Journal of Medical Virology,
Journal Year:
2023,
Volume and Issue:
95(6)
Published: June 1, 2023
Abstract
Accumulating
evidence
shows
that
SARS‐CoV‐2
can
potentially
trigger
autoimmune
processes,
which
be
responsible
for
the
long‐term
consequences
of
COVID‐19.
Therefore,
this
paper
aims
to
review
autoantibodies
reported
in
COVID‐19
convalescents.
Six
main
groups
were
distinguished:
(i)
against
components
immune
system,
(ii)
cardiovascular
(iii)
thyroid
autoantibodies,
(iv)
specific
rheumatoid
diseases,
(v)
antibodies
G‐protein
coupled
receptors,
and
(vi)
other
autoantibodies.
The
reviewed
here
clearly
highlights
infection
may
induce
humoral
responses.
However,
available
studies
share
number
limitations,
such
as:
(1)
sole
presence
does
not
necessarily
implicate
clinically‐relevant
risks,
(2)
functional
investigations
rarely
performed
it
is
often
unknown
whether
observed
are
pathogenic,
(3)
control
seroprevalence,
healthy,
noninfected
individuals
was
reported;
thus
sometimes
detected
result
or
accidental
post‐COVID‐19
detection,
(4)
correlated
with
symptoms
syndrome,
(5)
size
studied
small,
(6)
focused
predominantly
on
adult
populations,
(7)
age‐
sex‐related
differences
seroprevalence
explored,
(8)
genetic
predispositions
involved
generation
during
infections
investigated,
(9)
reactions
following
variants
vary
clinical
course
remain
unexplored.
Further
longitudinal
advocated
assess
link
between
identified
particular
outcomes
Journal of Translational Medicine,
Journal Year:
2022,
Volume and Issue:
20(1)
Published: March 22, 2022
Abstract
Background
Fatigue,
exertion
intolerance
and
post-exertional
malaise
are
among
the
most
frequent
symptoms
of
Post-COVID
Syndrome
(PCS),
with
a
subset
patients
fulfilling
criteria
for
Myalgic
Encephalomyelitis/Chronic
Fatigue
(ME/CFS).
As
SARS-CoV-2
infects
endothelial
cells,
causing
endotheliitis
damaging
endothelium,
we
investigated
dysfunction
(ED)
biomarkers
in
PCS.
Methods
We
studied
function
30
PCS
persistent
fatigue
as
well
15
age-
sex
matched
seronegative
healthy
controls
(HCs).
14
fulfilled
diagnostic
ME/CFS.
The
other
were
considered
to
have
Peripheral
was
assessed
by
reactive
hyperaemia
index
(RHI)
using
peripheral
arterial
tonometry
(PAT)
HCs.
In
larger
cohort
HCs,
including
post-COVID
reconvalescents
(PCHCs),
Endothelin-1
(ET-1),
Angiopoietin-2
(Ang-2),
Endocan
(ESM-1),
IL-8,
Angiotensin-Converting
Enzyme
(ACE)
ACE2
analysed
biomarkers.
Results
Five
ME/CFS
five
16
showed
ED
defined
diminished
RHI
(<
1.67),
but
none
HCs
exhibited
this
finding.
A
paradoxical
positive
correlation
age,
blood
pressure
BMI
found
not
patients.
ET-1
concentration
significantly
elevated
both
compared
PCHCs.
serum
Ang-2
lower
PCHCs
Conclusion
display
evidence
shown
altered
Different
associations
clinical
parameters
varying
biomarker
profiles
may
suggest
distinct
pathomechanisms
patient
subgroups.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Jan. 4, 2024
A
subgroup
of
patients
infected
with
SARS-CoV-2
remain
symptomatic
over
three
months
after
infection.
distinctive
symptom
long
COVID
is
post-exertional
malaise,
which
associated
a
worsening
fatigue-
and
pain-related
symptoms
acute
mental
or
physical
exercise,
but
its
underlying
pathophysiology
unclear.
With
this
longitudinal
case-control
study
(NCT05225688),
we
provide
new
insights
into
the
malaise
in
COVID.
We
show
that
skeletal
muscle
structure
lower
exercise
capacity
patients,
local
systemic
metabolic
disturbances,
severe
exercise-induced
myopathy
tissue
infiltration
amyloid-containing
deposits
muscles
worsen
induction
malaise.
This
highlights
novel
pathways
help
to
understand
suffering
from
other
post-infectious
diseases.
COVID-19,
with
persistent
and
new
onset
of
symptoms
such
as
fatigue,
post-exertional
malaise,
cognitive
dysfunction
that
last
for
months
impact
everyday
functioning,
is
referred
to
Long
COVID
under
the
general
category
post-acute
sequelae
SARS-CoV-2
infection
(PASC).
PASC
highly
heterogenous
may
be
associated
multisystem
tissue
damage/dysfunction
including
acute
encephalitis,
cardiopulmonary
syndromes,
fibrosis,
hepatobiliary
damages,
gastrointestinal
dysregulation,
myocardial
infarction,
neuromuscular
neuropsychiatric
disorders,
pulmonary
damage,
renal
failure,
stroke,
vascular
endothelial
dysregulation.
A
better
understanding
pathophysiologic
mechanisms
underlying
essential
guide
prevention
treatment.
This
review
addresses
potential
hypotheses
connect
long-term
health
consequences.
Comparisons
between
other
virus-initiated
chronic
syndromes
myalgic
encephalomyelitis/chronic
fatigue
syndrome
postural
orthostatic
tachycardia
will
addressed.
Aligning
identifying
potentially
regulated
common
underlining
pathways
necessary
true
nature
PASC.
The
discussed
contributors
include
from
injury
one
or
more
organs,
reservoirs
replicating
virus
its
remnants
in
several
tissues,
re-activation
latent
pathogens
Epstein-Barr
herpes
viruses
COVID-19
immune-dysregulated
environment,
interactions
host
microbiome/virome
communities,
clotting/coagulation
dysfunctional
brainstem/vagus
nerve
signaling,
dysautonomia
autonomic
dysfunction,
ongoing
activity
primed
immune
cells,
autoimmunity
due
molecular
mimicry
pathogen
proteins.
individualized
suggests
different
therapeutic
approaches
required
best
manage
specific
patients.
Trends in Endocrinology and Metabolism,
Journal Year:
2023,
Volume and Issue:
34(6), P. 321 - 344
Published: April 19, 2023
Acute
COVID-19
infection
is
followed
by
prolonged
symptoms
in
approximately
one
ten
cases:
known
as
Long
COVID.
The
disease
affects
~65
million
individuals
worldwide.
Many
pathophysiological
processes
appear
to
underlie
COVID,
including
viral
factors
(persistence,
reactivation,
and
bacteriophagic
action
of
SARS
CoV-2);
host
(chronic
inflammation,
metabolic
endocrine
dysregulation,
immune
autoimmunity);
downstream
impacts
(tissue
damage
from
the
initial
infection,
tissue
hypoxia,
dysbiosis,
autonomic
nervous
system
dysfunction).
These
mechanisms
culminate
long-term
persistence
disorder
characterized
a
thrombotic
endothelialitis,
endothelial
hyperactivated
platelets,
fibrinaloid
microclots.
abnormalities
blood
vessels
coagulation
affect
every
organ
represent
unifying
pathway
for
various
Cardiovascular Research,
Journal Year:
2022,
Volume and Issue:
119(2), P. 336 - 356
Published: July 25, 2022
Abstract
Long
COVID
has
become
a
world-wide,
non-communicable
epidemic,
caused
by
long-lasting
multiorgan
symptoms
that
endure
for
weeks
or
months
after
SARS-CoV-2
infection
already
subsided.
This
scientific
document
aims
to
provide
insight
into
the
possible
causes
and
therapeutic
options
available
cardiovascular
manifestations
of
long
COVID.
In
addition
chronic
fatigue,
which
is
common
symptom
COVID,
patients
may
present
with
chest
pain,
ECG
abnormalities,
postural
orthostatic
tachycardia,
newly
developed
supraventricular
ventricular
arrhythmias.
Imaging
heart
vessels
provided
evidence
chronic,
post-infectious
perimyocarditis
consequent
left
right
failure,
arterial
wall
inflammation,
microthrombosis
in
certain
patient
populations.
Better
understanding
underlying
cellular
molecular
mechanisms
will
aid
development
effective
treatment
strategies
its
manifestations.
A
number
have
been
proposed,
including
those
involving
direct
effects
on
myocardium,
microthrombotic
damage
endothelium,
persistent
inflammation.
Unfortunately,
existing
circulating
biomarkers,
coagulation,
inflammatory
markers,
are
not
highly
predictive
either
presence
outcome
when
measured
3
infection.
Further
studies
needed
understand
mechanisms,
identify
specific
guide
future
preventive
treatments
address
sequelae.
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2022,
Volume and Issue:
12
Published: April 5, 2022
Many
discharged
COVID-19
patients
affected
by
sequelae
experience
reduced
quality
of
life
leading
to
an
increased
burden
on
the
healthcare
system,
their
families
and
society
at
large.
Possible
pathophysiological
mechanisms
long
COVID
include:
persistent
viral
replication,
chronic
hypoxia
inflammation.
Ongoing
vascular
endothelial
damage
promotes
platelet
adhesion
coagulation,
resulting
in
impairment
various
organ
functions.
Meanwhile,
thrombosis
will
further
aggravate
vasculitis
contributing
deterioration.
Thus,
is
essentially
a
thrombotic
sequela.
Unfortunately,
there
currently
no
effective
treatment
for
COVID.
This
article
summarizes
evidence
coagulation
abnormalities
COVID,
with
focus
thrombosis.
Extracellular
vesicles
(EVs)
released
types
cells
can
carry
SARS-CoV-2
through
circulation
attack
distant
tissues
organs.
Furthermore,
EVs
express
tissue
factor
phosphatidylserine
(PS)
which
Given
persistence
virus,
inflammation
are
inevitable.
Pulmonary
structural
changes
such
as
hypertension,
embolism
fibrosis
common
The
impaired
lung
function
again
aggravates
abnormalities.
In
this
article,
we
also
summarize
recent
research
antithrombotic
therapy
COVID-19.
There
increasing
that
early
anticoagulation
be
improving
outcomes.
fact,
systemic
dysfunction
caused
key
factors
driving
complications
Early
prophylactic
prevent
release
or
remove
procoagulant
substances,
thereby
protecting
endothelium
from
damage,
reducing
sequelae,
long-COVID
patients.
The Lancet Regional Health - Europe,
Journal Year:
2023,
Volume and Issue:
28, P. 100595 - 100595
Published: Feb. 24, 2023
Few
studies
have
reported
the
long-term
health
effects
of
COVID-19.
The
regional
population-based
Linköping
COVID-19
study
(LinCoS)
included
all
patients
hospitalised
due
to
during
first
pandemic
wave.
Four
months
post-discharge,
over
40%
(185/433)
experienced
persisting
symptoms
and
activity/participation
limitations,
indicating
post-COVID-19
condition
(PCC).
present
follow-up
aimed
determine
recovery
among
these
24
post-admission.
This
prospective
cohort
from
LinCoS
with
PCC
at
four
post-discharge.
We
repeated
same
structured
interview
a
24-month
identify
their
impact
on
daily
life.
Intercurrent
issues
were
identified
by
reviewing
medical
records.
Of
185
4
181
alive
assessment
165
agreed
participate.
those,
21%
(35/165)
had
been
readmitted
hospital
for
various
causes
in
interim
period.
majority
(139/165,
84%)
problems
affecting
everyday
life
months.
Significant
improvements
seen
prevalence
magnitude
some
symptoms/limitations
compared
Cognitive,
sensorimotor,
fatigue
most
common
No
clear
difference
was
evident
between
individuals
treated
intensive
care
unit
(ICU)
non-ICU-treated
individuals.
Approximately
half
those
who
sick
leave
related
after
infection
is
one
report
2-year
outcomes
following
hospitalisation.
Despite
time,
we
found
high
need
rehabilitation
post
infection.
funded
Region
Östergötland.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Sept. 27, 2022
Most
patients
with
Post
COVID
Syndrome
(PCS)
present
a
plethora
of
symptoms
without
clear
evidence
organ
dysfunction.
A
subset
them
fulfills
diagnostic
criteria
myalgic
encephalomyelitis/chronic
fatigue
syndrome
(ME/CFS).
Symptom
severity
ME/CFS
correlates
natural
regulatory
autoantibody
(AAB)
levels
targeting
several
G-protein
coupled
receptors
(GPCR).
In
this
exploratory
study,
we
analyzed
serum
AAB
against
vaso-
and
immunoregulatory
receptors,
mostly
GPCRs,
in
80
PCS
following
mild-to-moderate
COVID-19,
40
fulfilling
ME/CFS.
Healthy
seronegative
(n=38)
asymptomatic
post
COVID-19
controls
(n=40)
were
also
included
the
study
as
control
groups.
We
found
lower
for
various
AABs
compared
to
at
least
one
group,
accompanied
by
alterations
correlations
among
AABs.
Classification
using
random
forest
indicated
ADRB2,
STAB1,
ADRA2A
strongest
classifiers
(AABs
stratifying
according
disease
outcomes)
outcomes.
Several
correlated
symptom
Remarkably,
vasomotor
associated
ADRB2
PCS/ME/CFS
patients.
Our
identified
dysregulation
involved
autonomous
nervous
system
(ANS),
vaso-,
immunoregulation
their
correlation
severity,
pointing
role
pathogenesis
PCS.