Nikhil Prasad Fact checked by:Thailand Medical News Team Dec 02, 2024 1 week, 2 days, 14 hours, 25 minutes ago
Medical News: Researchers from the University of Ottawa, Canada, and the University of Saskatchewan, Canada, have made a groundbreaking discovery in the fight against COVID-19. They have identified a small RNA molecule, miR-24-3p, that significantly inhibits the replication and spread of the SARS-CoV-2 virus, the pathogen responsible for the COVID-19 pandemic. This study opens new avenues for antiviral therapies that could potentially tackle emerging coronavirus strains.
MicroRNA Found to Inhibit SARS-CoV-2 Infection
This
Medical News report delves into how miR-24-3p works against the virus and its implications for future treatments.
What Are MicroRNAs
MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate gene expression. They act like switches, turning off specific genes by binding to messenger RNA. Researchers have previously studied miR-24-3p for its role in lipid regulation and its ability to control pathways like MAPK, which are crucial for cell signaling. Intriguingly, miR-24-3p also appears to influence viral infections, reducing the spread of viruses like hepatitis C and H5N1 influenza.
The Study
Led by researchers Parrish Evers, Spencer Uguccioni, and others, the team examined the effects of miR-24-3p on SARS-CoV-2. The scientists discovered that miR-24-3p inhibits the virus's ability to enter and replicate within human cells. This microRNA achieves its antiviral effects by targeting critical proteins such as furin, NRP1, NRP2, and SREBP2, which are essential for the virus to infect and replicate in host cells.
How miR-24-3p Works
The team found that miR-24-3p acts by targeting and downregulating critical host proteins that the SARS-CoV-2 virus exploits to infect human cells. These include furin, neuropilin-1 (NRP1), neuropilin-2 (NRP2), and SREBP2. These proteins are crucial for the virus to enter cells, replicate, and produce new infectious particles.
Furin, for instance, facilitates the cleavage of the viral spike protein, a process essential for the virus to gain entry into host cells. Meanwhile, NRP1 and NRP2 are co-receptors that enhance the virus’s ability to infect cells. SREBP2, on the other hand, regulates cholesterol synthesis, which plays a role in the viral lifecycle. By targeting these proteins, miR-24-3p disrupts multiple stages of the virus's life cycle, making it harder for the virus to survive and spread.
The Study Findings
The study revealed several key findings:
-Inhibition of Viral Entry and Replication: Experiments showed that cells treated with miR-24-3p had significantly lower levels of SARS-CoV-2 RNA, indicating reduced viral replication. The molecule also impaired the production and infectivity of new virus particles.
-Broad Antiviral Potential: Interestingly, miR-24-3p retained its antiviral activity against common SARS-CoV-2 mutations such as D614G and
N501Y. These mutations are associated with increased viral fitness and have been found in many variants of concern, including Delta and Omicron.
-Selective Action: While miR-24-3p effectively inhibited SARS-CoV-2, its impact on a related coronavirus, HCoV-229E, was minimal. This specificity highlights its targeted action against SARS-CoV-2-specific pathways.
-Mechanism Validation: The researchers confirmed that miR-24-3p directly downregulates its target proteins at both the mRNA and protein levels. This was validated through advanced laboratory techniques, including qPCR and western blotting.
Why This Matters
The emergence of escape mutants that can evade current vaccines and antiviral drugs is a growing concern. The study shows that miR-24-3p, by targeting host factors rather than the virus itself, has a robust mechanism less likely to be affected by viral mutations. This makes it a promising candidate for future therapeutic development, particularly for combating new variants.
Future Implications
Although miR-24-3p shows great promise, the researchers caution that targeting host proteins also comes with challenges. These proteins often play vital roles in normal cellular functions, so any therapeutic approach would need to balance antiviral efficacy with minimal side effects. For example, furin and neuropilins are involved in processes like tissue repair and angiogenesis.
However, the team believes that miR-24-3p could complement existing treatments and pave the way for multi-target antiviral strategies. Such approaches have been successful in treating other viral diseases like hepatitis C and HIV.
Conclusion
The discovery of miR-24-3p as a potent antiviral molecule represents a significant advancement in the fight against COVID-19. Its ability to target multiple stages of the viral lifecycle and its resilience against common mutations make it a promising tool for managing the current pandemic and future coronavirus outbreaks. While further research and clinical trials are needed, this small RNA molecule could become a key player in the arsenal against viral diseases.
The study findings were published in the peer-reviewed journal: Viruses.
https://www.mdpi.com/1999-4915/16/12/1844
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