Hepatology Communications,
Journal Year:
2021,
Volume and Issue:
6(2), P. 255 - 269
Published: Oct. 20, 2021
Liver
injury,
characterized
predominantly
by
elevated
aspartate
aminotransferase
and
alanine
aminotransferase,
is
a
common
feature
of
coronavirus
disease
2019
(COVID-19)
symptoms
caused
severe
acute
respiratory
syndrome-coronavirus
2
(SARS-CoV-2).
Additionally,
SARS-CoV-2
infection
associated
with
acute-on-chronic
liver
failure
in
patients
cirrhosis
has
notably
mortality
alcohol-related
compared
to
other
etiologies.
Direct
viral
the
remains
controversial,
alternative
pathophysiologic
explanations
for
its
hepatic
effects
are
an
area
active
investigation.
In
this
review,
we
discuss
inflammatory
environment
it
creates
on
endothelial
cells
platelets
more
generally
then
focus.
doing
this,
present
vascular
inflammation
thrombosis
as
potential
mechanism
injury
liver-related
complications
COVID-19.
Thrombotic
and
microvascular
complications
are
frequently
seen
in
deceased
COVID-19
patients.
However,
whether
this
is
caused
by
direct
viral
infection
of
the
endothelium
or
inflammation-induced
endothelial
activation
remains
highly
contentious.Here,
we
use
patient
autopsy
samples,
primary
human
cells
an
vitro
model
pulmonary
epithelial-endothelial
cell
barrier.We
show
that
express
very
low
levels
SARS-CoV-2
receptor
ACE2
protease
TMPRSS2,
which
blocks
their
capacity
for
productive
infection,
limits
to
produce
infectious
virus.
Accordingly,
can
only
be
infected
when
they
overexpress
ACE2,
exposed
high
concentrations
SARS-CoV-2.
We
also
does
not
infect
3D
vessels
under
flow
conditions.
further
demonstrate
a
co-culture
with
Endothelial
do
however
sense
respond
adjacent
epithelial
cells,
increasing
ICAM-1
expression
releasing
pro-inflammatory
cytokines.Taken
together,
these
data
suggest
vivo,
unlikely
may
occur
if
epithelium
denuded
(basolateral
infection)
load
present
blood
(apical
infection).
In
such
scenario,
whilst
occur,
it
contribute
amplification.
still
play
key
role
pathogenesis
sensing
mounting
response
Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
10
Published: Feb. 15, 2022
Severe
Acute
Respiratory
Syndrome
Coronavirus
2
(SARS-CoV-2)
was
first
identified
in
December
2019
as
a
novel
respiratory
pathogen
and
is
the
causative
agent
of
Corona
Virus
disease
(COVID-19).
Early
on
during
this
pandemic,
it
became
apparent
that
SARS-CoV-2
not
only
restricted
to
infecting
tract,
but
virus
also
found
other
tissues,
including
vasculature.
Individuals
with
underlying
pre-existing
co-morbidities
like
diabetes
hypertension
have
been
more
prone
develop
severe
illness
fatal
outcomes
COVID-19.
In
addition,
critical
clinical
observations
made
COVID-19
patients
include
hypercoagulation,
cardiomyopathy,
heart
arrythmia,
endothelial
dysfunction,
which
are
indicative
for
an
involvement
vasculature
pathology.
Hence,
review
summarizes
impact
infection
details
how
promotes
(chronic)
vascular
inflammation.
We
provide
general
overview
SARS-CoV-2,
its
entry
determinant
Angiotensin-Converting
Enzyme
II
(ACE2)
detection
extrapulmonary
tissue.
Further,
we
describe
relation
between
cardiovascular
diseases
(CVD)
their
Clinical
findings
changes
reviewed
detail
recent
evidence
from
vitro
studies
susceptibility
cells
discussed.
conclude
current
notions
contribution
events
long
term
consequences
COVID-19,
known
“Long-COVID-syndrome”.
Altogether,
our
provides
detailed
perspectives
influence
Future Microbiology,
Journal Year:
2022,
Volume and Issue:
17(7), P. 551 - 571
Published: March 10, 2022
There
is
limited
evidence
available
on
the
long-term
impact
of
SARS-CoV-2
infection
in
children.
In
this
article,
authors
analyze
recent
pediatric
long
Covid
and
lessons
learnt
from
a
post-Covid
unit
Rome,
Italy.
To
gain
better
understanding
concerns
raised
by
parents
physicians
relation
to
potential
consequences
novel
infection,
it
important
recognize
that
effect
post-infectious
disease
not
new
phenomenon.
Viruses,
Journal Year:
2023,
Volume and Issue:
15(2), P. 553 - 553
Published: Feb. 16, 2023
COVID-19
is
a
multisystemic
disease
caused
by
the
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2).
The
immunopathogenic
conditions
of
hyperinflammatory
response
that
cause
systemic
inflammation
are
extremely
linked
to
its
severity.
This
research
sought
review
immunopathological
elements
contribute
progression.
systematic
using
PUBMED,
LILACS,
MEDLINE,
and
SCIELO
databases
articles
between
May
2020
July
2022
with
following
search
terms
in
conjunction
“AND”:
“SARS-CoV-2”;
“COVID-19”;
“ARDS”
“Cytokine
Storm”.
quality
appraisal
risk
bias
were
assessed
JBI
checklists
Cochrane
Collaboration’s
RoB
2.0
ROBINS-I
tools,
respectively,
for
vitro
studies
pre-defined
standard
literature.
resulted
39
articles.
main
actors
this
denote
SARS-CoV-2
Spike
proteins,
cellular
proteases,
leukocytes,
cytokines,
proteolytic
cascades.
“cytokine
storm”
itself
brings
several
complications
host
through
cytokines
such
as
IL-6
chemokines
(such
CCL2),
which
influence
tissue
apoptosis
pyroptosis.
causes
unfavorable
outcomes
patients,
largely
dysregulation
immune
should
be
controlled
their
recovery.
Pharmacological Reports,
Journal Year:
2022,
Volume and Issue:
74(6), P. 1255 - 1278
Published: July 25, 2022
The
use
of
antiviral
COVID-19
medications
can
successfully
inhibit
SARS-CoV-2
replication
and
prevent
disease
progression
to
a
more
severe
form.
However,
the
timing
treatment
plays
crucial
role
in
this
regard.
Oral
drugs
provide
an
opportunity
manage
infection
without
need
for
hospital
admission,
easing
general
burden
that
have
on
healthcare
system.
This
review
paper
(i)
presents
potential
pharmaceutical
targets,
including
various
host-based
targets
viral-based
(ii)
characterizes
first-generation
anti-SARS-CoV-2
oral
(nirmatrelvir/ritonavir
molnupiravir),
(iii)
summarizes
clinical
progress
other
antivirals
COVID-19,
(iv)
discusses
ethical
issues
such
trials
(v)
challenges
associated
with
practice.
represent
part
strategy
adapt
long-term
co-existence
manner
prevents
from
being
overwhelmed.
It
is
pivotal
ensure
equal
fair
global
access
currently
available
those
authorized
future.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(2), P. 326 - 326
Published: Jan. 31, 2023
Oxidative
stress
and
endothelial
dysfunction
have
been
shown
to
play
crucial
roles
in
the
pathophysiology
of
COVID-19
(coronavirus
disease
2019).
On
these
grounds,
we
sought
investigate
impact
on
lipid
peroxidation
ferroptosis
human
cells.
We
hypothesized
that
oxidative
induced
by
cells
could
be
linked
outcome.
Thus,
collected
serum
from
patients
hospital
admission,
incubated
sera
with
cells,
comparing
effects
generation
reactive
oxygen
species
(ROS)
between
who
survived
did
not
survive.
found
non-survivors
significantly
increased
peroxidation.
Moreover,
markedly
regulated
expression
levels
main
markers
ferroptosis,
including
GPX4,
SLC7A11,
FTH1,
SAT1,
a
response
was
rescued
silencing
TNFR1
Taken
together,
our
data
indicate
survive
triggers