Angus C Wilson
New York University, NY·Microbiology & Immunology
Herpes simplex virus type 1 (HSV-1) infects more than 70% of people in the US and stays in the nervous system for life. HSV-1 manipulates the cells it infects in two ways.
- Fields
Microbiology & Immunology
Neuroscience
Biochemistry
- Topics
herpes simplex virus
herpesvirus
viral latency
- Grants
- 2 known grants, through Oct 2028
What they work on
- 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.
- Determine how neuronal factors rapidly mobilized during HSV-1 reactivation selectively block viral gene expression and stop the replication program at a defined stage.
- Characterize how the viral protein ICP27 relocates and disrupts the host machinery that installs, removes and reads m6A, a methyl mark on RNA, and the machinery that finishes RNA ends.
- Test whether ICP27-driven loss of m6A causes a widespread failure of transcription termination that preferentially harms host RNAs, and map m6A on viral RNAs to explain why viral transcripts escape.
More about the research
It can lie dormant in nerve cells and wake up under stress. During active infection, it also takes over the host cell's gene-expression machinery. The lab studies both sides of this relationship: what holds the virus in check inside neurons, and how the virus reshapes the host cell's RNA to favor its own replication.
Why it matters
Repeated reawakening of HSV-1 can damage nerve tissue and is considered a risk factor for neurodegenerative disease. Learning how neurons keep the virus dormant, and how the virus hijacks host RNA processing, could reveal targets for new antiviral therapies. It could also show how neurons can be protected from other kinds of damage.
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).
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.
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
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
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