Tzu Chi Medical Journal,
Год журнала:
2024,
Номер
36(2), С. 152 - 165
Опубликована: Март 25, 2024
Objectives:
The
protective
effects
and
related
mechanisms
of
Jing-Si
herbal
tea
(JSHT)
were
investigated
in
cellular
damage
mediated
by
pro-inflammatory
cytokines,
including
interleukin
(IL)-1β,
IL-6,
tumor
necrosis
factor-α,
on
normal
human
lung
fibroblast
multiomic
platform
analysis.
Materials
Methods:
silico
high-throughput
target
was
analyzed
using
pharmacophore
models
BIOVIA
Discovery
Studio
2022
with
ingenuity
pathway
analysis
software.
To
assess
cell
viability,
the
study
utilized
MTT
assay
technique.
In
addition,
IncuCyte
S3
ZOOM
System
implemented
for
continuous
monitoring
confluence
JSHT-treated
cytokine-injured
HEL
299
cells.
Cytokine
concentrations
determined
a
Quantibody
Human
Inflammation
Array.
Gene
expression
signaling
pathways
next-generation
sequencing.
Results:
JSHT
revealed
canonical
their
networks.
Glucocorticoid
receptor
is
potential
JSHT.
results
against
inflammatory
cytokines
Transcriptome
network
analyses
that
induction
helper
T
lymphocytes,
TNFSF12,
NFKB1-mediated
relaxin
signaling,
G-protein
coupled
play
important
roles
immune
regulatory
Conclusion:
findings
from
our
research
indicate
holds
promise
as
therapeutic
agent,
potentially
offering
advantageous
outcomes
treating
virus
infections
through
various
mechanisms.
Furthermore,
primary
bioactive
components
justify
extended
antiviral
drug
development,
especially
context
addressing
coronavirus.
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(7), С. 3507 - 3507
Опубликована: Март 23, 2022
Coronavirus
disease
2019
(COVID-19),
caused
by
the
severe
acute
respiratory
syndrome
2
(SARS-CoV-2),
has
been
one
of
most
devastating
pandemics
recent
times.
The
lack
potent
novel
antivirals
had
led
to
global
health
crises;
however,
emergence
and
approval
inhibitors
viral
main
protease
(Mpro),
such
as
Pfizer’s
newly
approved
nirmatrelvir,
offers
hope
not
only
in
therapeutic
front
but
also
context
prophylaxis
against
infection.
By
their
nature,
RNA
viruses
including
human
immunodeficiency
virus
(HIV)
have
inherently
high
mutation
rates,
lessons
learnt
from
previous
currently
ongoing
taught
us
that
these
can
easily
escape
selection
pressure
through
vital
target
amino
acid
residues
monotherapeutic
settings.
In
this
paper,
we
review
nirmatrelvir
its
binding
SARS-CoV-2
Mpro
draw
a
comparison
HIV
were
rendered
obsolete
resistance
mutations,
emphasizing
potential
pitfalls
design
may
be
important
relevance
long-term
use
SARS-CoV-2.
Cellular and Molecular Immunology,
Год журнала:
2022,
Номер
19(8), С. 872 - 882
Опубликована: Июнь 23, 2022
Most
deaths
from
the
COVID-19
pandemic
are
due
to
acute
respiratory
distress
syndrome
(ARDS)-related
failure.
Cytokine
storms
and
oxidative
stress
major
players
in
ARDS
development
during
virus
infections.
However,
it
is
still
unknown
how
regulated
by
viral
host
factors
response
SARS-CoV-2
infection.
Here,
we
found
that
activation
of
NRF2/HMOX1
significantly
suppressed
replication
multiple
cell
types
producing
metabolite
biliverdin,
whereas
impaired
axis
through
action
nonstructural
protein
NSP14.
Mechanistically,
NSP14
interacts
with
catalytic
domain
NAD-dependent
deacetylase
Sirtuin
1
(SIRT1)
inhibits
its
ability
activate
pathway.
Furthermore,
both
genetic
pharmaceutical
evidence
corroborated
novel
antiviral
activity
SIRT1
against
SARS-CoV-2.
Therefore,
our
findings
reveal
a
mechanism
which
dysregulates
antioxidant
defense
system
emphasize
vital
role
played
SIRT1/NRF2
Immunological Reviews,
Год журнала:
2022,
Номер
309(1), С. 12 - 24
Опубликована: Июль 1, 2022
Abstract
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS‐CoV‐2),
the
causative
agent
of
disease
2019
(COVID‐19),
has
caused
millions
deaths
in
past
two
years.
Although
initially
little
was
understood
about
this
virus,
recent
research
significantly
advanced
and
landed
interferons
(IFNs)
spotlight.
While
Type
I
III
IFN
have
long
been
known
as
central
to
antiviral
immunity,
case
COVID‐19
their
role
controversial.
However,
protective
function
is
now
well
supported
by
identification
human
deficiencies
responses
a
predictor
severity.
Here,
we
will
review
cell
types
pathways
that
lead
production
importance
timing
location
for
outcome.
We
further
discuss
mechanisms
SARS‐CoV‐2
uses
evade
responses,
current
efforts
implement
IFNs
therapeutics
treatment
COVID‐19.
It
essential
understand
relationships
between
better
inform
treatments
exploit
functions
alleviate
International Journal of Biological Sciences,
Год журнала:
2022,
Номер
18(15), С. 5827 - 5848
Опубликована: Янв. 1, 2022
The
rapid
dissemination
of
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2),
the
causative
agent
disease
2019
,
remains
a
global
public
health
emergency.The
host
immune
response
to
SARS-CoV-2
plays
key
role
in
COVID-19
pathogenesis.SARS-CoV-2
can
induce
aberrant
and
excessive
responses,
leading
cytokine
storm
syndrome,
autoimmunity,
lymphopenia,
neutrophilia
dysfunction
monocytes
macrophages.Pyroptosis,
proinflammatory
form
programmed
cell
death,
acts
as
defense
mechanism
against
infections.Pyroptosis
deprives
replicative
niche
by
inducing
lysis
infected
cells
exposing
virus
extracellular
attack.Notably,
has
evolved
sophisticated
mechanisms
hijack
this
death
mode
for
its
own
survival,
propagation
shedding.SARS-CoV-2-encoded
viral
products
act
modulate
various
components
pyroptosis
pathways,
including
inflammasomes,
caspases
gasdermins.SARS-CoV-2-induced
contriubtes
development
COVID-19-associated
immunopathologies
through
leakage
intracellular
contents,
disruption
system
homeostasis
or
exacerbation
inflammation.Therefore,
emerged
an
important
involved
immunopathogenesis.However,
entangled
links
between
pathogenesis
lack
systematic
clarification.In
review,
we
briefly
summarize
characteristics
COVID-19-related
immunopathologies.Moreover,
present
overview
interplay
infection
highlight
recent
research
advances
understanding
responsible
implication
pathways
pathogenesis,
which
will
provide
informative
inspirations
new
directions
further
investigation
clinical
practice.Finally,
discuss
potential
value
therapeutic
target
COVID-19.An
in-depth
discussion
underlying
be
conducive
identification
targets
exploration
effective
treatment
measures
aimed
at
conquering
SARS-CoV-2-induced
COVID-19.
Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 15, 2024
Mammalians
sense
antigenic
messages
from
infectious
agents
that
penetrate
the
respiratory
and
digestive
epithelium,
as
well
signals
damaged
host
cells
through
membrane
cytosolic
receptors.
The
transduction
of
these
triggers
a
personalized
response,
depending
on
nature
stimulus
host’s
genetics,
physiological
condition,
comorbidities.
Interferons
(IFNs)
are
primary
effectors
innate
immune
their
synthesis
is
activated
in
most
within
few
hours
after
pathogen
invasion.
IFNs
primarily
synthesized
infected
cells,
but
anti-infective
effect
extended
to
neighboring
by
autocrine
paracrine
action.
emergence
severe
acute
syndrome
coronavirus
2
(SARS‐CoV‐2)
pandemic
2019
was
stark
reminder
potential
threat
posed
newly
emerging
viruses.
This
has
also
triggered
an
overwhelming
influx
research
studies
aiming
unveil
mechanisms
protective
versus
pathogenic
responses
induced
SARS‐CoV‐2.
purpose
this
review
describe
role
vital
players
battle
against
SARS‐CoV-2
infection.
We
will
briefly
characterize
classify
IFNs,
present
inductors
IFN
synthesis,
sensors,
signaling
pathways,
then
discuss
controlling
evolution
SARS-CoV-2
infection
its
clinical
outcome.
Finally,
we
perspectives
controversies
regarding
prophylactic
therapeutic
The Journal of Immunology,
Год журнала:
2024,
Номер
212(10), С. 1540 - 1552
Опубликована: Март 22, 2024
Abstract
Severe
SARS-CoV-2
infection
is
associated
with
significant
immune
dysregulation
involving
different
cell
subsets.
In
this
study,
when
analyzing
critically
ill
COVID-19
patients
versus
those
mild
disease,
we
observed
a
reduction
in
total
and
memory
B
subsets
but
an
increase
naive
cells.
Moreover,
cells
from
displayed
impaired
effector
functions,
evidenced
by
diminished
proliferative
capacity,
reduced
cytokine,
Ab
production.
This
functional
impairment
was
accompanied
increased
apoptotic
potential
upon
stimulation
severely
patients.
Our
further
studies
revealed
the
expansion
of
expressing
coinhibitory
molecules
(PD-1,
PD-L1,
TIM-1,
VISTA,
CTLA-4,
Gal-9)
intensive
care
unit
(ICU)–admitted
not
disease.
The
receptor
expression
linked
to
altered
IgA
IgG
capacity
Also,
found
frequency
CD24hiCD38hi
regulatory
IL-10
mechanistic
that
upregulation
PD-L1
elevated
plasma
IL-6
levels
implies
connection
between
cytokine
storm
phenotype
function.
Finally,
our
metabolomic
analysis
showed
tryptophan
elevation
kynurenine
ICU-admitted
We
promotes
cells,
correlating
IL-6R
STAT1/STAT3
activation.
observations
provide
novel
insights
into
complex
interplay
dysregulation,
implicating
receptors,
IL-6,
potentially
contributing
pathogenesis
COVID-19.
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Июнь 7, 2024
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
is
responsible
for
the
distress
condition
known
as
COVID-19.
This
disease
broadly
affects
several
physiological
systems,
including
gastrointestinal,
renal,
and
central
nervous
(CNS)
significantly
influencing
patient’s
overall
quality
of
life.
Additionally,
numerous
risk
factors
have
been
suggested,
gender,
body
weight,
age,
metabolic
status,
renal
health,
preexisting
cardiomyopathies,
inflammatory
conditions.
Despite
advances
in
understanding
genome
pathophysiological
ramifications
COVID-19,
its
precise
origins
remain
elusive.
SARS-CoV-2
interacts
with
a
receptor-binding
domain
within
angiotensin-converting
enzyme
(ACE2).
receptor
expressed
various
organs
different
species,
humans,
abundance.
Although
COVID-19
has
multiorgan
manifestations,
main
pathologies
occur
lung,
pulmonary
fibrosis,
failure,
embolism,
secondary
bacterial
pneumonia.
In
post-COVID-19
period,
sequelae
may
occur,
which
causes,
direct
action
virus,
alteration
immune
response,
alterations
during
infection,
among
others.
Recognizing
serious
adverse
health
effects
associated
it
becomes
imperative
to
comprehensively
elucidate
discuss
existing
evidence
surrounding
this
viral
those
related
subsequent
consequences.
review
aims
contribute
comprehensive
impact
long-term
on
human
health.
AIMS Microbiology,
Год журнала:
2023,
Номер
9(2), С. 245 - 276
Опубликована: Янв. 1, 2023
<abstract>
<p>The
recent
pandemic
caused
by
the
SARS-CoV-2
virus
continues
to
be
an
enormous
global
challenge
faced
healthcare
sector.
Availability
of
new
vaccines
and
drugs
targeting
sequelae
COVID-19
has
given
world
hope
in
ending
pandemic.
However,
emergence
mutations
viral
genome
every
couple
months
different
parts
is
a
persistent
danger
public
health.
Currently
there
no
single
treatment
eradicate
risk
COVID-19.
The
widespread
transmission
due
Omicron
variant
necessitates
continued
work
on
development
implementation
effective
vaccines.
Moreover,
evidence
that
receptor
domain
spike
glycoprotein
led
decrease
current
vaccine
efficacy
escaping
antibody
recognition.
Therefore,
it
essential
actively
identify
mechanisms
which
evades
host
immune
system,
study
long-lasting
effects
develop
therapeutics
infections
humans
preclinical
models.
In
this
review,
we
describe
pathogenic
infection
as
well
innate
adaptive
responses
infection.
We
address
ongoing
need
provide
protection
against
variants
SARS-CoV-2,
validated
endpoint
assays
evaluate
immunogenicity
pipeline,
medications,
anti-viral
drug
therapies
health
measures,
will
required
successfully
end
pandemic.</p>
</abstract>
PLoS Pathogens,
Год журнала:
2023,
Номер
19(10), С. e1011702 - e1011702
Опубликована: Окт. 6, 2023
Coronaviruses
(CoVs)
are
a
family
of
the
largest
RNA
viruses
that
typically
cause
respiratory,
enteric,
and
hepatic
diseases
in
animals
humans,
imposing
great
threats
to
public
safety
animal
health.
Porcine
deltacoronavirus
(PDCoV),
newly
emerging
enteropathogenic
coronavirus,
causes
severe
diarrhea
suckling
piglets
all
over
world
poses
potential
risks
cross-species
transmission.
Here,
we
use
PDCoV
as
model
CoVs
illustrate
reciprocal
regulation
between
infection
host
antiviral
responses.
In
this
study,
downregulation
DNA
polymerase
delta
interacting
protein
3
(POLDIP3)
was
confirmed
infected
IPEC-J2
cells
by
isobaric
tags
for
relative
absolute
quantification
(iTRAQ)
Western
blotting
analysis.
Overexpression
POLDIP3
inhibits
infection,
whereas
knockout
(POLDIP3-/-)
CRISPR-Cas9
editing
significantly
promotes
indicating
novel
regulator
against
infection.
Surprisingly,
an
antagonistic
strategy
revealed
encoded
nonstructural
5
(nsp5)
responsible
reduction
via
its
3C-like
protease
cleavage
at
glutamine
acid
176
(Q176),
facilitating
due
loss
effects
cleaved
fragments.
Consistent
with
obtained
data
cell
vitro,
also
corroborated
infected-SPF
vivo.
Collectively,
unveiled
new
evolved
counteract
innate
immunity
nsp5-mediated
cleavage,
eventually
ensuring
productive
virus
replication.
Importantly,
further
demonstrated
nsp5s
from
PEDV
TGEV
harbor
conserved
function
cleave
porcine
Q176
despair
POLDIP3-mediated
effects.
addition,
nsp5
SARS-CoV-2
cleaves
human
POLDIP3.
Therefore,
speculate
coronaviruses
employ
similar
mechanisms
mediated
antagonize
responses
sustain
efficient