Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 8, 2025
Acute
COVID-19
infection
causes
significant
alterations
in
the
innate
and
adaptive
immune
systems.
While
most
individuals
recover
naturally,
some
develop
long
COVID
(LC)
syndrome,
marked
by
persistent
or
new
symptoms
weeks
to
months
after
SARS-CoV-2
infection.
Despite
its
prevalence,
there
are
no
clinical
tests
distinguish
LC
patients
from
those
fully
recovered.
Understanding
immunological
basis
of
is
essential
for
improving
diagnostic
treatment
approaches.
We
performed
deep
immunophenotyping
functional
assays
examine
profiles
patients,
with
active
COVID-19,
recovered
healthy
donors.
This
analysis
assessed
both
features,
identifying
potential
biomarkers
syndrome.
A
Binomial
Generalized
Linear
Model
(BGLM)
was
used
pinpoint
features
characterizing
LC.
exhibited
depletion
cell
subsets,
including
plasmacytoid
conventional
dendritic
cells,
classical,
non-classical,
intermediate
monocytes,
monocyte-derived
inflammatory
cells.
Elevated
basal
inflammation
observed
compared
whose
were
closer
donors
individuals.
However,
displayed
alterations,
reduced
T
subsets
(CD4,
CD8,
Tregs)
switched
memory
B
similar
patients.
Through
BGLM,
a
unique
signature
identified,
featuring
CD8
gd
cells
low
proliferative
capacity
diminished
expression
activation
homing
receptors.
The
findings
highlight
associated
characterized
dysregulation.
recovery
comparable
Recovered
individuals,
deficits
populations
evident,
differentiating
full
recovery.
These
provide
insights
into
pathogenesis
may
support
development
tools
targeted
therapies.
Journal of Personalized Medicine,
Год журнала:
2024,
Номер
14(2), С. 170 - 170
Опубликована: Янв. 31, 2024
Postural
orthostatic
tachycardia
syndrome
(POTS)
is
a
common
accompaniment
of
variety
chronic,
inflammatory
diseases,
including
long
COVID,
as
are
small,
insoluble,
'fibrinaloid'
microclots.
We
here
develop
the
argument,
with
accompanying
evidence,
that
fibrinaloid
microclots,
through
their
ability
to
block
flow
blood
microcapillaries
and
thus
cause
tissue
hypoxia,
not
simply
correlated
but
in
fact,
by
preceding
it,
may
be
chief
intermediary
POTS,
which
body's
exaggerated
'physiological'
response
hypoxia.
Similar
reasoning
accounts
for
symptoms
bundled
under
term
'fatigue'.
Amyloids
known
membrane
disruptors,
when
targets
nerve
membranes,
this
can
explain
neurotoxicity
hence
autonomic
nervous
system
dysfunction
contributes
POTS.
Taken
together
view,
we
indicate
microclots
serve
link
POTS
fatigue
COVID
manner
at
once
both
mechanistic
explanatory.
This
has
clear
implications
treatment
such
diseases.
medRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Апрель 5, 2024
Abstract
Outcomes
following
SARS-CoV-2
infection
are
variable;
whilst
the
majority
of
patients
recover
without
serious
complications,
a
subset
develop
prolonged
illness
termed
Long
COVID
or
post-acute
sequelae
(PASC).
The
pathophysiology
underlying
remains
unclear
but
appears
to
involve
multiple
mechanisms
including
persistent
inflammation,
coagulopathy,
autoimmunity,
and
organ
damage.
Studies
suggest
that
microclots,
also
known
as
fibrinaloids,
play
role
in
COVID.
In
this
context,
we
developed
method
quantify
microclots
investigated
relationship
between
microclot
counts
We
show
cohort,
platelet-poor
plasma
from
samples
had
higher
count
compared
control
groups
retained
wide
distribution
counts.
Recent
COVID-19
infections
were
seen
be
associated
with
than
equivalent
subsequent
time-dependent
reduction
Our
findings
could
potential
biomarker
disease
and/or
treatment
target
some
patients.
Journal of Infection and Public Health,
Год журнала:
2025,
Номер
18(3), С. 102652 - 102652
Опубликована: Янв. 5, 2025
With
the
outbreak
of
COVID-19
in
China,
a
large
number
patients
are
at
risk
long
COVID
after
recovery.
The
purpose
our
research
is
to
systematically
review
existing
clinical
studies
understand
current
prevalence
and
related
factors
China.
protocol
this
systematic
was
registered
on
PROSPERO
(CRD42024519375).
We
searched
six
electronic
databases
from
1st
January
2020-1st
March
2024.
Literature
screening,
data
extraction,
bias
assessment
were
independently
carried
out
by
two
reviewers.
Quality
included
evaluated
AHRQ
NOS.
meta-analysis
performed
R
software
4.2.3
derive
factors.
Overall,
50
with
65880
participants
included.
results
showed
that
(with
least
one
symptom)
among
approximately
%
(95
%Confidence
Interval
(CI)
42-58
%)
Although
we
conducted
meta-regression
subgroup
analysis,
heterogeneity
study
high.
But
Omicron
BA.2
variant
had
statistically
significant
effect
(P
=
0.0004).
three
most
common
symptoms
fatigue
(0.33,
95
%CI
0.28-0.39),
cognitive
decline
(0.30,
0.14-0.46)
shortness
breath
(0.29,
0.15-0.43).
Patients
severe
acute
phase
(Odds
Ratio
(OR)
1.57,
CI
1.39-1.77),
combined
2
comorbidities
(OR
1.80,
1.40-2.32),
3
2.13,
1.64-2.77),
advanced
age
1.02,
1.01-1.04),
female
1.58,
1.44-1.73)
for
prevalence.
Current
found
nearly
half
may
suffering
Establishing
recovery-support
platform
regular
follow-up
would
help
long-term
monitor
manage
patients,
especially
those
high-risk
population.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 8, 2025
Acute
COVID-19
infection
causes
significant
alterations
in
the
innate
and
adaptive
immune
systems.
While
most
individuals
recover
naturally,
some
develop
long
COVID
(LC)
syndrome,
marked
by
persistent
or
new
symptoms
weeks
to
months
after
SARS-CoV-2
infection.
Despite
its
prevalence,
there
are
no
clinical
tests
distinguish
LC
patients
from
those
fully
recovered.
Understanding
immunological
basis
of
is
essential
for
improving
diagnostic
treatment
approaches.
We
performed
deep
immunophenotyping
functional
assays
examine
profiles
patients,
with
active
COVID-19,
recovered
healthy
donors.
This
analysis
assessed
both
features,
identifying
potential
biomarkers
syndrome.
A
Binomial
Generalized
Linear
Model
(BGLM)
was
used
pinpoint
features
characterizing
LC.
exhibited
depletion
cell
subsets,
including
plasmacytoid
conventional
dendritic
cells,
classical,
non-classical,
intermediate
monocytes,
monocyte-derived
inflammatory
cells.
Elevated
basal
inflammation
observed
compared
whose
were
closer
donors
individuals.
However,
displayed
alterations,
reduced
T
subsets
(CD4,
CD8,
Tregs)
switched
memory
B
similar
patients.
Through
BGLM,
a
unique
signature
identified,
featuring
CD8
gd
cells
low
proliferative
capacity
diminished
expression
activation
homing
receptors.
The
findings
highlight
associated
characterized
dysregulation.
recovery
comparable
Recovered
individuals,
deficits
populations
evident,
differentiating
full
recovery.
These
provide
insights
into
pathogenesis
may
support
development
tools
targeted
therapies.