Peters B, Kleinstein S, Augustine A, Diray-Arce J, Becker P, Rouphael N, Altman M, Bosinger S, Eckalbar W, Network I, Calfee C, Aguilar O, Reed E, Greenland J, Calabrese D. MICBG406A polymorphism reduces risk of mechanical ventilation and death during viral acute lung injury. JCI Insight 2025, 10: e191951. PMID: 40608426, PMCID: PMC12333951, DOI: 10.1172/jci.insight.191951.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAcute lung injuryMHC class I polypeptide-related sequence BImmune profileLung injuryMechanical ventilationSARS-CoV-2Variant allelesAcute lung injury severityRisk of mechanical ventilationProfiles of peripheral bloodSoluble inflammatory mediatorsOdds of severe COVID-19Cox proportional hazards modelsSevere COVID-19SARS-CoV-2 infectionProportional hazards modelMultiple immune pathwaysNKG2D-activatingCOVID-19 severityNKG2D ligandsNK cellsViral burdenBronchoalveolar lavagePeripheral bloodHomozygous patientsType 2 immune responses are associated with less severe COVID-19 in a hospitalized cohort
Jayavelu N, Qi J, Milliren C, Ozonoff A, Liu S, Levy O, Baden L, Melamed E, McComsey G, Cairns C, Schaenman J, Shaw A, Hafler D, Corry D, Kheradmand F, Atkinson M, Brakenridge S, Higuita N, Metcalf J, Hough C, Messer W, Pulendran B, Nadeau K, Davis M, Geng L, Sesma A, Simon V, Krammer F, Bime C, Calfee C, Bosinger S, Eckalbar W, Steen H, Maecker H, Becker P, Augustine A, Holland S, Rosen L, Lee S, Vaysman T, Ozonoff A, Diray-Arce J, Chen J, Kho A, Milliren C, Hoch A, Chang A, McEnaney K, Barton B, Lentucci C, Murphy M, Saluvan M, Shaheen T, Liu S, Syphurs C, Albert M, Hayati A, Bryant R, Abraham J, Thomas S, Cooney M, Karoly M, Altman M, Jayavelu N, Presnell S, Kohr B, Jancsyk T, Arnett A, Peters B, Overton J, Vita R, Westendorf K, Overton J, Levy O, Steen H, van Zalm P, Fatou B, Smolen K, Viode A, van Haren S, Jha M, Stevenson D, Odumade O, Baden L, Mendez K, Lasky-Su J, Tong A, Rooks R, Desjardins M, Sherman A, Walsh S, Mitre X, Cauley J, Li X, Evans B, Montesano C, Licona J, Krauss J, Issa N, Chang J, Izaguirre N, Hutton S, Michelotti G, Wong K, Tebbutt S, Shannon C, Sekaly R, Fourati S, McComsey G, Harris P, Sieg S, Ribeiro S, Cairns C, Haddad E, Kutzler M, Bernui M, Cusimano G, Connors J, Woloszczuk K, Joyner D, Edwards C, Lee E, Lin E, Melnyk N, Powell D, Kim J, Goonewardene I, Simmons B, Smith C, Martens M, Croen B, Semenza N, Bell M, Furukawa S, McLin R, Tegos G, Rogowski B, Mege N, Ulring K, Schearer P, Sheidy J, Nagle C, Seyfert-Margolis V, Rouphael N, Bosinger S, Boddapati A, Tharp G, Pellegrini K, Johnson B, Panganiban B, Huerta C, Anderson E, Samaha H, Sevransky J, Bristow L, Beagle E, Cowan D, Hamilton S, Hodder T, Bechnak A, Cheng A, Mehta A, Ciric C, Spainhour C, Carter E, Scherer E, Usher J, Hellmeister K, Hussaini L, Hewitt L, Mcnair N, Ribeiro S, Wimalasena S, Fernandez-Sesma A, Simon V, Krammer F, Van Bakel H, Kim-Schulze S, Reiche A, Qi J, Lee B, Carreño J, Singh G, Raskin A, Tcheou J, Khalil Z, van de Guchte A, Farrugia K, Khan Z, Kelly G, Srivastava K, Eaker L, Bermúdez-González M, Mulder L, Beach K, Saksena M, Altman D, Kojic E, Sominsky L, Azad A, Bielak D, Kawabata H, Yellin T, Fried M, Sullivan L, Morris S, Kleiner G, Stadlbauer D, Dutta J, Xie H, Patel M, Nie K, Rahman A, Messer W, Hough C, Siegel S, Sullivan P, Lu Z, Brunton A, Strand M, Lyski Z, Coulter F, Micheleti C, Maecker H, Pulendran B, Nadeau K, Rosenberg-Hasson Y, Leipold M, Sigal N, Rogers A, Fernandes A, Manohar M, Do E, Chang I, Lee A, Blish C, Din H, Roque J, Geng L, Artandi M, Davis M, Ahuja N, Yang S, Chinthrajah S, Hagan T, Reed E, Schaenman J, Salehi-Rad R, Rivera A, Pickering H, Sen S, Elashoff D, Ward D, Brook J, Sanchez E, Llamas M, Perdomo C, Magyar C, Fulcher J, Erle D, Calfee C, Hendrickson C, Kangelaris K, Nguyen V, Lee D, Chak S, Ghale R, Gonzalez A, Jauregui A, Leroux C, Altamirano L, Rashid A, Willmore A, Woodruff P, Krummel M, Carrillo S, Ward A, Langelier C, Patel R, Wilson M, Dandekar R, Alvarenga B, Rajan J, Eckalbar W, Schroeder A, Fragiadakis G, Tsitsiklis A, Mick E, Guerrero Y, Love C, Maliskova L, Adkisson M, Leligdowicz A, Beagle A, Rao A, Sigman A, Samad B, Curiel C, Shaw C, Tietje-Ulrich G, Milush J, Singer J, Vasquez J, Tang K, Betancourt L, Santhosh L, Pierce L, Paz M, Matthay M, Thakur N, Rodriguez N, Sutter N, Jones N, Sinha P, Prasad P, Lota R, Rashid S, Asthana S, Bhide S, Lea T, Abe-Jones Y, Hafler D, Montgomery R, Shaw A, Kleinstein S, Gygi J, Pawar S, Konstorum A, Chen E, Cotsapas C, Wang X, Xu L, Dela Cruz C, Iwasaki A, Mohanty S, Nelson A, Zhao Y, Farhadian S, Asashima H, Chaudhary O, Coppi A, Fournier J, Muenker M, Nelson A, Raddassi K, Rainone M, Ruff W, Salahuddin S, Shulz W, Vijayakumar P, Wang H, Wunder E, Young H, Ko A, Wang X, Duchen D, Esserman D, Guan L, Brito A, Rothman J, Grubaugh N, Corry D, Kheradmand F, Song L, Nelson E, Metcalf J, Higuita N, Sinko L, Booth J, Drevets D, Brown B, Kraft M, Bime C, Mosier J, Erickson H, Schunk R, Kimura H, Conway M, Francisco D, Molzahn A, Wilson C, Schunk R, Hughes T, Sierra B, Atkinson M, Brakenridge S, Ungaro R, Manning B, Moldawer L, Oberhaus J, Guirgis F, Borresen B, Anderson M, Ehrlich L, Melamed E, Maguire C, Wylie D, Rousseau J, Hurley K, Geltman J, Siles N, Rogers J, Augustine A, Diray-Arce J, Haddad E, Sekaly R, Kraft M, Woodruff P, Erle D, Ehrlich L, Montgomery R, Becker P, Altman M, Fourati S. Type 2 immune responses are associated with less severe COVID-19 in a hospitalized cohort. Journal Of Allergy And Clinical Immunology Global 2025, 4: 100515. PMID: 40709330, PMCID: PMC12284355, DOI: 10.1016/j.jacig.2025.100515.Peer-Reviewed Original ResearchConceptsT2 immune responseClinical outcomesVirus loadImmune responseSARS-CoV-2Primary siteSusceptibility to respiratory viral infectionsType 2 immune responsesAntibody titersCellular markersPrimary site of infectionSeverity of respiratory illnessRespiratory viral infectionsIL-13 levelsDegree of respiratory supportAssociated with less severe COVID-19Site of infectionLow virus loadSevere COVID-19Effects of SARS-CoV-2Severe coronavirus diseaseDiagnosis of asthmaRespiratory supportCoronavirus severe acute respiratory syndrome coronavirus 2Blood cytometryMicrofluidics combined with electron microscopy for rapid and high-throughput mapping of antibody–viral glycoprotein complexes
Sewall L, de Paiva Froes Rocha R, Gibson G, Louie M, Xie Z, Bangaru S, Tran A, Ozorowski G, Mohanty S, Beutler N, Rogers T, Burton D, Shaw A, Batista F, Chocarro Ruiz B, Torrents de la Peña A, Ward A. Microfluidics combined with electron microscopy for rapid and high-throughput mapping of antibody–viral glycoprotein complexes. Nature Biomedical Engineering 2025, 1-14. PMID: 40461656, PMCID: PMC12404239, DOI: 10.1038/s41551-025-01411-x.Peer-Reviewed Original ResearchAltmetricConceptsStructure-based vaccine designVolumes of seraHA glycoproteinPolyclonal antibodiesImmune complexesAntibody responseVaccine designVaccine developmentHigh-throughput mappingCharacterization of immune complexesVaccinated individualsAntibodiesGlycoprotein complexViral glycoproteinsInvading pathogensEpitope mappingSeraSingle-particle electron microscopyGlycoproteinNegative-stain electron microscopyHormetic elevation of taurine restrains inflammaging by deactivating the NLRP3 inflammasome.
Guan C, Ryu S, Dong M, Youm YH, Mohanty S, Maeda R, Orliaguet L, Kim HH, Dlugos T, Smith SR, Ravussin E, Onyuru J, Wang A, Shaw AC, Hoffman HM, Kluger Y, Sugiura Y, Dixit VD. Hormetic elevation of taurine restrains inflammaging by deactivating the NLRP3 inflammasome. BioRxiv 2025 PMID: 40501605, DOI: 10.1101/2025.05.27.656381.Publications for non-academic audiencesHigh affinity CD16 polymorphism associated with reduced risk of severe COVID-19
Qualls A, Tsao T, Lui I, Lim S, Su Y, Chen E, Duchen D, Maecker H, Kim-Schulze S, Montgomery R, Krammer F, Langelier C, Levy O, Baden L, Melamed E, Ehrlich L, McComsey G, Sekaly R, Cairns C, Haddad E, Shaw A, Hafler D, Corry D, Kheradmand F, Atkinson M, Brakenridge S, Higuita N, Metcalf J, Hough C, Messer W, Pulendran B, Nadeau K, Davis M, Fernandez-Sesma A, Simon V, Kraft M, Bime C, Calfee C, Erle D, Schaenmann J, Ozonoff A, Peters B, Kleinstein S, Augustine A, Diray-Arce J, Becker P, Rouphael N, Network I, Goldman J, Calabrese D, Heath J, Wells J, Reed E, Lanier L, Pickering H, Aguilar O. High affinity CD16 polymorphism associated with reduced risk of severe COVID-19. JCI Insight 2025, 10: e191314. PMID: 40402577, PMCID: PMC12306582, DOI: 10.1172/jci.insight.191314.Peer-Reviewed Original ResearchCitationsAltmetricConceptsAntibody-dependent cellular cytotoxicitySevere COVID-19Anti-SARS-CoV-2 IgG titersNK cell-mediated immune responsesNK cell-mediated antibody-dependent cellular cytotoxicityHost-directed therapeutic strategiesSevere disease trajectoryCell-mediated immune responsesHospitalized COVID-19 patientsLevels of inflammatory mediatorsNatural killer cellsSevere respiratory complicationsImmunopathogenesis of COVID-19Activating Fc receptorsRisk of ICU admissionRisk of severe COVID-19SARS-CoV-2 infectionCOVID-19 patientsCOVID-19 cohortIn vitro reporter systemKiller cellsRespiratory complicationsCellular cytotoxicityViral loadImmunophenotypic assessmentHost-microbe multiomic profiling identifies distinct COVID-19 immune dysregulation in solid organ transplant recipients
Pickering H, Schaenman J, Phan H, Maguire C, Tsitsiklis A, Rouphael N, Higuita N, Atkinson M, Brakenridge S, Fung M, Messer W, Salehi-rad R, Altman M, Becker P, Bosinger S, Eckalbar W, Hoch A, Doni Jayavelu N, Kim-Schulze S, Jenkins M, Kleinstein S, Krammer F, Maecker H, Ozonoff A, Diray-Arce J, Shaw A, Baden L, Levy O, Reed E, Langelier C. Host-microbe multiomic profiling identifies distinct COVID-19 immune dysregulation in solid organ transplant recipients. Nature Communications 2025, 16: 586. PMID: 39794319, PMCID: PMC11723965, DOI: 10.1038/s41467-025-55823-z.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSolid organ transplant recipientsOrgan transplant recipientsTransplant recipientsInduction of pro-inflammatory genesSenescent T cellsTransitional B cellsImpaired viral clearanceImmune response to infectionAnti-spike IgG levelsNon-transplanted controlsFeatures of COVID-19Innate Immune Signaling PathwaysResponse to infectionPro-inflammatory genesSerum chemokinesViral clearanceImmune dysregulationT cellsImmune signaling pathwaysB cellsImmune featuresSex-matchedIgG levelsSevere diseaseTransplantation
2024
The human CD47 checkpoint is targeted by an immunosuppressive Aedes aegypti salivary factor to enhance arboviral skin infectivity
Marin-Lopez A, Huck J, Esterly A, Azcutia V, Rosen C, Garcia-Milian R, Sefik E, Vidal-Pedrola G, Raduwan H, Chen T, Arora G, Halene S, Shaw A, Palm N, Flavell R, Parkos C, Thangamani S, Ring A, Fikrig E. The human CD47 checkpoint is targeted by an immunosuppressive Aedes aegypti salivary factor to enhance arboviral skin infectivity. Science Immunology 2024, 9: eadk9872-eadk9872. PMID: 39121194, PMCID: PMC11924945, DOI: 10.1126/sciimmunol.adk9872.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSuppress antiviral responsesArthropod proteinsPathogen replicationAntiviral responseProtein AVertebrate hostsMosquito salivary proteinsUp-regulatedBlood feedingHuman macrophagesPleomorphic effectsSkin infectionsZika virus disseminationInhibit proinflammatory responsesSalivary proteinsProteinNatural ligandWhite blood cellsHuman skin explantsProinflammatory responseMosquito salivaVirus disseminationHuman CD47Salivary factorsArbovirus infection
Clinical Trials
Current Trials
Immune Response Analysis in Lymph Node Tissue
HIC ID2000032631RoleSub InvestigatorPrimary Completion Date04/30/2027Recruiting ParticipantsEffects of circadian regulation and sleep on immune responses
HIC ID2000027037RolePrincipal InvestigatorPrimary Completion Date02/28/2025Recruiting ParticipantsGenderBothAge21+ yearsImpact of HIV Infection on Immunologic, Transcriptomic, and Metabolomic Signatures
HIC ID1608018239RoleSub InvestigatorPrimary Completion Date09/01/2021Recruiting ParticipantsGenderBothAge18+ years
Clinical Care
Overview
Albert C. Shaw, MD, PhD, is an infectious diseases specialist who provides care for individuals with a variety of infections, including those that affect older adults. He focuses on how age-related changes in the body’s defenses can make people more vulnerable to infection and immune system complications.
As a professor of medicine at Yale School of Medicine, Dr. Shaw studies the ways in which the immune system’s first line of defense, called the innate immune system, changes with age. This includes investigating how these shifts might reduce vaccine effectiveness and contribute to ongoing, low-grade inflammation that can harm overall health. He also examines how circadian rhythms—biological processes that follow a 24-hour cycle—may regulate immune responses, as well as how certain treatments for opioid use disorder might influence inflammation.
Dr. Shaw earned his medical degree from Harvard Medical School and completed a doctorate at Harvard University. He then pursued an internal medicine residency and an infectious diseases fellowship at Massachusetts General Hospital.
Clinical Specialties
Infectious Diseases
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- October 15, 2025Source: Everyday Health
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- August 27, 2025
Yale Pepper Center Seeks Letters of Intent For Aging Research 2025 - 2026
- February 19, 2025Source: MSN
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- November 19, 2024Source: Yahoo
What are the symptoms of foodborne illnesses like E. coli? What to know amid a new carrot recall.
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