Clinton Jones
Oklahoma State University, OK·Microbiology & Immunology
Once a person catches herpes simplex virus type 1 (HSV-1), the virus hides for life in nerve cells. It lies dormant in the trigeminal ganglia (nerve clusters in the face) and in the brain.
- Fields
Microbiology & Immunology
Neuroscience
Genetics
- Topics
herpes simplex virus
latency
reactivation
- Grants
- 1 known grant, through Mar 2031
What they work on
- Test whether HSV-1 reactivation is impaired in mice carrying an S134A mutation in the glucocorticoid receptor (stress hormone receptor) that blocks its hormone-independent activation.
- Determine whether crosstalk between the glucocorticoid receptor and other nuclear hormone receptors drives reactivation in latently infected mice and human sensory neurons.
- Identify sex-specific genes that regulate reactivation from latency by comparing GRS229A, S134A-GR and normal C57BL/6 mice.
- Test whether pioneer transcription factors GR and KLF4, which can open packed DNA, remodel chromatin at key HSV-1 promoters early in reactivation.
More about the research
Stress can wake the virus up, a process called reactivation. In some people, reactivation causes recurring eye disease or encephalitis, a serious brain inflammation. Acyclovir does not greatly reduce reactivation, and no vaccine exists. Learning exactly how stress triggers the virus could point to new ways to prevent it.
Why it matters
Recurring HSV-1 eye disease and herpes encephalitis arise when stress reactivates the virus from nerve cells. Current drugs do little to prevent this, and no vaccine exists. Pinpointing how stress hormone receptors and pioneer transcription factors restart the virus could reveal new therapeutic strategies to reduce reactivation. Sex-specific findings may also explain why the risk differs between people.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Donna Neumann
University of Wisconsin-Madison, WI·Microbiology & Immunology
Define how chromatin insulators in the HSV-1 genome form loops that silence viral genes during latency, using human neurons and Chromosome Conformation Capture circular sequencing (4C-seq).
Shaochung Hsia
University of Maryland Eastern Shore, MD·Microbiology & Immunology
Test whether a single nucleotide change in the thyroid hormone receptor element of a key HSV-1 regulatory sequence disrupts hormone-driven epigenetic control of latency and reactivation, using computer-guided mutagenesis and synthetic-genome chimeric viruses.
Angus C Wilson
New York University, NY·Microbiology & Immunology
Identify the viral reactivation signature that neurons recognize when latent HSV-1 reawakens, using cultured primary neurons as a model of latency and reactivation together with single-cell technologies.
The school
Oklahoma State University: 15 labs on PI Pages, $254M a year on research, 238 research doctorates a year.
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