Researchers from University of Pennsylvania’s School of Medicine reveal that altering the molecular interactions between the flu virus and host genes stunts virus replication.
Influenza A virus is a single stranded, segmented RNA virus that causes 250,000 to 500,000 deaths per year worldwide according to a report by World Health Organization (WHO). There are vaccines and antiviral drugs against several flu viruses however, it is crucial to understand influenza virus-host relations at a molecular level in order to identify host susceptibility targeted by flu viruses, which could benefit in creating new therapeutic options.
The team of researchers led by Kristin W. Lynch, PhD, chair of the department of Biochemistry and Biophysics from University of Pennsylvania’s School of Medicine suggest that restricting RNA slicing mechanism between flu A virus and human RNA proteins can halt the replication of viruses. DNA and RNA are nucleic acids with base pairs of nucleotides as a complementary language. The process of a single gene encoding a single protein as DNA transcribes into messenger RNA was widely thought as straightforward. However, alternative RNA splicing consisting of a single gene encoding multiple proteins was also evident in viruses. The eight single-stranded RNA segments of flu genome are responsible for alternative slicing, where three of the segments produce two essential viral proteins each to gain access of the host cells. The mutating sequences of viral genome to prevent host proteins from binding resulted in incorrect slicing of RNA, eventually slowing the spread of virus by halting replication. Slicing of RNA creates an imbalance between the two viral messenger RNAs and stops it from infecting the host cells. It is a fundamental step in viral-host interaction and can lead to efficient anti-viral remedies. He study was published in the journal Nature Communications on June 22, 2018.