UCSD - University of California - San Diego

05/01/2026 | Press release | Distributed by Public on 05/01/2026 10:17

New Grant Targets Viral Toxins that Exacerbate Viral Diseases

Published Date

May 01, 2026

Article Content

Coefficient Giving, the philanthropic funder and advisor formerly known as Open Philanthropy, has awarded a grant for a new study on how viruses may have evolved a little-known process that enables them to disseminate, promoting disease development and spread, or pathogenesis.

The $600,000 grant to University of California San Diego biologist Scott Biering will support research on a newly discovered class of virulence factors, called viral toxins, that are used by viruses to compromise integrity of cellular barriers, promoting viral pathogenesis and expediting virus spread.

Postdoctoral researcher Vasiliya Kril and Assistant Professor Scott Biering.

Biering, who joined the Department of Molecular Biology (School of Biological Sciences) in 2023, is focused on understanding how viruses infect cells and cause disease, with a goal of identifying targets for new therapies. He previously led a comparative investigation on SARS-CoV-2, the virus behind the COVID pandemic, and dengue virus, a mosquito-spread pathogen. From these studies he found that vascular leak, a process in which blood plasma escapes through capillary walls, is a common signature of viral infection. The study showed that vascular leak may provide an evolutionary advantage for viral pathogens.

The Coefficient Giving funding will support new studies of the mechanisms underlying virus-triggered vascular leak as a method viruses employ to spread throughout the body. The project is considered "high-risk, high-reward," given the broad scope of work and unexpected finding that viral leak is a driver of viral dissemination.

Said Biering: "Ultimately, this research will contribute to our understanding of the evolutionary reasons why viruses trigger pathogenesis and facilitate the production of a new arsenal of anti-leak therapeutics which can be used against newly emerging viruses long before vaccines are developed, constituting the first line of defense."

Credit: iStock/Design Cells

The new study will focus on a class of proteins, which Biering has described as viral toxins, that initiate a breakdown of cellular structures and barriers. This work, led by postdoctoral researcher Vasiliya Kril, will seek to discover and characterize novel viral toxins from families of viruses that cause severe disease in broad populations of humans, including viruses transmitted by insect vectors, as well as respiratory and gastrointestinal viral pathogens. While only three such viruses have been documented in published scientific studies, Biering's lab has now identified viral toxins from several additional biomedically relevant virus families for which the mechanisms underlying disease spread is mostly a mystery. The goal is to discover factors that are critical for viral toxins to trigger leak and to repurpose drugs to block this process.

Working under the hypothesis that viruses from highly divergent families developed intriguingly similar strategies, the scientists will use a variety of research techniques to understand the molecular mechanisms of viral toxins at the cellular level. Finding a common root ultimately could lead to broad-ranging antiviral therapeutic targets.

"This project has the ambition to understand how multiple diverse human viruses invade our bodies and induce severe disease. How can a virus go from the skin to the blood and infect different organs, even the brain?" said Kril. "Understanding these common strategies will open new avenues for anti-viral therapeutics, perhaps anti-leak therapeutics, that can reduce infection and severe disease in the context of already known or new, emerging pathogens."

Illustration from "The contribution of viral toxins to infection and pathogenesis," by Biering et al, published in mBio, March 13, 2026. This illustration shows how viral toxins from four viruses including dengue virus (DENV), SARS-CoV-2, Ebola virus (EBOV) and Crimean-Congo Hemorrhagic Fever virus (CCHFV) interact with endothelial cells and trigger endothelial dysfunction resulting in vascular leak.
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