Thomas E. Shenk
Princeton University · Molecular Biology
Active 1970–2025
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About
Thomas E. Shenk is the James A. Elkins Professor of Life Sciences, Emeritus, in the Department of Molecular Biology at Princeton University. He is a virologist who has investigated gene functions and the pathogenesis of adenovirus, a DNA tumor virus, and human cytomegalovirus (HCMV), a member of the herpes family of viruses. His research focuses on understanding the molecular mechanisms underlying HCMV replication and pathogenesis, as well as viral latency. His laboratory employs genetic, biochemical, proteomic, and metabolomic approaches to study the HCMV life cycle, including how the virus blocks host cell defenses and alters cellular metabolism during infection. Key areas of his work include identifying viral proteins such as pUL38 that interact with host cellular complexes, studying how HCMV induces metabolic pathways like glycolysis and lipid biosynthesis, and developing models for viral latency. His research also explores the role of cellular long non-coding RNAs, such as HSATII RNA, in viral replication. Dr. Shenk is a fellow of the American Academy of Microbiology and the American Academy of Arts and Sciences, and a member of the U.S. National Academy of Sciences and the U.S. Institute of Medicine. He has served as past president of the American Society for Virology and the American Society for Microbiology, and has been a member of the board of directors of Merck & Co. He currently serves on the boards of the Fox Chase Cancer Center, The Hepatitis B Foundation, and…
Research topics
- Virology
- Immunology
- Medicine
- Political Science
- Pathology
- Biology
Selected publications
Role of PDGF receptor-α during human cytomegalovirus entry into fibroblasts
Proceedings of the National Academy of Sciences · 2018-10-01 · 97 citations
articleOpen accessSenior authorCorrespondingHuman CMV (HCMV) exhibits a broad cell tropism that depends on two virion glycoprotein complexes: a trimeric complex (gH/gL/gO) that facilitates viral infection primarily in fibroblasts and a pentameric complex (gH/gL/pUL128-pUL130-pUL131A) that mediates infection in epithelial and endothelial cells. We performed genome-wide CRISPR screens in which the PDGF receptor-α (PDGFRα) was identified as the most significant cellular gene product essential for infection by HCMV virions containing only tri…
Proceedings of the National Academy of Sciences · 2017-09-05 · 72 citations
articleOpen accessSenior authorCorrespondingHuman cytomegalovirus (HCMV) is the prototypical human β-herpes virus. Here we perform a systems analysis of the HCMV host-cell transcriptome, using gene set enrichment analysis (GSEA) as an engine to globally map the host-pathogen interaction across two cell types. Our analysis identified several previously unknown signatures of infection, such as induction of potassium channels and amino acid transporters, derepression of genes marked with histone H3 lysine 27 trimethylation (H3K27me3), and in…
A tumor-specific endogenous repetitive element is induced by herpesviruses
Nature Communications · 2019-01-03 · 46 citations
articleOpen accessTandem satellite repeats account for 3% of the human genome. One of them, Human Satellite II (HSATII), is highly expressed in several epithelial cancers and cancer cell lines. Here we report an acute induction of HSATII RNA in human cells infected with two herpes viruses. We show that human cytomegalovirus (HCMV) IE1 and IE2 proteins cooperate to induce HSATII RNA affecting several aspects of the HCMV replication cycle, viral titers and infected-cell processes. HSATII RNA expression in tissue fr…
Proceedings of the National Academy of Sciences · 2020-11-30 · 28 citations
articleOpen accessSenior authorCorrespondingPericentromeric human satellite II (HSATII) repeats are normally silent but can be actively transcribed in tumor cells, where increased HSATII copy number is associated with a poor prognosis in colon cancer, and in human cytomegalovirus (HCMV)-infected fibroblasts, where the RNA facilitates viral replication. Here, we report that HCMV infection or treatment of ARPE-19 diploid epithelial cells with DNA-damaging agents, etoposide or zeocin, induces HSATII RNA expression, and a kinase-independent f…
Proceedings of the National Academy of Sciences · 2019-09-03 · 28 citations
articleOpen accessHuman cytomegalovirus (HCMV) manipulates many aspects of host cell biology to create an intracellular milieu optimally supportive of its replication and spread. Our study reveals that levels of several components of the purinergic signaling system, including the P2Y2 and P2X5 receptors, are elevated in HCMV-infected fibroblasts. Knockdown and drug treatment experiments demonstrated that P2Y2 enhances the yield of virus, whereas P2X5 reduces HCMV production. The HCMV IE1 protein induces P2Y2 expr…
Recent grants
NIH · $399k · 2014
NIH · $3.7M · 2011
NIH · $1.8M · 2016
Frequent coauthors
- 34 shared
Felicia Goodrum
University of Arizona
- 31 shared
Miklós Tóth
Cornell University
- 29 shared
Jay A. Nelson
Ambrx (United States)
- 27 shared
Kevin P. High
Cincinnati Children's Hospital Medical Center
- 27 shared
David A. Ornelles
Wake Forest University
- 26 shared
Eain A. Murphy
SUNY Upstate Medical University
- 26 shared
Craig T. Jordan
- 26 shared
Anny Usheva
Bryn Mawr College
Labs
Shenk LabPI
Awards & honors
- 2013 Intellectual Property Accelerator Award, Princeton Univ…
- 2012 Arthur Kornberg and Paul Berg Lifetime Achievement Awar…
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