Influenza A (flu A) hijacks host proteins for viral RNA splicing and blocking these interactions caused replication of the virus to slow, which could point to novel strategies for antiviral therapies.
Influenza A virus is a common human pathogen that causes 250,000 to 500,000 deaths per year worldwide.
“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,”
whose lab focuses on the specific mechanisms and patterns of alternative RNA splicing and how it relates to human disease,
The transcription of DNA into messenger RNA the process of a single gene encoding a single protein isn’t as straightforward as once thought.
The phenomenon of alternative RNA splicing where a single gene can encode multiple proteins was discovered over 30 years ago in viruses.
The flu A genome is comprised of eight single-strand segments of RNA. Three of these segments use alternative splicing to produce two essential viral proteins each, which are important in helping the virus gain entry into host cells.
Working with cultures of human lung cells, the team’s proposed mechanism of how flu A virus interacts with human RNA splicing machinery suggests that keeping human splicing proteins from binding to the viral genome would help to stop its replication.
As a result, the researchers found that mutating sequences of the viral genome to prevent host proteins from binding caused viral RNA to splice incorrectly and eventually halt replication thus slowing the spread of the virus in the body.
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