Richard Park, PhD
Associate Research ScientistDownloadHi-Res Photo
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Associate Research Scientist
Appointments
Pediatric Infectious Diseases
Associate Research ScientistPrimary
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Education & Training
- PhD
- Johns Hopkins University (2003)
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Richard Park's published research.
I. George Miller Jr, MD
Publications
2026
Playing both sides – Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells
Daigle D, Creasy-Marrazzo A, Gradoville L, El-Guindy A, Mukherjee R, Das S, Baral B, Rousseau B, Park R, McIntosh M, Miller G, Bhaduri-McIntosh S. Playing both sides – Epstein-Barr Virus accumulates select cellular transcripts to counter virus-mediated host shut-off in lytic cells. PLOS Pathogens 2026, 22: e1014211. PMID: 42113877, PMCID: PMC13225664, DOI: 10.1371/journal.ppat.1014211.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsEpstein-Barr virusHost shutoffGenome replicationCellular transcriptionLytic cycleHost genesGene expressionDownregulation of host gene expressionEfficient genome replicationRNA-binding proteinsHost gene expressionHost shut-offLytic cellsEpstein-Barr virus lytic cycleHost protein synthesisFinely tuned regulationViral gene expressionBurkitt lymphoma linesTranscriptional demandBurkitt's lymphoma cellsHost transcriptionTranscript abundanceLymphoma cellsVirion packagingLymphoma lines
2015
DNA Damage Signaling Is Induced in the Absence of Epstein—Barr Virus (EBV) Lytic DNA Replication and in Response to Expression of ZEBRA
Wang'ondu R, Teal S, Park R, Heston L, Delecluse H, Miller G. DNA Damage Signaling Is Induced in the Absence of Epstein—Barr Virus (EBV) Lytic DNA Replication and in Response to Expression of ZEBRA. PLOS ONE 2015, 10: e0126088. PMID: 25950714, PMCID: PMC4423948, DOI: 10.1371/journal.pone.0126088.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAtaxia Telangiectasia Mutated ProteinsCell LineChromobox Protein Homolog 5DeoxyribonucleasesDNA DamageDNA ReplicationDNA, ViralEpstein-Barr Virus InfectionsGene Expression Regulation, NeoplasticHerpesvirus 4, HumanHistonesHumansImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsPhosphorylationProtein Serine-Threonine KinasesSignal TransductionTrans-ActivatorsTumor Suppressor p53-Binding Protein 1Viral ProteinsConceptsDNA damage responseEBV lytic cycleLytic DNA replicationDNA replicationDDR activationEpstein-Barr virusExpression of ZEBRALytic cycleGene expressionCellular DNA damage responseDNA damageDNA damaging reagentsDNA damage signalingCellular gene expressionViral DNA replicationLytic viral DNA replicationZEBRA mutantsDamage signalingLytic cycle progressionViral lytic DNA replicationViral DNA amplificationEBV gene productsDamage responseReplication compartmentsDDR pathways
2013
Latency of Epstein–Barr virus is disrupted by gain-of-function mutant cellular AP-1 proteins that preferentially bind methylated DNA
Yu KP, Heston L, Park R, Ding Z, Wang’ondu R, Delecluse HJ, Miller G. Latency of Epstein–Barr virus is disrupted by gain-of-function mutant cellular AP-1 proteins that preferentially bind methylated DNA. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 8176-8181. PMID: 23625009, PMCID: PMC3657822, DOI: 10.1073/pnas.1301577110.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
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