Long non-coding RNA BCAR4 is required for efficient influenza A virus replication
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 6, 2025
Abstract
Long
non-coding
RNAs
(lncRNAs)
regulate
diverse
biological
processes,
including
influenza
A
virus
(IAV)
infection.
However,
the
understanding
of
lncRNAs
in
IAV
infection
is
limited.
By
using
both
bioinformatic
analyses
and
virological
assays,
we
showed
that
lncRNA
BCAR4
expression
can
be
highly
induced
by
multiple
different
subtypes.
was
required
for
propagation
Genetic
inactivation
inhibited
growth.
Investigation
cycle
revealed
a
suppressed
viral
RNA
transcription
replication,
attenuated
protein
synthesis
-deficient
cells.
potentially
interacted
with
cellular
splicing-associated
proteins
activation
associated
NS
segment.
These
findings
suggest
important
role
regulation
Importance
serve
as
critical
regulators
processes
how
engage
remains
unclear.
Here
show
universally
Deletion
reduced
multiplication.
In
cycle,
deficiency
decreased
transcription,
replication
biosynthesis.
binding
to
host
splicing
protein,
segment
.
Our
results
highlight
Язык: Английский
Human long noncoding RNA VILMIR is induced by major respiratory viral infections and modulates the host interferon response
Journal of Virology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 25, 2025
ABSTRACT
Long
noncoding
RNAs
(lncRNAs)
are
a
newer
class
of
transcripts
identified
as
key
regulators
biological
processes.
Here,
we
aimed
to
identify
novel
lncRNA
targets
that
play
critical
roles
in
major
human
respiratory
viral
infections
by
systematically
mining
large-scale
transcriptomic
data
sets.
Using
bulk
RNA-sequencing
(RNA-seq)
analysis,
previously
uncharacterized
lncRNA,
named
virus-inducible
modulator
interferon
response
(
VILMIR
),
was
consistently
upregulated
after
vitro
influenza
infection
across
multiple
epithelial
cell
lines
and
A
virus
subtypes.
also
severe
acute
syndrome
coronavirus
2
(SARS-CoV-2)
syncytial
(RSV)
.
We
experimentally
confirmed
the
interferon-beta
(IFN-β)
treatment
A549
line
found
expression
robustly
induced
IFN-β
dose-
time-specific
manner.
Single-cell
RNA-seq
analysis
bronchoalveolar
lavage
fluid
samples
from
disease
2019
(COVID-19)
patients
uncovered
various
types,
including
at
least
five
immune
cells.
The
upregulation
cells
further
T
monocyte
lines,
SUP-T1
THP-1,
treatment.
Finally,
knockdown
reduced
magnitude
host
transcriptional
responses
both
Together,
our
results
show
is
interferon-stimulated
gene
(ISG)
regulates
may
be
potential
therapeutic
target
for
upon
mechanistic
investigation.
IMPORTANCE
Identifying
factors
regulate
developing
new
therapeutics.
Human
long
have
been
regulatory
during
processes;
however,
majority
functions
within
antiviral
remain
unknown.
In
this
study,
influenza,
2,
virus.
demonstrated
an
several
types.
Our
reveal
present
infections.
Язык: Английский
Positive Regulation of Cellular Proteins by Influenza Virus for Productive Infection
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(8), С. 3584 - 3584
Опубликована: Апрель 10, 2025
Influenza
viruses
cause
annual
epidemics
and
occasional
pandemics
through
respiratory
tract
infections,
giving
rise
to
substantial
morbidity
mortality
worldwide.
extensively
interact
with
host
cellular
proteins
exploit
a
variety
of
pathways
accomplish
their
infection
cycle.
Some
the
that
display
negative
effects
on
virus
are
degraded
by
virus.
However,
there
also
various
upregulated
influenza
at
expression
and/or
activation
levels.
It
has
been
well-established
large
number
antiviral
such
as
type
I
interferon-stimulated
genes
elevated
viral
infection.
On
other
hand,
many
induced
directly
virus,
which
considered
pro-viral
factors
often
indispensable
for
rigorous
propagation
or
pathogenicity.
Here,
we
review
recent
advances
in
our
understanding
deemed
be
utilized
The
focus
is
placed
functions
these
mechanisms
associated
promoting
amplification,
evading
immunity,
enhancing
Investigating
process
how
hijack
could
provide
framework
inventing
host-factor-targeted
drugs
conquer
influenza.
Язык: Английский