January 2024 - A research team at Washington State University (WSU) received a four-year, $1.2 million grant from the National Institutes of Health to study how herpes simplex virus type 1 (HSV-1) fuses with and enters host cells. The goal is to understand this entry mechanism in enough detail to eventually block it, which would prevent the virus from establishing infection in the first place.
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SHOP NOW & SAVE 15%The project is led by professors Jin Liu and Prashanta Dutta at the Voiland College of Engineering and Architecture, alongside professor Anthony Nicola at the College of Veterinary Medicine.
Their focus is the moment a virus merges with a cell membrane to initiate infection, a process called viral fusion. "Virus fusion is a highly complex, multistage and multiscale process.
The associated protein interactions and structural changes are extremely complicated and high-dimensional", said Liu. "A combination of knowledge from different disciplines, and expertise from both state-of-the-art numerical modeling and biological experiments, is the key to tackle down the problem."
Physics-Based Machine Learning to Model Viral Entry
Rather than relying purely on data-driven machine learning, the WSU team is developing a physics-based approach.
Their algorithm incorporates fundamental principles from physics and chemistry to model cell-virus interactions at multiple scales, allowing the simulation to capture biological behavior that purely statistical models would miss.
PhD students Ryan Odstrcil and Amir Birjandi in the School of Mechanical and Materials Engineering are leading the computational modeling work.
PhD student Albina Makio, from WSU’s Immunology and Infectious Disease program, is conducting the experimental research by directly observing cell-virus interactions in the lab to validate the models.
The computational models produced by this research are expected to generate testable predictions that can guide future experiments. A detailed mechanistic understanding of viral fusion could inform the design of new antiviral drugs and vaccines that work by blocking entry rather than replication.
Broader Implications for Antiviral Research
Although the research uses HSV-1 as its model system, the findings are expected to apply more broadly. As Liu noted, "the knowledge and strategies will be applicable to many other viruses that infect cells a similar way, such as HIV and SARS-CoV-2." Better models of viral entry could accelerate antiviral development across multiple diseases, not just herpes.
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