Vasoactive Intestinal Peptide Can Reduce the Ability of SARS-Cov-2 to Infect Human Cells
Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 17, 2025 2 hours, 38 minutes ago
Medical News: Scientists Explore How a Natural Peptide Might Help in the Fight Against COVID-19
A team of international researchers has uncovered new insights into how a natural compound called vasoactive intestinal peptide (VIP) may play a role in reducing the ability of the SARS-CoV-2 virus to infect human cells. The study was conducted by scientists from the University Medical Center Freiburg and the University of Heidelberg in Germany, as well as the University of Florence in Italy. Their findings could open the door to new therapeutic strategies for COVID-19 and potentially other viral infections.
Vasoactive Intestinal Peptide Can Reduce the Ability of SARS-Cov-2 to Infect Human Cells
How the Virus Enters Human Cells
The SARS-CoV-2 virus, which causes COVID-19, enters human cells by binding its spike protein to a receptor called angiotensin-converting enzyme 2 (ACE2). This is followed by a process involving another protein, transmembrane serine protease 2 (TMPRSS2), which helps the virus penetrate the cells. If these proteins are present in high amounts on the surface of human cells, the virus can enter more easily, leading to higher infection rates.
This
Medical News report highlights that scientist have long been searching for ways to block the virus from entering cells. Some drugs attempt to neutralize the spike protein, while others work by blocking ACE2 or TMPRSS2. However, researchers in this latest study focused on a different approach - using VIP, a molecule known for its immune-modulating properties, to influence the availability of these key entry proteins.
VIP Reduces the Presence of ACE2 and TMPRSS2
In laboratory experiments, the researchers treated human epithelial cells with VIP and found that it significantly reduced the presence of both ACE2 and TMPRSS2 at multiple levels. VIP suppressed the genes responsible for producing these proteins, meaning the cells created less of them. It also decreased the surface expression of these proteins, effectively making it harder for the virus to find entry points into the cell.
Further analysis revealed another unexpected mechanism - VIP increased the activity of an enzyme called ADAM10. This enzyme acts like a molecular pair of scissors, cutting off ACE2 and TMPRSS2 from the cell surface, a process known as "shedding." With fewer of these proteins available on the cell surface, the ability of SARS-CoV-2 to infect the cells was significantly reduced.
Evidence From Lab Experiments
To confirm the importance of this discovery, the scientists performed experiments using a specially designed non-infectious version of the SARS-CoV-2 virus, known as a pseudovirus. This virus mimics the real virus’s entry process but does not cause disease. They found that cells treated with VIP had significantly fewer infections compared to untreated cells, further proving that VIP weakens the virus’s ability to enter human cells.
In another crucial test, the team used VIP r
eceptor antagonists - molecules that block VIP’s activity - to see if this would reverse the effects. When they did so, the levels of ACE2 and TMPRSS2 remained high, confirming that VIP was directly responsible for reducing these viral entry points.
What These Findings Mean for COVID19 Treatment
This study sheds light on an exciting new avenue for treating COVID-19. VIP’s ability to both reduce the production of ACE2 and TMPRSS2 and to enhance their shedding from cell surfaces suggests that it may be a useful therapeutic agent. The researchers believe this could be especially beneficial for high-risk patients, such as those with chronic lung conditions, who have been found to have elevated levels of ACE2 in their airways.
Beyond COVID-19, these findings may have implications for other respiratory viruses that rely on similar mechanisms to enter cells. By reducing the presence of key receptors, VIP could serve as a broader antiviral strategy.
Conclusion
The study presents compelling evidence that VIP can reduce the ability of SARS-CoV-2 to infect human cells by targeting ACE2 and TMPRSS2. Through genetic suppression and enhanced shedding via the enzyme ADAM10, VIP effectively weakens the virus’s entry pathways. These findings suggest that further research into VIP-based therapies could lead to new treatments not only for COVID-19 but also for other viral infections that use similar mechanisms to infect human cells.
The study findings were published in the peer-reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/26/6/2666
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