Using gene editing, researchers at the Fred Hutchinson Cancer Research Center (Fred Hutch) have successfully removed latent herpes simplex virus 1 (HSV-1) — the virus responsible for oral herpes — from infected mice.
HSV-1 is a widespread human pathogen that can produce oral ulcers and neonatal herpes in those infected, along with increasing their risk for acquiring human immunodeficiency virus (HIV). Primary infection begins at the skin, but HSV-1 typically invades neurons in the peripheral nervous system, where it can lie dormant for life. At any time, it can reactivate from its dormant, or latent, state and cause lesions or ulcers on the skin. Current antiviral therapies for oral herpes can reduce infection severity and reactivation frequency, but they do not eliminate the latent HSV-1 itself.
Gene editing technologies, such as CRISPR-Cas9 and meganucleases (i.e., molecular DNA scissors), offer the possibility of disrupting or eliminating latent HSV-1. Scientists have achieved in vivo gene editing of the HSV genome through...
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