Blocking of viral replication
At the center of the study is the CRISPR/Cas13d system, which – unlike the better-known Cas9 – cuts RNA rather than DNA. The researchers developed short guide RNAs (crRNAs) that recognize specific sections of the hepatitis E virus. “Our approach uses the ability of Cas13 to specifically recognize and destroy viral RNA,” explains Yannick Brüggemann. In cell culture experiments, this led to a significant reduction in viral replication and the production of infectious virus particles.
crRNAs targeting a region of the viral genome called ORF1 were particularly effective. They significantly reduced both the number of infected cells and viral production, while cell viability remained unaffected. “This shows that we can attack the virus very specifically without harming the cells,” says Eike Steinmann.
A small combination is sufficient
Another focus was identifying as few crRNAs as possible that could still cover many viral variants. Using bioinformatic analyses, the team showed that just three to four different crRNAs are enough to target the majority of known hepatitis E virus variants. This combination could help counteract the rapid adaptability of viruses. “With just a few targeted components, a broad effect can be achieved,” says Emely Richter.
Prospects for new antiviral strategies
The study provides an important proof of concept for CRISPR-based antiviral approaches against hepatitis E. However, further steps are needed before clinical application—particularly regarding safe and efficient delivery within the body.
JHEP Reports
Experimental study
Cells
Development of a CRISPR-Cas13-based Antiviral Strategy Against Hepatitis E Virus
4-May-2026