According to new research published in the Nature Communications journal, the blocking of interactions between influenza A (flu A) that takes control of host proteins for viral RNA can slow down the progression of the virus.
This research was conducted by Dr. Kristin W. Lynch, chair of the department of Biochemistry and Biophysics in the Perelman School of Medicine at the University of Pennsylvania, and doctoral student Matthew Thompson.
They discovered that the infection with flu A can diminish the splicing of some host genes, which could lead to brand new strategies for advanced antiviral therapies.
‘’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,” said Dr. Lynch, whose research focused on the specific mechanisms and patterns of alternative RNA splicing and how it relates to human disease.
The process of a single gene encoding a single protein is not forthright as once thought which is the transcription of DNA into messenger RNA.
30 years ago, alternative RNA splicing was discovered in viruses where a single gene has the ability to encode multiple proteins instead of just one.
The researchers observed that mutating sequences of the viral genome to prevent host proteins from binding caused viral RNA to splice incorrectly. It interrupted replication which led to a slow outspread of the virus in the body.
“Regulating splicing of the two viral proteins is a fundamental step in viral-host interaction and so a potentially new antiviral remedy,” Dr. Lynch stated.
There has to be a balance between the two viral messenger RNAs so the virus can triumphantly infect host cells and replicate.
Dr. Lynch and her team work to expand their knowledge of the complexities of viral reproduction in host cells.