Nikhil Prasad Fact checked by:Thailand Medical News Team Oct 18, 2025 1 day, 7 hours, 35 minutes ago
Medical News: A Promising Approach Against Oral Herpes
A new study by researchers from Hiroshima University, Hiroshima University Hospital, Tokyo University of Pharmacy and Life Science, and The University of Tokyo has revealed that a new class of antiviral drugs known as Pin1 inhibitors could stop the herpes simplex virus type 1 (HSV-1) from replicating. HSV-1 is the virus responsible for cold sores or fever blisters, which affect over half the world’s population. Once a person is infected, the virus remains dormant in their body but can reactivate at any time, especially during stress, illness, or weakened immunity.
New Antivirals May Stop Cold Sores by Reinforcing Cell Walls
This
Medical News report highlights how these Pin1 inhibitors offer a new way to fight HSV-1 infections that go beyond traditional antivirals. Most existing drugs only target viral enzymes or replication mechanisms, which can lead to drug resistance over time. By contrast, the Pin1 inhibitors focus on a key host enzyme involved in the virus’s ability to replicate and spread, making them a potentially safer and longer-lasting solution.
The Role of the Pin1 Enzyme
The study focused on a specific enzyme called peptidyl-prolyl cis-trans isomerase NIMA-interacting 1, or Pin1. This enzyme plays a crucial role in controlling how proteins fold and function within cells. When viruses infect human cells, they often hijack Pin1 to manipulate cell structure and function to their advantage. Previous research has already linked Pin1 to viral infections such as cytomegalovirus and SARS-CoV-2, as well as to diseases like cancer and heart failure.
Researchers discovered that HSV-1-infected cells tend to overexpress Pin1, making it an ideal therapeutic target. By introducing Pin1 inhibitors—particularly one compound known as H-77—scientists were able to block the virus’s ability to reproduce and spread. Even at very low concentrations, the inhibitors effectively suppressed viral replication in infected cells.
How Pin1 Inhibitors Trap the Virus
One of the most remarkable findings of this study is how these inhibitors physically prevent the virus from escaping the cell nucleus. Normally, HSV-1 creates viral particles inside the cell nucleus and then breaks through a protective layer called the nuclear lamina to exit and infect new cells. When Pin1 is overexpressed, this protective layer becomes weak and allows the virus to escape.
However, when cells were treated with the Pin1 inhibitor H-77, the nuclear lamina became thicker and more stable, creating what researchers described as an “impregnable defensive wall.” This structural reinforcement traps the virus inside the cell, preventing it from spreading to others. Laboratory imaging confirmed that cells treated with H-77 had no infectious viral particles escaping their nuclei.
Future of Pin1-Based Antivirals
The researchers believe that this discovery could lead to a new genera
tion of antiviral drugs that work by targeting host factors instead of the virus itself. Such “host-directed therapeutics” could significantly reduce the chances of drug resistance and have broader applications for other viral infections. The next steps involve optimizing these compounds for safety and effectiveness in humans and testing them against other viruses in the herpes family.
Conclusion
The study offers a major step forward in developing more resilient antiviral therapies that stop viral spread by strengthening the body’s own cellular defenses. By focusing on the host enzyme Pin1, scientists may have found a way to halt cold sore outbreaks before they begin—without the risk of resistance that plagues current treatments. If further trials succeed, this could revolutionize how chronic viral infections like HSV-1 are managed and treated worldwide.
The study findings were published in the peer reviewed journal: Antiviral Research.
https://www.sciencedirect.com/science/article/pii/S0166354225001706
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