University of Utah Discovers Cas12a2 'Shredder' CRISPR: Destroys Viral-Infected and Cancer Cells Without Editing

Researchers at University of Utah Health publish findings on a newly characterized CRISPR system — Cas12a2 — that operates on a fundamentally different principle from all existing CRISPR therapeutics. While standard CRISPR-Cas9, base editors, and prime editors are designed to make precise edits to the genome at specific target sites, Cas12a2 acts as a non-specific nuclease 'shredder' that, once activated by detecting a target RNA sequence (e.g., a viral RNA), begins indiscriminately cleaving all single-stranded nucleic acids (RNA and DNA) inside the cell. This hyperactivation mechanism destroys the infected or malignant cell from the inside, halting viral replication and killing the diseased cell while leaving unactivated cells (those without the viral or cancer marker RNA) unaffected. The mechanism is distinct from CAR-T or other cell-killing approaches: Cas12a2 does not require immune cell engineering — it could theoretically be delivered directly into infected or tumor cells using LNPs or viral vectors. The University of Utah team demonstrated proof-of-concept in cell culture models of viral infection and cancer, showing selective cell death in target-positive cells. Potential applications include: antiviral therapeutics (where Cas12a2 destroys cells harboring active virus before it replicates), cancer therapy (detecting cancer-specific RNA to trigger tumor cell destruction), and antimicrobial therapy. The discovery adds a new tool to the CRISPR toolkit beyond editing, potentially addressing diseases where precise gene correction is not the goal but eliminating specific cell populations is.