Clinton Jones

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Sitlington Professor of Infectious Diseases

Oklahoma State University

United States

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About

Clinton Jones is the Sitlington Professor of Infectious Diseases at Oklahoma State University System, USA. His research primarily focuses on the mechanisms of reactivation and replication of alpha-herpesviruses, including human and bovine strains. Recent articles explore the role of glucocorticoid receptors in viral latency and neuro-inflammation linked to viral infections.

Recent Grants

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Regulation of latency-reactivation cycle by ORF2 and beta-catenin/Wnt signaling pathway.

Open Date: 2018-07-01

Close Date: 2021-06-01

Grant: Close

Regulation of beta-catenin in neurons during the HSV-1 latency-reactivation cycle.

Open Date: 2018-01-01

Close Date: 2020-12-01

Grant: Close

Analysis of Bovine Herpesvirus 1 Stress Induced Reactivation from Latency.

Open Date: 2014-08-01

Close Date: 2018-09-01

Articles (19)

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2020

Collaborators (6)

Peter Hoyt

Oklahoma State University

UNITED STATES

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Madhan Subramanian

Oklahoma State University

UNITED STATES

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Fouad Elmayet

Research Assistant Professor

Oklahoma State University

UNITED STATES

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Jeffery Ostler

Oklahoma State University

UNITED STATES

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Kelly Harrison

Assistant Professor

Oklahoma State University

UNITED STATES

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Vanessa Claire Santos

Graduate Teaching Assistant

Oklahoma State University

UNITED STATES

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Clinton Jones

Research Interests

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About

Recent Grants

Articles (19)

Glucocorticoid receptor occupancy of key bovine alphaherpesvirus 1 (BoHV-1) promoters correlates with chromatin remodeling during reactivation from latency

Human alpha-herpesvirus 1 (HSV-1) viral replication and reactivation from latency are expedited by the glucocorticoid receptor

Murine nasal-associated lymphoid tissue (NALT) harbors human alphaherpesvirus 1 (HSV-1) DNA during latency, and dexamethasone triggers viral replication

Examination of neuro-inflammation and senescence in brainstem of aged mice latently infected with human alphaherpesvirus 1 (HSV-1)

Glucocorticoid receptor and specificity protein 1 (Sp1) or Sp3, but not the antibiotic Mithramycin A, stimulates human alphaherpesvirus 1 (HSV-1) replication

Glucocorticoid receptor and specificity protein 1 (Sp1) or Sp3 transactivate HSV-1 ICP0 promoter sequences but a GC-rich binding antibiotic, Mithramycin A, impairs reactivation from latency

A cell cycle regulator, E2F2, and glucocorticoid receptor cooperatively transactivate the bovine alphaherpesvirus 1 immediate early transcription unit 1 promoter

Specificity protein 1 (Sp1) and glucocorticoid receptor (GR) stimulate bovine alphaherpesvirus 1 (BoHV-1) replication and cooperatively transactivate the immediate early transcription unit 1 promoter

Intimate Relationship Between Stress and Human Alpha-Herpes Virus 1 (HSV-1) Reactivation from Latency

Slug, a Stress-Induced Transcription Factor, Stimulates Herpes Simplex Virus 1 Replication and Transactivates a cis -Regulatory Module within the VP16 Promoter

Impaired glucocorticoid receptor function attenuates herpes simplex virus 1 production during explant-induced reactivation from latency in female mice

Stress Triggers Expression of Bovine Herpesvirus 1 Infected Cell Protein 4 (bICP4) RNA during Early Stages of Reactivation from Latency in Pharyngeal Tonsil

Herpes Simplex Virus Type 1 Preferentially Enhances Neuro-Inflammation and Senescence in Brainstem of Female Mice

Regulation of herpes simplex virus type 1 latency-reactivation cycle and ocular disease by cellular signaling pathways

Progesterone Sporadically Induces Reactivation from Latency in Female Calves but Proficiently Stimulates Bovine Herpesvirus 1 Productive Infection

A Pioneer Transcription Factor and Type I Nuclear Hormone Receptors Synergistically Activate the Bovine Herpesvirus 1 Infected Cell Protein 0 (ICP0) Early Promoter

Transactivation of Herpes Simplex Virus 1 (HSV-1) Infected Cell Protein 4 Enhancer by Glucocorticoid Receptor and Stress-Induced Transcription Factors Requires Overlapping Krüppel-Like Transcription Factor 4/Sp1 Binding Sites

Specific Akt Family Members Impair Stress-Mediated Transactivation of Viral Promoters and Enhance Neuronal Differentiation: Important Functions for Maintaining Latency

Herpes simplex virus 1 regulates β-catenin expression in TG neurons during the latency-reactivation cycle

Collaborators (6)

Peter Hoyt

Madhan Subramanian

Fouad Elmayet

Jeffery Ostler

Kelly Harrison

Vanessa Claire Santos

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