Shaochung Hsia
University of Maryland Eastern Shore, MD·Microbiology & Immunology
Herpes simplex virus type 1 (HSV-1) behaves very differently depending on which cell it infects. In most cells it copies itself in under a day, switching on roughly 90 genes.
- Fields
Microbiology & Immunology
Neuroscience
Pharmacology
- Topics
herpes simplex virus
viral latency
reactivation
- Grants
- 1 known grant, through Jun 2029
What they work on
- 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.
- Determine whether thyroid hormone increases voltage-gated sodium channel function in neurons by upregulating growth factors through MAPK/ERK signaling, a pathway that relays growth signals to the nucleus.
- Test the hypothesis that thyroid hormone antagonists increase HSV-1 reactivation in latently infected mice, and measure degrees of latency and reactivation under hormone or antagonist treatment.
- Determine how thyroid hormone alters cytokine production that regulates sodium channel activity, through changes in signaling pathways or intracellular trafficking of the channels.
- Build an enrichment academy at UMES in which students manufacture adeno-associated virus (AAV) gene delivery vectors and apply them to express a dominant-negative thyroid hormone receptor in neurons for HSV-1 studies.
More about the research
In nerve cells it can instead go quiet, a dormant state called latency, and later wake up and cause painful neurological complications with large health and economic costs. What decides whether the virus sleeps or wakes is still unclear. This project pursues an unexpected lead: thyroid hormone, the hormone that sets the body's metabolic pace.
Why it matters
HSV-1 reactivation causes recurrent, painful conditions such as shingles and a range of nerve complications, with substantial health and economic burden. Understanding how thyroid hormone keeps the virus dormant in neurons could point toward new drugs that prevent reactivation. The project also trains underrepresented undergraduate and high school students in virology and gene-delivery techniques.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Clinton Jones
Oklahoma State University, OK·Microbiology & Immunology
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.
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).
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
University of Maryland Eastern Shore: 2 labs on PI Pages, $13M a year on research, 17 research doctorates a year.
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