Current Pharmaceutical Design,
Journal Year:
2022,
Volume and Issue:
28(22), P. 1780 - 1797
Published: May 22, 2022
Coronavirus
disease
2019
(COVID-19)
continues
to
spread
globally
despite
the
discovery
of
vaccines.
Many
people
die
due
COVID-19
as
a
result
catastrophic
consequences,
such
acute
respiratory
distress
syndrome,
pulmonary
embolism,
and
disseminated
intravascular
coagulation
caused
by
cytokine
storm.
Immunopathology
immunogenetic
research
may
assist
in
diagnosing,
predicting,
treating
severe
storm
associated
with
COVID-19.
This
paper
reviews
immunopathogenesis
variants
that
play
role
Although
various
immune-related
genetic
have
been
investigated
relation
COVID-19,
NOD-like
receptor
protein
3
(NLRP3)
interleukin
18
(IL-18)
not
assessed
for
their
potential
significance
clinical
outcome.
Here,
we
a)
summarize
current
understanding
etiology
pathophysiology
storm;
b)
construct
analyze
protein-protein
interaction
(PPI)
networks
(using
enrichment
annotation
analysis)
based
on
NLRP3
IL18
all
genes,
which
were
established
Our
PPI
network
analyses
predict
useful
drug
targets
prevent
onset
including
key
antiviral
pathways
Toll-Like-Receptor
cascades,
signaling,
RIG-induction
interferon
(IFN)
α/β,
(IL)-1,
IL-6,
IL-12,
IL-18,
tumor
necrosis
factor
signaling;
SARS-CoV-2
innate
immune
evasion
participation
MYD88
MAVS
The
be
used
more
outcomes,
thereby
opening
door
targeted
preventive
treatments.
Journal of Medical Virology,
Journal Year:
2023,
Volume and Issue:
95(4)
Published: April 1, 2023
Abstract
In
patients
with
severe
COVID‐19,
acute
respiratory
distress
syndrome
(ARDS),
multiple
organ
dysfunction
(MODS),
and
even
mortality
can
result
from
cytokine
storm,
which
is
a
hyperinflammatory
medical
condition
caused
by
the
excessive
uncontrolled
release
of
pro‐inflammatory
cytokines.
High
levels
numerous
crucial
cytokines,
such
as
interleukin‐1
(IL‐1),
IL‐2,
IL‐6,
tumor
necrosis
factor‐α,
interferon
(IFN)‐γ,
IFN‐induced
protein
10
kDa,
granulocyte‐macrophage
colony‐stimulating
factor,
monocyte
chemoattractant
protein‐1,
IL‐10
so
on,
have
been
found
in
COVID‐19.
They
participate
cascade
amplification
pathways
responses
through
complex
inflammatory
networks.
Here,
we
review
involvements
these
critical
cytokines
SARS‐CoV‐2
infection
discuss
their
potential
roles
triggering
or
regulating
help
to
understand
pathogenesis
So
far,
there
rarely
effective
therapeutic
strategy
for
storm
besides
using
glucocorticoids,
proved
fatal
side
effects.
Clarifying
key
involved
network
will
develop
an
ideal
intervention,
neutralizing
antibody
certain
inhibitor
some
signal
pathways.
Life Sciences,
Journal Year:
2023,
Volume and Issue:
319, P. 121531 - 121531
Published: Feb. 27, 2023
SARS-CoV-2
virus
has
attracted
a
lot
of
attention
globally
due
to
the
autoimmune
and
inflammatory
processes
that
were
observed
during
development
Covid-19
disease.
Excessive
activation
immune
response
triggering
autoantibodies
synthesis
as
well
an
excessive
cytokines
onset
cytokine
storm
vital
role
in
disease
outcome
occurring
complications.
This
scenario
is
reminiscent
infiltration
lymphocytes
monocytes
specific
organs
increased
production
chemoattractants
noted
other
diseases.
The
main
goal
this
study
investigate
complex
occur
find
similarities
with
diseases
such
multiple
sclerosis
(MS),
acute
respiratory
distress
syndrome
(ARDS),
rheumatoid
arthritis
(RA)
Kawasaki
advance
existing
diagnostic
therapeutic
protocols.
therapy
Interferon-gamma
(IFN-γ)
use
S1P
receptor
modulators
showed
promising
results.
However,
there
are
many
unknowns
about
these
mechanisms
possible
novel
therapies.
Therefore,
inflammation
autoimmunity
triggered
by
should
be
further
investigated
improve
procedures
protocols
for
Covid-19.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 28, 2024
The
COVID-19
pandemic
continues
to
cause
severe
global
disruption,
resulting
in
significant
excess
mortality,
overwhelming
healthcare
systems,
and
imposing
substantial
social
economic
burdens
on
nations.
While
most
of
the
attention
therapeutic
efforts
have
concentrated
acute
phase
disease,
a
notable
proportion
survivors
experience
persistent
symptoms
post-infection
clearance.
This
diverse
set
symptoms,
loosely
categorized
as
long
COVID,
presents
potential
additional
public
health
crisis.
It
is
estimated
that
1
5
exhibit
clinical
manifestations
consistent
with
COVID.
Despite
this
prevalence,
mechanisms
pathophysiology
COVID
remain
poorly
understood.
Alarmingly,
evidence
suggests
cases
within
condition
develop
debilitating
or
disabling
symptoms.
Hence,
urgent
priority
should
be
given
further
studies
equip
systems
for
its
management.
review
provides
an
overview
available
information
emerging
condition,
focusing
affected
individuals’
epidemiology,
pathophysiological
mechanisms,
immunological
inflammatory
profiles.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Nov. 1, 2021
More
than
one
and
a
half
years
have
elapsed
since
the
commencement
of
coronavirus
disease
2019
(COVID-19)
pandemic,
world
is
struggling
to
contain
it.
Being
caused
by
previously
unknown
virus,
in
initial
period,
there
had
been
an
extreme
paucity
knowledge
about
mechanisms,
which
hampered
preventive
therapeutic
measures
against
COVID-19.
In
endeavor
understand
pathogenic
extensive
experimental
studies
conducted
across
globe
involving
cell
culture-based
experiments,
human
tissue
organoids,
animal
models,
targeted
various
aspects
disease,
viz.,
viral
properties,
tropism
organ-specific
pathogenesis,
involvement
physiological
systems,
immune
response
infection.
The
vastly
accumulated
scientific
on
all
COVID-19
has
currently
changed
scenario
from
great
despair
hope.
Even
though
spectacular
progress
made
these
aspects,
multiple
gaps
are
remaining
that
need
be
addressed
future
studies.
Moreover,
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
variants
emerged
onset
first
wave,
with
seemingly
greater
transmissibility/virulence
escape
capabilities
wild-type
strain.
this
review,
we
narrate
pandemic
regarding
mechanisms
body,
including
virus-host
interactions,
pulmonary
other
systemic
manifestations,
immunological
dysregulations,
complications,
host-specific
vulnerability,
long-term
health
consequences
survivors.
Additionally,
provide
brief
review
current
evidence
explaining
molecular
imparting
transmissibility
virulence
emerging
SARS-CoV-2
variants.
Brazilian Journal of Nephrology,
Journal Year:
2021,
Volume and Issue:
43(4), P. 551 - 571
Published: May 28, 2021
Abstract
Acute
kidney
injury
(AKI)
in
hospitalized
patients
with
COVID-19
is
associated
higher
mortality
and
a
worse
prognosis.
Nevertheless,
most
have
mild
symptoms,
about
5%
can
develop
more
severe
symptoms
involve
hypovolemia
multiple
organ
dysfunction
syndrome.
In
pathophysiological
perspective,
SARS-CoV-2
infection
characterized
by
numerous
dependent
pathways
triggered
hypercytokinemia,
especially
IL-6
TNF-alpha,
leading
to
systemic
inflammation,
hypercoagulability,
dysfunction.
Systemic
endotheliitis
direct
viral
tropism
proximal
renal
tubular
cells
podocytes
are
important
mechanisms
critical
infection,
clinical
presentation
ranging
from
proteinuria
and/or
glomerular
hematuria
fulminant
AKI
requiring
replacement
therapies.
Glomerulonephritis,
rhabdomyolysis,
nephrotoxic
drugs
also
damage
COVID-19.
Thus,
independent
risk
factors
for
infection.
We
provide
comprehensive
review
of
the
literature
emphasizing
impact
acute
involvement
evolutive
prognosis
Journal of Medical Virology,
Journal Year:
2022,
Volume and Issue:
94(5), P. 1886 - 1892
Published: Jan. 28, 2022
In
late
2019,
an
outbreak
of
coronavirus
disease
2019
(COVID-19)
arose,
caused
by
severe
acute
respiratory
syndrome
type
2
(SARS-CoV-2).
This
rapidly
became
a
public
health
event
international
concern.
addition
to
the
most
typical
symptoms
dyspnea,
numerous
patients
with
COVID-19
exhibited
systemic
symptoms,
such
as
cardiovascular
disease,
liver
and
kidney
failure,
disorders
in
coagulation.
At
present,
clinical
data
indicates
that
who
are
critically
ill
die
from
multiple
organ
dysfunction
syndromes
(MODS).
Moreover,
entry
SARS-CoV-2
into
cells
causing
pathology
progressive
failure
is
precisely
mediated
human
angiotensin-converting
enzyme
protein.
plays
role
maintaining
both
fluid
electrolyte
homeostasis,
ensuring
stability
internal
environment.
Therefore,
present
review
aimed
investigate
pathogenesis
MODS
infection
based
on
current
previous
studies.
Inflammation Research,
Journal Year:
2021,
Volume and Issue:
71(1), P. 39 - 56
Published: Nov. 21, 2021
The
COVID-19
pandemic
created
a
worldwide
debilitating
health
crisis
with
the
entire
humanity
suffering
from
deleterious
effects
associated
high
infectivity
and
mortality
rates.
While
significant
evidence
is
currently
available
online
targets
various
aspects
of
disease,
both
inflammatory
noninflammatory
kidney
manifestations
secondary
to
infection
are
still
largely
underrepresented.
In
this
review,
we
summarized
current
knowledge
about
COVID-19-related
manifestations,
their
pathologic
mechanisms
as
well
pharmacotherapies
used
treat
patients
COVID-19.
We
also
shed
light
on
effect
these
medications
functions
that
can
further
enhance
renal
damage
illness.
Kidney360,
Journal Year:
2021,
Volume and Issue:
2(6), P. 924 - 936
Published: April 14, 2021
Abstract
Key
Points
Using
an
antigen
capture
assay
to
detect
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
spike
S1
protein,
we
found
that
the
protein
is
present
in
urine
of
25%
patients
with
disease
2019
(COVID-19).
Further,
24%
and
21%
adult
COVID-19
have
high
levels
albumin
cystatin
C,
respectively.
The
presence
SARS-CoV-2
suggests
renal
abnormalities
resulting
from
COVID-19.
Background
infection
has,
as
April
2021,
affected
>133
million
people
worldwide,
causing
>2.5
deaths.
Because
large
majority
individuals
infected
are
asymptomatic,
major
concerns
been
raised
about
possible
long-term
consequences
infection.
Methods
Wedeveloped
samples
COVID-19whose
diagnosis
was
confirmed
by
positive
PCR
results
nasopharyngeal
swabs
(NP-PCR+)
forSARS-CoV-2.
We
used
a
collection
233
132
participants
Yale
New
Haven
Hospital
Children’s
Philadelphia
were
obtained
during
pandemic
(106
NP-PCR+
26
NP-PCR−),
20
collected
before
pandemic.
Results
Our
analysis
identified
23
out
91
(25%)
(Ur-S+).
Interestingly,
although
all
children
Ur-S−,
one
child
who
NP-PCR−
be
for
their
urine.
Of
adults
Ur-S+,
only
individual
showed
detectable
viral
RNA
further
had
respectively,
Among
albuminuria
(>0.3
mg/mg
creatinine),
statistical
correlation
could
between
Conclusions
Together,
our
data
four
develop
abnormalities,
such
albuminuria.
Awareness
effect
these
findings
warranted.
Atherosclerosis,
Journal Year:
2021,
Volume and Issue:
322, P. 39 - 50
Published: Feb. 15, 2021
The
new
coronavirus
disease
(COVID-19)
is
a
systemic
disease.
Mounting
evidence
depict
signs
and
symptoms
involving
multiple
organs,
most
of
which
supported
by
pathological
data.
A
plausible
link
to
these
manifestations
vascular
endothelial
dysfunction/damage.
However,
much
the
current
knowledge
relies
on
opinion
incipient
evidence.
We
aim
objectively
appraise
association
between
COVID-19
disease,
specifically
endotheliitis
vasculitis.