Coronavirus
nonstructural
protein
2
(Nsp2)
is
regarded
as
a
virulence
determinant
and
plays
critical
role
in
virus
replication,
innate
immunity.
Screening
identifying
host
cell
proteins
that
interact
with
viral
an
effective
way
to
reveal
the
functions
of
proteins.
In
this
study,
interacted
transmissible
gastroenteritis
(TGEV)
Nsp2
were
identified
using
immunoprecipitation
combined
LC-MS/MS.
77
putative
interaction
protein-protein
(PPI)
was
constructed.
The
found
be
associated
various
subcellular
locations
functional
categories
through
Gene
Ontology
(GO)
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
enrichment
analysis.
It
hypothesized
interacting
TGEV
are
mainly
involved
formation
cytoplasmic
translation
initiation
complex,
mRNA
binding,
ribosomes,
proteasomes.
Among
these,
ATP5B,
core
subunit
mitochondrial
ATP
synthase
further
studied.
Coimmunoprecipitation
(Co-IP)
indirect
immunofluorescence
(IFA)
results
confirmed
ATP5B.
Furthermore,
downregulation
ATP5B
expression
promote
suggesting
might
function
negative
regulator
replication.
Collectively,
our
offer
additional
insights
into
provide
novel
antiviral
target
against
TGEV.
Genes,
Год журнала:
2024,
Номер
15(2), С. 165 - 165
Опубликована: Янв. 26, 2024
Porcine
epidemic
diarrhea
(PED)
virus
(PEDV)
is
one
of
the
main
pathogens
causing
in
piglets
and
fattening
pigs.
The
clinical
signs
PED
are
vomiting,
acute
diarrhea,
dehydration,
mortality
resulting
significant
economic
losses
becoming
a
major
challenge
pig
industry.
PEDV
possesses
various
crucial
structural
functional
proteins,
which
play
important
roles
viral
structure,
infection,
replication,
assembly,
release,
as
well
escaping
host
innate
immunity.
Over
past
few
years,
there
has
been
progress
study
pathogenesis,
revealing
role
interaction
between
proteins
cytokines
infection.
At
present,
control
measure
against
vaccine
immunization
sows,
but
protective
effect
for
emerging
strains
still
insufficient,
no
ideal
safe
efficient
vaccine.
Although
scientists
have
persistently
delved
their
research
into
intricate
structure
functionalities
genome
pathogenic
mechanism
remains
incompletely
elucidated.
Here,
we
focus
on
reviewing
nonstructural
to
facilitate
understanding
biological
processes
such
infection
pathogenesis.
Viruses,
Год журнала:
2024,
Номер
16(3), С. 474 - 474
Опубликована: Март 20, 2024
A
defining
feature
of
a
productive
viral
infection
is
the
co-opting
host
cell
resources
for
replication.
Despite
repertoire
molecular
functions
and
biological
counter
measures,
viruses
still
subvert
defenses
to
take
control
cellular
factors
such
as
RNA
binding
proteins
(RBPs).
RBPs
are
involved
in
virtually
all
steps
mRNA
life,
forming
ribonucleoprotein
complexes
(mRNPs)
highly
ordered
regulated
process
fate
stability
cell.
As
such,
hallmark
takeover
reshaping
modulate
gene
expression
evade
immune
responses
by
altering
RBP
interactions.
Here,
we
provide
an
extensive
review
work
this
area,
particularly
on
duality
formation
RNP
that
can
be
either
pro-
or
antiviral.
Overall,
review,
highlight
various
ways
co-opt
regulate
outcome
gathering
novel
insights
gained
from
research
studies
field.
Journal of Virology,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 10, 2025
Porcine
epidemic
diarrhea,
as
a
porcine
diarrhea
virus
(PEDV)-induced
infectious
intestinal
condition
typified
by
emesis,
dehydration,
and
anorexia,
leads
to
death
rates
high
100%
among
suckling
piglets.
Given
the
existing
commercial
vaccines,
it
is
essential
study
host-virus
interactions
formulate
efficient
anti-viral
regimes.
This
concerned
host
factor
POLM
(a
DNA
polymerase
family
member)
that
exerts
an
effect
against
PEDV
proliferation.
Our
results
indicated
expression
was
increased
following
infection
regulated
transcription
FOXA1.
In
addition,
our
findings
targeted
degraded
structural
proteins
(N,
S2,
M)
autophagy
pathway
inhibit
could
recruit
E3
ubiquitination
ligase
MARCH8
for
N,
M
protein
ubiquitination,
which
subsequently
recognized
p62,
cargo
receptor,
translocation
autophagic
lysosome,
therefore
degrading
preventing
summary,
we
showed
novel
therapeutic
target
combating
PEDV,
i.e.,
using
POLM-MARCH8-p62-autophagosome
degrade
proteins.IMPORTANCEPEDV
coronavirus
causes
mortality
in
piglets,
poses
significant
economic
damage
swine
farming.
During
infection,
cells
may
promote
natural
immune
response
suppress
viral
replication
through
variety
of
potential
factors.
this
study,
found
upregulation
FOXA1
factor)
during
infection.
It
be
new
replication,
interacted
with
(an
ubiquitin
ligase)
p62
receptor)
facilitate
degradation
via
process.
Apart
from
elucidating
previously
unidentified
function
POLM,
also
provides
perspective
studying
factors
act
regulators
anti-PEDV
pathways.
Veterinary Research,
Год журнала:
2025,
Номер
56(1)
Опубликована: Март 24, 2025
Abstract
Porcine
epidemic
diarrhea
is
an
acute
contagious
disease
caused
by
porcine
virus
(PEDV),
which
severely
constrains
the
development
of
global
swine
industry.
Host
restriction
factors
constitute
a
vital
defensive
barrier
against
viral
infections,
typically
interacting
with
viruses
at
specific
stages
their
replication
process
to
disrupt
it.
Considering
that
traditional
PEDV
vaccines
often
struggle
effectively
activate
mucosal
immunity
in
sows
and
thereby
fail
provide
reliable
passive
piglets
via
milk,
this
review
focuses
on
host
play
crucial
roles
restricting
infection
replication.
The
aim
identify
potential
targets
for
anti-PEDV
drugs
offer
insights
exploration
novel
vaccine
adjuvants.
Journal of Virology,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 29, 2025
ABSTRACT
Cells
utilize
proteasomes
and
selective
autophagy
to
degrade
ubiquitin-labeled
viral
proteins
inhibit
proliferation.
Midnolin,
a
midbrain
nucleolar
protein,
is
reported
use
ubiquitin-independent
proteasomal
degradation
various
nuclear
including
transcription
factors
encoded
by
the
immediate-early
genes.
However,
it
remains
unclear
whether
midnolin
can
protein
hinder
replication.
In
this
study,
degraded
porcine
epidemic
diarrhea
virus
(PEDV)
S1/S2/M/E
suppress
PEDV
Midnolin
has
two
essential
structural
domains:
Catch
domain
ubiquitin-like
domain.
We
found
that
of
concerted
target
both
proteasome
autophagy.
Furthermore,
study
indicated
individual
through
pathway,
which
recruited
E3
ubiquitinating
enzyme
MARCH8
ubiquitinate
proteins,
ubiquitinated
were
recognized
Tollip
transported
lysosome
for
degradation.
Collectively,
not
only
pathway
but
also
revealed
new
mechanism
midnolin-mediated
restriction,
where
using
(Catch)-MARCH8-Tollip-autophagosome
pathway.
IMPORTANCE
Proteasomes
are
ways
proliferation
in
cells.
proteins.
unknown.
we
During
degradation,
domains
exerted
vital
role.
The
interact
addition,
Overall,
have
discovered
acts
as
host
factor
antiviral
function.
Journal of Virology,
Год журнала:
2024,
Номер
99(1)
Опубликована: Дек. 13, 2024
Infection
with
porcine
epidemic
diarrhea
virus
(PEDV)
results
in
enormous
economic
damage
to
the
global
swine
industry.
PEDV
starts
its
life
cycle
by
binding
receptors
of
host
cells
and
adsorbing
onto
cellular
surfaces.
However,
it
is
still
unknown
how
adsorbs
surface
mechanism
beneath
interplay
cell
transmembrane
protein
proteins.
FSTL1,
which
a
secreted
glycoprotein,
participates
diverse
pathological
physiological
processes,
including
immune
modulation
proliferation
differentiation.
The
protein,
TLR4,
serves
as
pattern
recognition
receptor
recognizing
broad
spectrum
pathogens,
exerts
crucial
effect
on
system.
In
this
study,
we
identified
that
FSTL1
promoted
infection.
Further
studies
demonstrated
interactive
relationship
between
structural
proteins
(N
S2).
addition,
also
confirmed
TLR4
interacted
N,
S1,
S2
surface.
Moreover,
interaction
induced
viral
adsorption
cells.
This
study
offers
explicit
evidence
act
mediators
for
interacting
N/S
proteins.IMPORTANCEAs
highly
infectious
(PEDV)-induced
intestinal
condition
swine,
(PED)
100%
death
rate
among
suckling
piglets
poses
serious
burden
farming.
Therefore,
essential
investigate
infection,
replication,
proliferation.
Virus
begins
remains
unclear
revealed
N
proteins,
while
(N,
thoroughly
methodically
was
engaged
internalization
attachment
processes
promoting
N\S
A
defining
feature
of
a
productive
infection
is
the
co-opting
host
cell
resources
for
viral
replication.
Despite
their
repertoire
molecular
functions,
viruses
subvert
defenses
to
take
control
cellular
factors
such
as
RNA
binding
proteins
(RBPs).
RBPs
are
involved
in
virtually
all
steps
mRNA
life
forming
ribonucleoprotein
complexes
(mRNPs)
highly
ordered
and
regulated
process
fate
stability
cell.
Thus,
hallmark
this
takeover
reshape
modulate
gene
expression
evade
immune
responses.
Here
we
provide
an
extensive
review
work
area,
particularly
how
host-viral
interplay
influences
RBP
functions
Overall,
review,
highlight
myriad
ways
can
regulate
either
pro-viral
or
antiviral
manner
by
gathering
novel
insights
gained
from
research
studies
field.