With
a
global
tally
of
more
than
500
million
cases
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infections
to
date,
there
are
growing
concerns
about
the
post-acute
sequelae
SARS-CoV-2
infection
(PASC),
also
known
as
long
COVID.
Recent
studies
suggest
that
exaggerated
immune
responses
key
determinants
severity
and
outcomes
initial
well
subsequent
PASC.
The
complexity
innate
adaptive
in
period
requires
in-depth
mechanistic
analyses
identify
specific
molecular
signals
cell
populations
which
promote
PASC
pathogenesis.
In
this
review,
we
examine
current
literature
on
mechanisms
dysregulation
COVID-19
limited
emerging
data
immunopathology
While
phases
may
share
some
parallel
immunopathology,
it
is
likely
quite
distinct
heterogeneous,
thus
requiring
large-scale
longitudinal
patients
with
without
after
an
infection.
By
outlining
knowledge
gaps
PASC,
hope
provide
avenues
for
novel
research
directions
will
ultimately
lead
precision
therapies
restore
healthy
function
patients.
Nature Communications,
Journal Year:
2022,
Volume and Issue:
13(1)
Published: Jan. 18, 2022
Pregnant
women
represent
a
high-risk
population
for
severe/critical
COVID-19
and
mortality.
However,
the
maternal-fetal
immune
responses
initiated
by
SARS-CoV-2
infection,
whether
this
virus
is
detectable
in
placenta,
are
still
under
investigation.
Here
we
show
that
infection
during
pregnancy
primarily
induces
unique
inflammatory
at
interface,
which
largely
governed
maternal
T
cells
fetal
stromal
cells.
also
associated
with
humoral
cellular
blood,
as
well
mild
cytokine
response
neonatal
circulation
(i.e.,
umbilical
cord
blood),
without
compromising
T-cell
repertoire
or
initiating
IgM
responses.
Importantly,
not
detected
placental
tissues,
nor
sterility
of
placenta
compromised
viral
infection.
This
study
provides
insight
into
triggered
emphasizes
rarity
Bioscience Reports,
Journal Year:
2021,
Volume and Issue:
41(8)
Published: July 30, 2021
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-Cov-2)-induced
infection,
the
cause
of
disease
2019
(COVID-19),
is
characterized
by
unprecedented
clinical
pathologies.
One
most
important
pathologies,
hypercoagulation
and
microclots
in
lungs
patients.
Here
we
study
effect
isolated
SARS-CoV-2
spike
protein
S1
subunit
as
potential
inflammagen
sui
generis.
Using
scanning
electron
fluorescence
microscopy
well
mass
spectrometry,
investigate
this
to
interact
with
platelets
fibrin(ogen)
directly
blood
hypercoagulation.
platelet-poor
plasma
(PPP),
show
that
may
interfere
flow.
Mass
spectrometry
also
showed
when
added
healthy
PPP,
it
results
structural
changes
β
γ
fibrin(ogen),
complement
3,
prothrombin.
These
proteins
were
substantially
resistant
trypsinization,
presence
S1.
suggest
that,
part,
circulation
contribute
COVID-19
positive
patients
substantial
impairment
fibrinolysis.
Such
lytic
result
persistent
large
have
noted
here
previously
samples
This
observation
relevance
treatment
hypercoagulability
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
The Lancet Respiratory Medicine,
Journal Year:
2023,
Volume and Issue:
11(8), P. 739 - 754
Published: July 17, 2023
Individuals
with
SARS-CoV-2
infection
can
develop
symptoms
that
persist
well
beyond
the
acute
phase
of
COVID-19
or
emerge
after
phase,
lasting
for
weeks
months
initial
illness.
The
post-acute
sequelae
COVID-19,
which
include
physical,
cognitive,
and
mental
health
impairments,
are
known
collectively
as
long
COVID
post-COVID-19
condition.
substantial
burden
this
multisystem
condition
is
felt
at
individual,
health-care
system,
socioeconomic
levels,
on
an
unprecedented
scale.
Survivors
COVID-19-related
critical
illness
risk
respiratory
distress
syndrome,
sepsis,
chronic
illness,
these
multidimensional
morbidities
might
be
difficult
to
differentiate
from
specific
effects
COVID-19.
We
provide
overview
manifestations
in
adults.
explore
various
organ
systems,
describe
potential
pathophysiological
mechanisms,
consider
challenges
providing
clinical
care
support
survivors
manifestations.
Research
needed
reduce
incidence
optimise
therapeutic
rehabilitative
patients.
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2021,
Volume and Issue:
11
Published: July 6, 2021
SARS-CoV-2
infection
can
cause
fatal
inflammatory
lung
pathology,
including
thrombosis
and
increased
pulmonary
vascular
permeability
leading
to
edema
hemorrhage.
In
addition
the
lung,
cytokine
storm-induced
cascade
also
affects
other
organs.
infection-related
inflammation
is
characterized
by
endotheliopathy
in
Whether
causes
directly
infecting
endothelial
cells
not
known
focus
of
present
study.
We
observed
1)
co-localization
with
cell
marker
CD31
lungs
SARS-CoV-2-infected
mice
expressing
hACE2
intranasal
delivery
adenovirus
5-hACE2
(Ad5-hACE2
mice)
non-human
primates
at
both
protein
RNA
levels,
2)
proteins
immunogold
labeling
electron
microscopic
analysis.
detected
autopsied
tissue
obtained
from
patients
who
died
severe
COVID-19.
Comparative
analysis
sequencing
data
infected
Ad5-hACE2
Ad5-empty
(control)
revealed
upregulated
KRAS
signaling
pathway,
a
well-known
pathway
for
cellular
activation
dysfunction.
Further,
we
showed
that
infects
mature
mouse
aortic
(AoECs)
were
activated
performing
an
sprouting
assay
prior
exposure
SARS-CoV-2.
This
was
demonstrated
CD34
immunostaining
detection
viral
particles
studies.
Moreover,
AoECs
became
positive
ACE-2
but
quiescent
AoECs.
Together,
our
results
indicate
pneumocytes,
vivo
ex
vivo,
which
may
contribute
cardiovascular
complications
infection,
multipleorgan
failure.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Feb. 5, 2021
The
Severe
Acute
Respiratory
Syndrome
Coronavirus
2
(SARS-CoV-2)
is
a
fast
spreading
virus
leading
to
the
development
of
Disease-2019
(COVID-19).
and
critical
cases
are
characterized
by
damage
respiratory
system,
endothelial
inflammation,
multiple
organ
failure
triggered
an
excessive
production
proinflammatory
cytokines,
culminating
in
high
number
deaths
all
over
world.
Sedentarism
induces
worse,
continuous,
progressive
consequences
health.
On
other
hand,
physical
activity
provides
benefits
health
improves
low-grade
systemic
inflammation.
aim
this
review
elucidate
effects
fitness,
immune
defense,
its
contribution
mitigate
severe
inflammatory
response
mediated
SARS-CoV-2.
Physical
exercise
effective
therapeutic
strategy
SARS-CoV-2
infection.
In
sense,
studies
have
shown
that
acute
myokines
secreted
tissues
into
bloodstream,
supporting
modulatory
effect.
Therefore,
maintaining
influence
balance
system
increases
vigilance,
also
might
promote
potent
against
infectious
diseases
chronic
associated
with
forms
COVID-19.
Protocols
maintain
practice
suggested
been
strongly
established,
such
as
home-based
(HBE)
outdoor-based
(OBE).
regard,
HBE
help
reduce
levels
inactivity,
bed
rest,
sitting
time,
impacting
on
adherence
activity,
promoting
related
exercise,
attracting
patients
different
stages
treatment
for
parallel,
OBE
must
improve
health,
but
prevent
COVID-19
outcomes
populations.
conclusion,
or
models
can
be
progress
infection,
coadjutant
therapy
at
ages
conditions.
Journal of Neuroinflammation,
Journal Year:
2022,
Volume and Issue:
19(1)
Published: Jan. 20, 2022
Abstract
Background
Comprehensive
data
on
the
cerebrospinal
fluid
(CSF)
profile
in
patients
with
COVID-19
and
neurological
involvement
from
large-scale
multicenter
studies
are
missing
so
far.
Objective
To
analyze
systematically
CSF
COVID-19.
Methods
Retrospective
analysis
of
150
lumbar
punctures
127
PCR-proven
symptoms
seen
at
17
European
university
centers
Results
The
most
frequent
pathological
finding
was
blood-CSF
barrier
(BCB)
dysfunction
(median
QAlb
11.4
[6.72–50.8]),
which
present
58/116
(50%)
samples
without
pre-/coexisting
CNS
diseases
(group
I).
remained
elevated
>
14d
(47.6%)
even
30d
(55.6%)
after
onset.
total
protein
54/118
(45.8%)
65.35
mg/dl
[45.3–240.4])
strongly
correlated
QAlb.
white
cell
count
(WCC)
increased
14/128
(11%)
(mostly
lympho-monocytic;
median
10
cells/µl,
100
only
4).
An
albuminocytological
dissociation
(ACD)
found
43/115
(37.4%)
samples.
l
-lactate
26/109
(24%;
3.04
mmol/l
[2.2–4]).
CSF-IgG
50/100
(50%),
but
peripheral
origin,
since
QIgG
normal
almost
all
cases,
as
were
QIgA
QIgM.
In
58/103
(56%)
pattern
4
oligoclonal
bands
(OCB)
compatible
systemic
inflammation
present,
while
CSF-restricted
OCB
2/103
(1.9%).
SARS-CoV-2-CSF-PCR
negative
76/76
Routine
findings
35%.
Cytokine
levels
frequently
(often
associated
BCB
dysfunction)
serum,
partly
remaining
positive
high
for
weeks/months
(939
tests).
Of
note,
a
SARS-CoV-2-IgG-antibody
index
(AI)
2/19
(10.5%)
unusually
WCC
both
them
interleukin-6
(IL-6)
one
(not
tested
other).
Anti-neuronal/anti-glial
autoantibodies
mostly
absent
serum
(1509
disorders
II
[
N
=
19];
including
multiple
sclerosis,
JC-virus-associated
immune
reconstitution
inflammatory
syndrome,
HSV/VZV
encephalitis/meningitis,
lymphoma,
anti-Yo
subarachnoid
hemorrhage),
representative
respective
disease.
Conclusions
is
mainly
characterized
by
disruption
absence
intrathecal
inflammation,
endotheliopathy.
Persistent
cytokine
may
contribute
to
acute
‘long
COVID’.
Direct
infection
SARS-CoV-2,
if
occurring
all,
seems
be
rare.
Broad
differential
diagnostic
considerations
recommended
avoid
misinterpretation
treatable
coexisting
complications