HSV‑1 hides in nerve cells, where today’s antivirals can’t reach it. A team at Temple University’s Center for Neurovirology and Gene Editing is testing whether CRISPR, a gene-editing tool, can cut the virus’s own DNA so it can no longer make new copies. Their results appeared in Molecular Therapy – Nucleic Acids.
What the researchers did
- They packaged CRISPR-Cas9 into a harmless delivery virus (AAV2) and aimed it at one of two HSV‑1 genes the virus needs to replicate and reactivate: ICP0 or ICP27.
- They first tested it in a standard laboratory cell line, where it strongly suppressed HSV‑1 replication.
- They then grew cerebral organoids: small 3D clusters of human brain tissue made from stem cells. They infected them with HSV‑1, created a model of dormant (latent) infection, and then triggered the virus to wake up.
What they found
In the organoids, CRISPR aimed at either gene significantly reduced viral rebound from latency. The authors conclude that gene editing could become a way to eliminate the hidden reservoir and treat complications of HSV‑1.
Why organoids matter
Mouse studies can’t show everything about how HSV behaves in human nerve tissue. Organoids are one step closer: real human cells, arranged in three dimensions. They sit between simple dish experiments and animal studies on the road to a clinical trial.
What to keep in mind
This is laboratory research. Organoids have no immune system or blood supply, and they model brain tissue rather than the sensory nerve ganglia where herpes usually hides. Delivering gene editing safely to every infected neuron in a human body remains the central challenge for the whole field.