Penn study reveals new therapeutic target for
slowing the spread of flu virus
by http://outbreaknewstoday.com/author/press-release/" rel="nofollow - Press
Release
June 23, 2018
Influenza A (flu A) hijacks host proteins for
viral RNA splicing and blocking these interactions caused replication
of the virus to slow, according to new research https://www.nature.com/articles/s41467-018-04779-4" rel="nofollow - published
in Nature Communications by Kristin
W. Lynch, PhD, chair of the department of Biochemistry and Biophysics
in the Perelman School of Medicine at the University of Pennsylvania,
and doctoral student Matthew Thompson. Their results also suggest
that infection with flu A may reduce splicing of some host genes,
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,” said Lynch,
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.
A balance between the two viral messenger RNAs
must be maintained for the virus to successfully infect host cells
and replicate. “Regulating splicing of the two viral proteins is a
fundamental step in viral-host interaction and so a potentially new
anti-viral remedy,” Lynch said.
For now, her team is refining their understanding
of the intricacies of viral reproduction in host cells. Their hope is
to one day identify a specific molecular target for antiviral
medications that can be used in the clinic.
Source
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