Sick Woman. Flu. Woman Caught Cold. Sneezing into Tissue

(© Subbotina Anna -

RIVERSIDE, Calif. — A case of the flu is a seasonal annoyance for countless people, but researchers from UC Riverside may soon change all that. Are we finally on the cusp of ridding the world of influenza? It may sound too good to be true, but study authors report the discovery of a new way to block one specific strain of the influenza virus from accessing the human protein it needs to replicate in our cells.

While these findings are just the beginning, researchers are hopeful their discovery will one day lead to very effective flu treatments. Moreover, this work may prove relevant in the fight against COVID-19 as well.

While the flu is more of an inconvenience than life-threatening illness for many, it still kills thousands of people annually – especially very young or very old patients. The CDC estimates the flu is responsible for somewhere between 12,000 to 50,000 American deaths annually.

Current flu vaccines — which work by “teaching” the body’s immune system how to recognize and attack influenza — are not universally effective. Currently, medical science doesn’t fully grasp why this is the case. Many scientists theorize flu vaccine inefficiency is probably the result of complexities in the immune system and viral mutations.

The new method doesn’t rely on the immune system to stop the flu

The only way the flu virus can make people sick is by infecting and entering our cells. From there, it goes on to replicate and infect more cells. Importantly, Jiayu Liao, an associate professor of bioengineering at UC Riverside, previously discovered that the two most common varieties of the flu (Influenza A, Influenza B) need a unique human protein in order to successfully proliferate in human cells.

This latest study builds on that discovery. Study authors found that by blocking this necessary protein, they can stop the Influenza B virus from replicating. Without the protein, the flu virus is totally unable to amplify itself within cells.

Now, the Influenza B virus specifically uses a human cellular process called SUMOylation to change a gene called M1. The M1 gene serves multiple roles in the influenza viral life cycle. SUMOylation usually happens when small ubiquitin-like modifier (SUMO) proteins both attach to and detach from other proteins. These actions change their biochemical activities and functions.

Liao’s latest experiments show that a SUMOylation inhibitor called STE025 can completely block the Influenza B virus from replicating. When researchers treated the influenza B virus with the SUMOyaltion inhibitor, it resulted in a lack of SUMOylation on the M1 protein. In other words, the virus couldn’t replicate in human cells.

What about the other common variety of the flu?

Influenza A also has SUMOylated proteins, which means it may be just as susceptible to the SUMOyaltion inhibitor.

In conclusion, study authors add that more research is necessary to better understand Influenza B’s dependence on SUMOylation. Still, the discovery that STE025 stops SUMOylation and prevents flu virus replication is a major towards wiping out the flu.

The study is published in the journal Viruses.

About John Anderer

Born blue in the face, John has been writing professionally for over a decade and covering the latest scientific research for StudyFinds since 2019. His work has been featured by Business Insider, Eat This Not That!, MSN, Ladders, and Yahoo!

Studies and abstracts can be confusing and awkwardly worded. He prides himself on making such content easy to read, understand, and apply to one’s everyday life.

Our Editorial Process

StudyFinds publishes digestible, agenda-free, transparent research summaries that are intended to inform the reader as well as stir civil, educated debate. We do not agree nor disagree with any of the studies we post, rather, we encourage our readers to debate the veracity of the findings themselves. All articles published on StudyFinds are vetted by our editors prior to publication and include links back to the source or corresponding journal article, if possible.

Our Editorial Team

Steve Fink


Chris Melore


Sophia Naughton

Associate Editor