Author

Catherine A. Lewis

University of North Carolina at Chapel HillORCID 0000-0001-7848-869XUnclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Microbiology· 1 Molecular Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Assay:ChIP-seq· 1 Research Focus:differential expression· 1 Assay:DNA methylation· 1 Research Focus:gene regulatory network inference· 1 Research Focus:host-pathogen & immune response· 1

Frequent Co-Authors

David M. MargolisiD· 2 shared Edward P. BrowneiD· 2 shared Allison A RowleyiD· 1 shared Brian RichardsoniD· 1 shared Fei Zou· 1 shared Genevieve CluttoniD· 1 shared Jackson J. PetersoniD· 1 shared Jeremy M. SimoniD· 1 shared

Activity by Year

2023-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersMicrobiology

David M. MargolisORCID

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2 papers

Recent·Most cited

MicrobiologyPLoS PathogensPeer-reviewedSep 3, 2025

HIV-1 accessory protein Vpr possesses a cryptic p300-dependent transcription-promoting activity that is blocked by histone deacetylases in CD4+ T cells.

Catherine A. Lewis, David M. Margolis, Edward P. Browne

This study identifies Vpr's transcription-promoting activity in HIV-1 latency, showing it is inhibited by HDACs and contributes to reservoir formation in CD4+ T cells.

2 citations

humanbulk RNA-seq

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Molecular BiologyCell chemical biologyPeer-reviewedDec 1, 2023

A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV infected cells

Jackson J. Peterson, Catherine A. Lewis, Samuel D. Burgos…·Edward P. Browne

The paper identifies HDAC inhibitors as agents that prevent HIV latency by maintaining viral expression and altering memory T cell phenotypes in infected cells.

32 citationstop 4%

humanDNA methylation

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