Viruses are rather helpless on their own; they require a host cell to reproduce and thrive. Influenza A, the virus that causes flu infections and leads to 250,000 to 500,00 deaths each year, has only eight single strands segments of RNA, but hijacks host proteins to snip three of these segments in different ways to produce a variety of proteins, a process known as alternative splicing.

In a paper in the journal Nature Communications, Perelman School of Medicine researchers led by Kristen W. Lynch, chair of the Department of Biochemistry and Biophysics, and doctoral student Matthew Thompson, found that blocking the interactions between the flu virus and host splicing machinery slowed down the rate the virus replicated in host cells. Using cultured human lung cells, they also showed that flu infections altered how host proteins were spliced. The findings point to potential new targets for flu treatments.

“Although vaccines and some antiviral drugs are available, it is crucial to understand influenza virus-host interactions at a molecular level in order to identify host vulnerabilities targeted by flu viruses, which could lead to developing new therapeutic options,” Lynch says.