Donna Neumann
University of Wisconsin-Madison, WI·Microbiology & Immunology
Herpes simplex virus 1 (HSV-1) is a leading cause of blindness in the US. After an initial infection, the virus hides in a dormant, or latent, state inside sensory nerve cells.
- Fields
Microbiology & Immunology
Genetics
Neuroscience
- Topics
herpes simplex virus 1
ocular herpes
herpes keratitis
- Grants
- 1 known grant, through Jan 2031
What they work on
- 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).
- Determine how loss of chromatin insulator function at the start of reactivation allows expression of anterograde transport genes that move new virus from neurons back toward the eye.
- Test whether depleting viral proteins with rAAV-delivered siRNAs, or editing viral genomes with rAAV-delivered CRISPR, blocks reactivation or depletes latent reservoirs in eye infections.
More about the research
From time to time it reactivates, travels back along the nerve to the cornea, and can spread to other people. Repeated reactivations damage the eye, yet no antiviral drug can prevent them because scientists do not know how reactivation starts and completes.
Why it matters
Recurrent ocular HSV-1 is the leading infectious cause of blindness in the US, and no drug prevents reactivation. By defining how viral DNA loops control reactivation, this work could lead to gene-silencing or gene-editing therapies that block flare-ups, reduce hidden virus reservoirs, and limit spread to new people.
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.
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.
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.
The school
University of Wisconsin-Madison: 91 labs on PI Pages, $1.9B a year on research, 854 research doctorates a year.
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