Journal of Investigative Medicine,
Journal Year:
2023,
Volume and Issue:
71(5), P. 545 - 562
Published: March 6, 2023
In
late
2019,
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
triggered
the
global
disease
2019
(COVID-19)
pandemic.
Although
most
infections
cause
a
self-limited
comparable
to
other
upper
viral
pathogens,
portion
of
individuals
develop
illness
leading
substantial
morbidity
and
mortality.
Furthermore,
an
estimated
10%–20%
SARS-CoV-2
are
followed
by
post-acute
sequelae
COVID-19
(PASC),
or
long
COVID.
Long
COVID
is
associated
with
wide
variety
clinical
manifestations
including
cardiopulmonary
complications,
persistent
fatigue,
neurocognitive
dysfunction.
Severe
hyperactivation
increased
inflammation,
which
may
be
underlying
in
subset
individuals.
However,
immunologic
mechanisms
driving
development
still
under
investigation.
Early
pandemic,
our
group
others
observed
immune
dysregulation
persisted
into
convalescence
after
COVID-19.
We
subsequently
cohort
experiencing
demonstrated
SARS-CoV-2-specific
CD4
+
CD8
T-cell
responses
antibody
affinity
patients
symptoms.
These
data
suggest
symptoms
due
chronic
activation
presence
antigen.
This
review
summarizes
literature
date
detailing
how
these
observations
relate
addition,
we
discuss
recent
findings
support
antigen
evidence
that
this
phenomenon
contributes
local
systemic
inflammation
heterogeneous
nature
seen
BMJ,
Journal Year:
2022,
Volume and Issue:
unknown, P. e069676 - e069676
Published: May 18, 2022
Abstract
Objective
To
estimate
associations
between
covid-19
vaccination
and
long
covid
symptoms
in
adults
with
SARS-CoV-2
infection
before
vaccination.
Design
Observational
cohort
study.
Setting
Community
dwelling
population,
UK.
Participants
28
356
participants
the
Office
for
National
Statistics
COVID-19
Infection
Survey
aged
18-69
years
who
received
at
least
one
dose
of
an
adenovirus
vector
or
mRNA
vaccine
after
testing
positive
infection.
Main
outcome
measure
Presence
12
weeks
over
follow-up
period
3
February
to
5
September
2021.
Results
Mean
age
was
46
years,
55.6%
(n=15
760)
were
women,
88.7%
(n=25
141)
white
ethnicity.
Median
141
days
from
first
(among
all
participants)
67
second
(83.8%
participants).
6729
(23.7%)
reported
any
severity
once
during
follow-up.
A
associated
initial
12.8%
decrease
(95%
confidence
interval
−18.6%
−6.6%,
P<0.001)
odds
covid,
subsequent
data
compatible
both
increases
decreases
trajectory
(0.3%
per
week,
95%
−0.6%
1.2%
P=0.51).
8.8%
−14.1%
−3.1%,
P=0.003)
a
by
0.8%
week
(−1.2%
−0.4%
P<0.001).
Heterogeneity
not
found
sociodemographic
characteristics,
health
status,
hospital
admission
acute
covid-19,
type
(adenovirus
mRNA),
duration
Conclusions
The
likelihood
observed
evidence
suggested
sustained
improvement
dose,
median
days.
Vaccination
may
contribute
reduction
population
burden
although
longer
is
needed.
Frontiers in Medicine,
Journal Year:
2023,
Volume and Issue:
10
Published: June 2, 2023
Some
patients
remain
unwell
for
months
after
"recovering"
from
acute
COVID-19.
They
develop
persistent
fatigue,
cognitive
problems,
headaches,
disrupted
sleep,
myalgias
and
arthralgias,
post-exertional
malaise,
orthostatic
intolerance
other
symptoms
that
greatly
interfere
with
their
ability
to
function
can
leave
some
people
housebound
disabled.
The
illness
(Long
COVID)
is
similar
myalgic
encephalomyelitis/chronic
fatigue
syndrome
(ME/CFS)
as
well
persisting
illnesses
follow
a
wide
variety
of
infectious
agents
following
major
traumatic
injury.
Together,
these
are
projected
cost
the
U.S.
trillions
dollars.
In
this
review,
we
first
compare
ME/CFS
Long
COVID,
noting
considerable
similarities
few
differences.
We
then
in
extensive
detail
underlying
pathophysiology
two
conditions,
focusing
on
abnormalities
central
autonomic
nervous
system,
lungs,
heart,
vasculature,
immune
gut
microbiome,
energy
metabolism
redox
balance.
This
comparison
highlights
how
strong
evidence
each
abnormality,
illness,
helps
set
priorities
future
investigation.
review
provides
current
road
map
literature
biology
both
illnesses.
Nature Neuroscience,
Journal Year:
2024,
Volume and Issue:
27(3), P. 421 - 432
Published: Feb. 22, 2024
Abstract
Vascular
disruption
has
been
implicated
in
coronavirus
disease
2019
(COVID-19)
pathogenesis
and
may
predispose
to
the
neurological
sequelae
associated
with
long
COVID,
yet
it
is
unclear
how
blood–brain
barrier
(BBB)
function
affected
these
conditions.
Here
we
show
that
BBB
evident
during
acute
infection
patients
COVID
cognitive
impairment,
commonly
referred
as
brain
fog.
Using
dynamic
contrast-enhanced
magnetic
resonance
imaging,
COVID-associated
Transcriptomic
analysis
of
peripheral
blood
mononuclear
cells
revealed
dysregulation
coagulation
system
a
dampened
adaptive
immune
response
individuals
Accordingly,
showed
increased
adhesion
human
endothelial
vitro,
while
exposure
serum
from
induced
expression
inflammatory
markers.
Together,
our
data
suggest
sustained
systemic
inflammation
persistent
localized
dysfunction
key
feature
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
COVID-19
global
pandemic
caused
by
the
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
has
infected
hundreds
of
millions
individuals.
Following
infection,
a
subset
can
develop
wide
range
chronic
symptoms
affecting
diverse
organ
systems
referred
to
as
post-acute
sequelae
SARS-CoV-2
(PASC),
also
known
long
COVID.
A
National
Institutes
Health-sponsored
initiative,
RECOVER:
Researching
COVID
Enhance
Recovery,
sought
understand
basis
in
large
cohort.
Given
that
occur
COVID,
mechanisms
may
underlie
these
be
diverse.
In
this
review,
we
focus
on
emerging
literature
supporting
role(s)
viral
persistence
or
reactivation
viruses
play
PASC.
Persistence
RNA
antigens
is
reported
some
organs,
yet
mechanism
which
they
do
so
and
how
associated
with
pathogenic
immune
responses
unclear.
Understanding
RNA,
antigen
other
reactivated
relate
specific
inflammatory
drive
PASC
provide
rationale
for
treatment.
Cells,
Journal Year:
2023,
Volume and Issue:
12(5), P. 816 - 816
Published: March 6, 2023
The
development
of
long-term
symptoms
coronavirus
disease
2019
(COVID-19)
more
than
four
weeks
after
primary
infection,
termed
"long
COVID"
or
post-acute
sequela
COVID-19
(PASC),
can
implicate
persistent
neurological
complications
in
up
to
one
third
patients
and
present
as
fatigue,
"brain
fog",
headaches,
cognitive
impairment,
dysautonomia,
neuropsychiatric
symptoms,
anosmia,
hypogeusia,
peripheral
neuropathy.
Pathogenic
mechanisms
these
long
COVID
remain
largely
unclear;
however,
several
hypotheses
both
nervous
system
systemic
pathogenic
such
SARS-CoV2
viral
persistence
neuroinvasion,
abnormal
immunological
response,
autoimmunity,
coagulopathies,
endotheliopathy.
Outside
the
CNS,
SARS-CoV-2
invade
support
stem
cells
olfactory
epithelium
leading
alterations
function.
infection
may
induce
abnormalities
innate
adaptive
immunity
including
monocyte
expansion,
T-cell
exhaustion,
prolonged
cytokine
release,
which
cause
neuroinflammatory
responses
microglia
activation,
white
matter
abnormalities,
microvascular
changes.
Additionally,
clot
formation
occlude
capillaries
endotheliopathy,
due
protease
activity
complement
contribute
hypoxic
neuronal
injury
blood-brain
barrier
dysfunction,
respectively.
Current
therapeutics
target
pathological
by
employing
antivirals,
decreasing
inflammation,
promoting
regeneration.
Thus,
from
laboratory
evidence
clinical
trials
literature,
we
sought
synthesize
pathophysiological
pathways
underlying
potential
therapeutics.
EClinicalMedicine,
Journal Year:
2023,
Volume and Issue:
61, P. 102089 - 102089
Published: July 1, 2023
The
coronavirus
disease
2019
(COVID-19)
pandemic
has
drastically
perturbed
the
epidemiology
of
Respiratory
Syncytial
Virus
(RSV)
respiratory
tract
infections
in
children.
reasons
for
this
are
not
clear.
In
article,
we
review
current
literature
and
critically
discuss
different
theories
to
explain
why
RSV
changed
during
COVID-19
pandemic.
Proposed
mechanisms
include
decreased
viral
immunity
vulnerable
age
groups
caused
by
prolonged
lack
circulation
early
pandemic,
potential
Severe
Acute
Syndrome
Corona
2
(SARS-CoV-2)-induced
immune
dysregulation,
interactions
between
SARS-CoV-2
RSV,
modifications
health-seeking
behaviors
as
well
heath
systems
factors.
Research
genomics
phylogeny,
more
robust
immunology
research
is
needed
guide
prevention
health
care
resource
planning.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: June 10, 2022
Several
COVID-19
convalescents
suffer
from
the
post-acute
COVID-syndrome
(PACS)/long
COVID,
with
symptoms
that
include
fatigue,
dyspnea,
pulmonary
fibrosis,
cognitive
dysfunctions
or
even
stroke.
Given
scale
of
worldwide
infections,
long-term
recovery
and
integrative
health-care
in
nearest
future,
it
is
critical
to
understand
cellular
molecular
mechanisms
as
well
possible
predictors
longitudinal
post-COVID-19
responses
convalescent
individuals.
The
immune
system
T
cell
alterations
are
proposed
drivers
COVID
syndrome.
However,
despite
number
studies
on
COVID-19,
many
them
addressed
only
severe
short-term
responses.
Here,
we
performed
mild,
moderate
COVID-19-convalescent
patients,
at
two
time
points
(3
6
months
infection),
assess
dynamics
cells
landscape,
integrated
patients-reported
symptoms.
We
show
among
subsets
exhibit
different,
severity-
time-dependent
dynamics,
result
a
polarization
towards
an
exhausted/senescent
state
CD4+
CD8+
perturbances
Tregs.
In
particular,
high
proportion
CD57+
terminal
effector
cells,
together
significant
decrease
naïve
population,
augmented
granzyme
B
IFN-γ
production
unresolved
inflammation
after
infection.
Mild
showed
increased
naïve,
decreased
central
memory
Treg
subsets.
Patients
all
severity
groups
can
be
predisposed
long
symptoms,
fatigue
not
necessarily
related
dysfunctions,
was
found
convalescents.
conclusion,
functional
remodeling
could
seen
two-step
process,
leading
distinct
states
Our
data
imply
attenuation
blocking
might
influence
post-COVID
either
search
for
any
treatment
prevent
PACS
further
complications
mandatory
patients
SARS-CoV-2
infection,
those
suffering
COVID-19.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: Nov. 1, 2023
Abstract
There
have
been
hundreds
of
millions
cases
coronavirus
disease
2019
(COVID-19),
which
is
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2).
With
the
growing
population
recovered
patients,
it
crucial
to
understand
long-term
consequences
and
management
strategies.
Although
COVID-19
was
initially
considered
an
illness,
recent
evidence
suggests
that
manifestations
including
but
not
limited
those
cardiovascular,
respiratory,
neuropsychiatric,
gastrointestinal,
reproductive,
musculoskeletal
systems
may
persist
long
after
phase.
These
persistent
manifestations,
also
referred
as
COVID,
could
impact
all
patients
with
across
full
spectrum
illness
severity.
Herein,
we
comprehensively
review
current
literature
on
highlighting
its
epidemiological
understanding,
vaccinations,
organ-specific
sequelae,
pathophysiological
mechanisms,
multidisciplinary
In
addition,
psychological
psychosomatic
factors
underscored.
Despite
these
findings
diagnostic
therapeutic
strategies
based
previous
experience
pilot
studies
remain
inadequate,
well-designed
clinical
trials
should
be
prioritized
validate
existing
hypotheses.
Thus,
propose
primary
challenges
concerning
biological
knowledge
gaps
efficient
remedies
well
discuss
corresponding
recommendations.