medRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 11, 2024
Abstract
Background
SARS-CoV-2
infection
may
lead
to
Post-COVID
Syndrome
(PCS),
characterized
by
debilitating
symptoms
like
persistent
fatigue,
cardiovascular
symptoms,
and
cognitive
dysfunction.
Persistent
endothelial
dysfunction
(ED)
is
a
potential
driver
of
ongoing
symptoms.
Yet,
the
underlying
biological
mechanisms
remain
unclear.
Methods
In
this
prospective
observational
study,
we
41
PCS
patients
24
healthy
controls
(HC,
matched
out
n
=
204,
recruited
before
pandemic)
investigated
effect
Spike
protein
1
(S1)
plasma
from
on
human
retinal
cells
(HREC).
Results
Plasma
samples
exhibited
significantly
elevated
erythropoietin,
VEGF
MCP-1
alongside
decreased
IL-6
levels
compared
HC.
Low
Haemoglobin
Haematocrit
were
negatively
associated
with
severity.
positively
correlated
Anti-S1
IgG
in
upregulated
mRNA
level
HREC
exposed
S1.
Additionally,
S1
exposure
promoted
ROS
production
transiently
activated
HIF-1α
HREC.
activation
HIF-2α
led
disrupted
integrity.
severely
affected
showed
increased
compromised
barrier
function.
Treatment
Belzutifan,
inhibitor,
restored
integrity
or
PCS-plasma.
Conclusion
These
findings
suggest
that
HIF-2α-mediated
ED
might
be
therapeutical
target
for
Belzutifan.
Trial
registration
URL:
https://www.clinicaltrials.gov
;
Unique
identifier:
NCT05635552
Novelty
significance
What
Is
Known?
Endothelial
consequence
acute
syndrome
(PCS)
Patients
show
inflammation
markers.
proteins
can
persist
up
12
months
post-infection,
driving
immune
activation.
New
Information
Does
This
Article
Contribute?
haemoglobin
(Hb)
high
correlate
higher
low
Hb
C19-YRS
severity
score.
exhibit
Erythropoietin
(EPO)
when
alone
patient’s
induce
primarily
through
Both
cause
oxidative
stress
disrupting
Inhibition
effectively
restores
plasma.
circulation
spike
sustain
chronic
PCS.
Here
exhibits
which
correlates
IgG.
was
titres
Levels
EPO
patients,
more
pronounced
observed
cells,
both
activation,
rather
than
NF-κB.
factors
significant
stress,
evidenced
turn
disrupts
Notably,
restore
function,
offering
therapeutic
Graphical
Brain Communications,
Journal Year:
2024,
Volume and Issue:
6(2)
Published: Jan. 1, 2024
Abstract
Components
that
comprise
our
brain
parenchymal
and
cerebrovascular
structures
provide
a
homeostatic
environment
for
proper
neuronal
function
to
ensure
normal
cognition.
Cerebral
insults
(e.g.
ischaemia,
microbleeds
infection)
alter
cellular
physiologic
processes
within
the
neurovascular
unit
contribute
cognitive
dysfunction.
COVID-19
has
posed
significant
complications
during
acute
convalescent
stages
in
multiple
organ
systems,
including
brain.
Cognitive
impairment
is
prevalent
complication
patients,
irrespective
of
severity
SARS-CoV-2
infection.
Moreover,
overwhelming
evidence
from
vitro,
preclinical
clinical
studies
reported
SARS-CoV-2-induced
pathologies
components
are
associated
with
impairment.
Neurovascular
disruption
alters
coupling
response,
critical
mechanism
regulates
cerebromicrovascular
blood
flow
meet
energetic
demands
locally
active
neurons.
Normal
processing
achieved
through
response
involves
coordinated
action
cells
(i.e.
neurons
glia)
cell
types
endothelia,
smooth
muscle
pericytes).
However,
current
work
on
COVID-19-induced
yet
investigate
as
causal
factor.
Hence,
this
review,
we
aim
describe
SARS-CoV-2's
effects
how
they
can
impact
decline
disease.
Additionally,
explore
potential
therapeutic
interventions
mitigate
Given
great
both
individuals
public
health,
necessity
effort
fundamental
scientific
research
application
becomes
imperative.
This
integrated
endeavour
crucial
mitigating
deficits
induced
by
its
subsequent
burden
especially
vulnerable
population.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: April 22, 2024
Introduction:
Although
post-COVID-19
syndrome
(PCS)
with
cognitive
impairment
is
increasingly
encountered
in
primary
care,
evidence-based
recommendations
for
its
appropriate
management
are
lacking.
Methods:
A
systematic
literature
search
evaluating
the
diagnosis
and
treatment
of
associated
PCS
was
conducted.
Practical
PCS-associated
care
summarized,
based
on
an
evaluation
pharmacological
plausibility
clinical
applications.
Results:
Currently,
pathology
remains
unclear
no
high-quality
data
to
support
targeted
interventions.
Existing
approaches
directed
towards
symptom
relief
where
counseling
chronicity
disease
regular
reassessments
at
4-
8-week
intervals
considered
reasonable.
Patients
should
be
informed
encouraged
adopt
a
healthy
lifestyle
that
centers
around
balanced
nutrition
physical
activities.
They
may
also
benefit
from
intake
vitamins,
micronutrients,
probiotics.
The
administration
Ginkgo
biloba
extract
could
offer
safe
potentially
beneficial
option.
Other
non-pharmacological
measures
include
physiotherapy,
digitally
supported
training,
and,
if
indicated,
ergotherapy
or
speech
therapy.
In
most
patients,
symptoms
improve
within
8
weeks.
If
serious,
ambiguous,
when
new
occur,
specialized
diagnostic
such
as
comprehensive
neurocognitive
testing
neuroimaging
initiated.
Very
few
patients
would
require
inpatient
rehabilitation.
Conclusion:
debilitating
condition
affect
daily
functioning
reduce
work
productivity.
Management
multidisciplinary
approach,
centering
physical,
cognitive,
therapies.
Trends in Endocrinology and Metabolism,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 1, 2024
When
acute
SARS-CoV-2
infections
cause
symptoms
that
persist
longer
than
3
months,
this
condition
is
termed
long
COVID.
Symptoms
experienced
by
patients
often
include
myalgia,
fatigue,
brain
fog,
cognitive
impairments,
and
post-exertional
malaise
(PEM),
which
the
worsening
of
following
mental
or
physical
exertion.
There
little
consensus
on
pathophysiology
exercise-induced
PEM
skeletal-muscle-related
symptoms.
In
opinion
article
we
highlight
intrinsic
mitochondrial
dysfunction,
endothelial
abnormalities,
a
muscle
fiber
type
shift
towards
more
glycolytic
phenotype
as
main
contributors
to
reduced
exercise
capacity
in
The
mechanistic
trigger
for
induce
unknown,
but
rapid
skeletal
tissue
damage
intramuscular
infiltration
immune
cells
contribute
PEM-related
Progress in Retinal and Eye Research,
Journal Year:
2024,
Volume and Issue:
102, P. 101285 - 101285
Published: June 24, 2024
There
is
an
increasing
body
of
knowledge
regarding
how
COVID-19
may
be
associated
with
ocular
disease
varying
severity
and
duration.
This
article
discusses
the
literature
on
manifestations
COVID-19,
including
appraisal
current
evidence,
suggested
mechanisms
action,
comorbidities
risk
factors,
timing
from
initial
infection
to
diagnosis
clinical
red
flags.
The
primarily
comprises
case
reports
series
which
inevitably
lack
control
groups
evidence
support
causality.
However,
these
early
data
have
prompted
development
larger
population-based
laboratory
studies
that
are
emerging.
As
new
become
available,
a
better
true
effects
eye
will
possible.
While
pandemic
was
officially
declared
no
longer
"global
health
emergency"
by
World
Health
Organization
(WHO)
in
May
2023,
numbers
continue
rise.
Reinfection
different
variants
predicted
lead
growing
cumulative
burden
disease,
particularly
as
more
chronic,
multi-organ
sequelae
apparent
potentially
significant
implications.
postulated
due
three
main
mechanisms:
firstly,
there
dysregulated
immune
response
linked
inflammatory
disease;
secondly,
patients
greater
tendency
towards
hypercoagulable
state,
leading
prothrombotic
events;
thirdly,
severe
requiring
hospitalisation
immunosuppressed
administered
corticosteroids
or
such
diabetes
mellitus
at
increased
secondary
infections,
endophthalmitis
rhino-orbital-mucormycosis.
Reported
ophthalmic
associations
therefore,
include
range
conditions
conjunctivitis,
scleritis,
uveitis,
endogenous
endophthalmitis,
corneal
graft
rejection,
retinal
artery
vein
occlusion,
non-arteritic
ischaemic
optic
neuropathy,
glaucoma,
neurological
orbital
sequelae.
With
need
consider
telemedicine
consultation
view
COVID-19's
infectivity,
understanding
present
during
following
essential
ensure
appropriately
triaged,
prompt
in-person
examination
for
management
sight-threatening
life-threatening
diseases.
Open Forum Infectious Diseases,
Journal Year:
2024,
Volume and Issue:
11(9)
Published: Aug. 27, 2024
Abstract
While
the
acute
manifestations
of
infectious
diseases
are
well
known,
in
some
individuals,
symptoms
can
either
persist
or
appear
after
period.
Postviral
fatigue
syndromes
recognized
with
other
viral
infections
and
described
coronavirus
disease
2019
(COVID-19).
We
have
a
growing
number
individuals
that
for
weeks,
months,
years.
Here,
we
share
evidence
regarding
abnormalities
associated
postacute
sequelae
COVID-19
(PASC)
therapeutics.
describe
physiological
biochemical
seen
reporting
PASC.
several
evidence-based
interventions
to
offer
patients.
It
is
expected
this
understanding
mechanisms
driving
PASC
benefits
certain
therapeutics
may
not
only
lead
better
outcomes
those
but
also
potential
treating
postinfectious
sequelae.
Frontiers in Neurology,
Journal Year:
2025,
Volume and Issue:
16
Published: March 26, 2025
Introduction
Cognitive
symptoms
are
reported
in
the
vast
majority
of
individuals
with
long-COVID
and
there
is
growing
support
to
suggest
neurovascular
mechanisms
may
play
a
role.
Older
adults
at
increased
risk
for
developing
complications
associated
COVID-19,
including
heightened
cognitive
decline.
Cerebrovascular
Reactivity
(CVR),
marker
health,
has
been
linked
age
related
decline
role
long-COVID,
however,
this
not
yet
explored.
Methods
The
present
study
examined
group
differences
CVR
31
older
compared
cognitively
unimpaired
without
symptoms.
Follow
up
analyses
were
conducted
examine
how
was
both
subjective
neuropsychological
(NP)
test
performance.
A
subject-specific
approach,
Distribution-Corrected
Z-scores
(DisCo-Z),
used.
Results
Analyses
revealed
demonstrated
significantly
greater
incidence
extreme
clusters
within
brain
(>100
voxels)
functional
networks
thought
drive
attention
executive
function.
Extreme
positive
positively
number
negatively
correlated
NP
Discussion
These
findings
among
first
provide
link
between
functioning
changes
relevant
aging
mechanistic
studies
long-COVID.