SARS-CoV-2, the virus that causes COVID-19, has caused more than 3.8 million deaths worldwide. Several vaccines are now being deployed globally, yet advances in effective treatments, including engineered monoclonal antibodies, and small molecule antiviral agents, have been less successful.
This highlights the need for innovative approaches that simultaneously suppress viral replication and circumvent viral escape from host immunity and antiviral therapeutics.
Now, Scientists at the Peter Doherty Institute for Infection and Immunity (Doherty Institute) and Peter MacCallum Cancer Centre have taken a step toward a new treatment for stopping the transmission of viruses such as SARS-CoV-2. They have found that Crispr Gene Editing Technology can prevent virus transmission in human cells.
Using the CRISPR Gene Editing tool, scientists successfully block the transmission of the SARS-CoV-2 virus in infected human cells. In addition, this Gene editing technology can also be used to eliminate abnormal RNAs that drive children’s cancers.
In this Crispr Cas Gene Editing, an enzyme (CRISPR-Cas13b) plays an important role. The enzyme binds to target RNAs and degrades part of the virus’s genome to replicate inside cells.
Professor Lewin said, “while the pandemic response was focussed on rolling out protective vaccines, there remained an urgent need for treatments specific to COVID-19 patients.”
“The flexibility of CRISPR-Cas13 – which only needs the viral sequence – means we can look to design antivirals for COVID-19 and any new emerging viruses rapidly.”
Dr. Fareh said, “there were signs this approach could also be applied to a host of existing viruses and be a game-changer for how they are currently treated.”
“Unlike conventional antiviral drugs, the power of this tool lies in its design-flexibility and adaptability, which make it a suitable drug against a multitude of pathogenic viruses including influenza, Ebola, and possibly HIV.”
- Fareh, M., Zhao, W., Hu, W. et al. Reprogrammed CRISPR-Cas13b suppresses SARS-CoV-2 replication and circumvents its mutational escape through mismatch tolerance. Nat Commun 12, 4270 (2021). DOI: 10.1038/s41467-021-24577-9