International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(16), P. 12648 - 12648
Published: Aug. 10, 2023
Long
COVID,
also
called
post-acute
sequelae
of
SARS-CoV-2,
is
characterized
by
a
multitude
lingering
symptoms,
including
impaired
cognition,
that
can
last
for
many
months.
This
symptom,
often
"brain
fog",
affects
the
life
quality
numerous
individuals,
increasing
medical
complications
as
well
healthcare
expenditures.
The
etiopathogenesis
SARS-CoV-2-induced
cognitive
deficit
unclear,
but
most
likely
cause
chronic
inflammation
maintained
viral
remnant
thriving
in
select
body
reservoirs.
These
sanctuaries
are
comprised
fused,
senescent
cells,
microglia
and
astrocytes,
pathogen
convert
into
neurotoxic
phenotypes.
Moreover,
enteric
nervous
system
contains
neurons
glia,
virus
lingers
gastrointestinal
tract
well,
accounting
intestinal
symptoms
long
COVID.
Fusogens
proteins
overcome
repulsive
forces
between
cell
membranes,
allowing
to
coalesce
with
host
cells
enter
cytoplasm.
In
intracellular
compartment,
hijacks
actin
cytoskeleton,
fusing
each
other
engendering
pathological
syncytia.
Cell-cell
fusion
enables
infect
healthy
neighboring
cells.
We
surmise
syncytia
formation
drives
impairment
facilitating
"seeding"
hyperphosphorylated
Tau,
documented
COVID-19.
our
previous
work,
we
hypothesized
SARS-CoV-2
induces
premature
endothelial
senescence,
permeability
blood-brain
barrier.
migration
microbes
and/or
their
components
circulation,
eventually
reaching
brain
where
they
may
induce
dysfunction.
For
example,
translocated
lipopolysaccharides
or
microbial
DNA
Tau
hyperphosphorylation,
memory
problems.
this
perspective
article,
examine
pathogenetic
mechanisms
potential
biomarkers
cell-free
DNA,
interleukin
22,
phosphorylated
beneficial
effect
transcutaneous
vagal
nerve
stimulation.
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
Human Genomics,
Journal Year:
2022,
Volume and Issue:
16(1)
Published: June 1, 2022
Abstract
COVID-19,
which
is
caused
by
the
SARS-CoV-2,
has
ravaged
world
for
past
2
years.
Here,
we
review
current
state
of
research
into
disease
with
focus
on
its
history,
human
genetics
and
genomics
transition
from
pandemic
to
endemic
phase.
We
are
particularly
concerned
lack
solid
information
initial
phases
that
highlighted
necessity
better
preparation
face
similar
future
threats.
On
other
hand,
gratified
progress
genetic
susceptibility
investigations
believe
now
time
explore
The
latter
will
require
worldwide
vigilance
cooperation,
especially
in
emerging
countries.
In
phase,
vaccination
rates
have
lagged
developed
countries
should
assist,
as
warranted,
bolstering
worldwide.
also
discuss
status
vaccines
outlook
COVID-19.
Pharmacology Research & Perspectives,
Journal Year:
2022,
Volume and Issue:
10(1)
Published: Jan. 13, 2022
Abstract
Infection
of
humans
with
SARS‐CoV‐2
virus
causes
a
disease
known
colloquially
as
“COVID‐19”
symptoms
ranging
from
asymptomatic
to
severe
pneumonia.
Initial
pathology
is
due
the
binding
ACE‐2
protein
on
endothelial
cells
lining
blood
vessels
and
entering
these
in
order
replicate.
Viral
replication
oxidative
stress
elevated
levels
reactive
oxygen
species.
Many
(~60%)
infected
people
appear
have
eliminated
their
body
after
28
days
resume
normal
activity.
However,
significant
proportion
(~40%)
experience
variety
(loss
smell
and/or
taste,
fatigue,
cough,
aching
pain,
“brain
fog,”
insomnia,
shortness
breath,
tachycardia)
12
weeks
are
diagnosed
syndrome
named
“LONG
COVID.”
Longitudinal
clinical
studies
group
subjects
who
were
been
compared
non‐infected
matched
subjects.
A
cohort
can
be
identified
by
battery
cytokine
markers
persistent,
low
level
grade
inflammation
often
self‐report
two
or
more
troubling
symptoms.
There
no
drug
that
will
relieve
effectively.
It
hypothesized
drugs
activate
intracellular
transcription
factor,
nuclear
factor
erythroid‐derived
2‐like
2
(NRF2)
may
increase
expression
enzymes
synthesize
antioxidant,
glutathione
quench
free
radicals
causing
stress.
The
hormone
melatonin
has
an
activator
NRF2
relatively
safe
chemical
for
most
ingest
chronically.
Thus,
it
option
consideration
re‐purposing
COVID”
experiencing
depression,
fog”
but
not
tachycardia.
Appropriately
designed
trials
required
evaluate
melatonin.
Psychiatry and Clinical Neurosciences,
Journal Year:
2022,
Volume and Issue:
77(2), P. 84 - 93
Published: Nov. 17, 2022
Although
some
patients
have
persistent
symptoms
or
develop
new
following
coronavirus
disease
2019
(COVID-19)
infection,
neuropsychiatric
aspects
of
long
COVID
are
not
well
known.
This
review
summarizes
and
provides
an
update
on
the
dimensions
COVID.
Its
manifestations
commonly
include
fatigue,
cognitive
impairment,
sleep
disorders,
depression,
anxiety,
post-traumatic
stress
disorder.
There
no
specific
tests
for
COVID,
but
characteristic
findings
such
as
hypometabolism
positron
emission
tomography
been
reported.
The
possible
mechanisms
inflammation,
ischemic
effects,
direct
viral
invasion,
social
environmental
changes.
Some
patient
characteristics
severity
complications
acute
COVID-19
infection
may
be
associated
with
increased
risk
symptoms.
Long
resolve
spontaneously
persist,
depending
type
established
treatments
lacking,
various
psychological
pharmacological
attempted.
Vaccination
against
plays
a
key
role
in
prevention
disease.
With
differences
among
SARS-CoV-2
variants,
including
omicron
variant,
likely
to
change
future.
Further
studies
clarifying
effective
warranted.
Frontiers in Microbiology,
Journal Year:
2023,
Volume and Issue:
13
Published: Jan. 13, 2023
Coronaviruses
can
cause
serious
respiratory
tract
infections
and
may
also
impact
other
end
organs
such
as
the
central
nervous
system,
lung
heart.
The
coronavirus
disease
2019
(COVID-19)
has
had
a
devastating
on
humanity.
Understanding
mechanisms
that
contribute
to
pathogenesis
of
infections,
will
set
foundation
for
development
new
treatments
attenuate
with
coronaviruses
host
cells
tissues.
During
infection
cells,
trigger
an
imbalance
between
increased
production
reactive
oxygen
species
(ROS)
reduced
antioxidant
responses
leads
redox
stress.
Subsequently,
stress
contributes
antiviral
virus-induced
inflammation
apoptosis
ultimately
drive
cell
tissue
damage
organ
disease.
However,
there
is
limited
understanding
how
different
including
SARS-CoV-2,
manipulate
cellular
machinery
drives
responses.
This
review
aims
elucidate
involved
in
replication
associated
inflammation,
apoptotic
pathways,
autoimmunity,
vascular
dysfunction
collectively
multiorgan
damage.
Biomedicines,
Journal Year:
2022,
Volume and Issue:
10(12), P. 3113 - 3113
Published: Dec. 2, 2022
Many
people
infected
with
the
SARS-CoV-2
suffer
long-term
symptoms,
such
as
"brain
fog",
fatigue
and
clotting
problems.
Explanations
for
"long
COVID"
include
immune
imbalance,
incomplete
viral
clearance
potentially,
mitochondrial
dysfunction.
As
conditions
sub-optimal
function
are
associated
initial
severity
of
disease,
their
prior
health
could
be
key
in
resistance
to
long
COVID
recovery.
The
SARs
virus
redirects
host
metabolism
towards
replication;
response,
can
metabolically
react
control
virus.
Resolution
is
normally
achieved
after
stress
activates
a
hormetic
negative
feedback
mechanism.
It
therefore
possible
that,
some
individuals
function,
"tip"
into
chronic
inflammatory
cycle.
This
might
explain
main
including
platelet
Long
thus
described
virally
induced
self-perpetuating
imbalanced
non-resolving
state
characterised
by
dysfunction,
where
reactive
oxygen
species
continually
drive
inflammation
shift
glycolysis.
would
suggest
that
sufferer's
needs
"tipped"
back
using
stimulus,
physical
activity,
calorie
restriction,
or
chemical
compounds
mimic
these
enhancing
perhaps
combination
inhibitors
quell
response.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(13), P. 10458 - 10458
Published: June 21, 2023
Long
COVID
(LC)
encompasses
a
constellation
of
long-term
symptoms
experienced
by
at
least
10%
people
after
the
initial
SARS-CoV-2
infection,
and
so
far
it
has
affected
about
65
million
people.
The
etiology
LC
remains
unclear;
however,
many
pathophysiological
pathways
may
be
involved,
including
viral
persistence;
chronic,
low-grade
inflammatory
response;
immune
dysregulation
defective
reactivation
latent
viruses;
autoimmunity;
persistent
endothelial
dysfunction
coagulopathy;
gut
dysbiosis;
hormonal
metabolic
dysregulation;
mitochondrial
dysfunction;
autonomic
nervous
system
dysfunction.
There
are
no
specific
tests
for
diagnosis
LC,
clinical
features
laboratory
findings
biomarkers
not
specifically
relate
to
LC.
Therefore,
is
paramount
importance
develop
validate
that
can
employed
prediction,
prognosis
its
therapeutic
response,
although
this
effort
hampered
challenges
pertaining
non-specific
nature
majority
manifestations
in
spectrum,
small
sample
sizes
relevant
studies
other
methodological
issues.
Promising
candidate
found
some
patients
markers
systemic
inflammation,
acute
phase
proteins,
cytokines
chemokines;
reflecting
persistence,
herpesviruses
endotheliopathy,
coagulation
fibrinolysis;
microbiota
alterations;
diverse
proteins
metabolites;
biomarkers;
cerebrospinal
fluid
biomarkers.
At
present,
there
only
two
reviews
summarizing
they
do
cover
entire
umbrella
current
biomarkers,
their
link
etiopathogenetic
mechanisms
or
diagnostic
work-up
comprehensive
manner.
Herein,
we
aim
appraise
synopsize
available
evidence
on
typical
classification
based
pathogenetic
main
symptomatology
frame
epidemiological
aspects
syndrome
furthermore
assess
limitations
as
well
potential
implications
interventions.
The Neuroscientist,
Journal Year:
2023,
Volume and Issue:
30(4), P. 421 - 439
Published: Sept. 11, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2),
the
causative
agent
of
disease
2019
(COVID-19),
could
affect
brain
structure
and
function.
SARS-CoV-2
can
enter
through
different
routes,
including
olfactory,
trigeminal,
vagus
nerves,
blood
immunocytes.
may
also
from
peripheral
a
disrupted
blood-brain
barrier
(BBB).
The
neurovascular
unit
in
brain,
composed
neurons,
astrocytes,
endothelial
cells,
pericytes,
protects
parenchyma
by
regulating
entry
substances
blood.
astrocytes
highly
express
angiotensin
converting
enzyme
(ACE2),
indicating
that
BBB
be
disturbed
lead
to
derangements
tight
junction
adherens
proteins.
This
leads
increased
permeability,
leakage
components,
movement
immune
cells
into
parenchyma.
cross
microvascular
an
ACE2
receptor–associated
pathway.
exact
mechanism
dysregulation
COVID-19/neuro-COVID
is
not
clearly
known,
nor
development
long
COVID.
Various
biomarkers
indicate
severity
neurologic
complications
COVID-19
help
objectively
diagnose
those
developing
review
highlights
importance
disruption,
as
well
some
potentially
useful
COVID-19,
COVID/neuro-COVID.
Archives of Microbiology & Immunology,
Journal Year:
2023,
Volume and Issue:
07(02)
Published: Jan. 1, 2023
Long
Covid
is
one
of
the
most
prevalent
and
puzzling
conditions
that
arose
with
pandemic.
Covid-19
infection
generally
resolves
within
several
weeks
but
some
experience
new
or
lingering
symptoms.
Though
there
no
formal
definition
for
such
symptoms
CDC
boadly
describes
long
as
persons
having
a
wide
range
new,
recurring
sustained
health
issues
four
more
after
first
being
infected
SARS-CoV2.
The
WHO
defines
manifestation
from
"probable
confirmed"
start
approximately
3
months
onset
acute
last
than
2
months.
Numerous
studies
have
looked
at
implications
on
various
organs.
Many
specific
mechanisms
been
proposed
changes.
In
this
article,
we
provide
an
overview
main
by
which
induces
end-organ
damage
in
recent
research
studies.
We
also
review
treatment
options,
current
clinical
trials,
other
potential
therapeutic
avenues
to
control
followed
information
about
effect
vaccination
Covid.
Lastly,
discuss
questions
knowledge
gaps
present
understanding
believe
effects
has
quality
life,
future
life
expectancy
are
required
better
understand
eventually
prevent
treat
disease.
acknowledge
not
limited
those
article
it
may
affect
offspring
therefore,
deem
important
identify
prognostic
targets
condition.
American Journal of Medicine Open,
Journal Year:
2024,
Volume and Issue:
11, P. 100068 - 100068
Published: Feb. 14, 2024
The
virus
called
SARS-CoV-2
emerged
in
2019
and
quickly
spread
worldwide,
causing
COVID-19.
It
has
greatly
impacted
on
everyday
life,
healthcare
systems,
the
global
economy.
In
order
to
save
as
many
lives
possible,
precautions
such
social
distancing,
quarantine,
testing
policies
were
implemented,
effective
vaccines
developed.
A
growing
amount
of
data
collected
worldwide
allowed
characterization
this
new
disease,
which
turned
out
be
more
complex
than
other
common
respiratory
tract
infections.
An
increasing
number
convalescents
presented
with
a
variety
non-specific
symptoms
emerging
after
acute
infection.
This
possible
health
problem
was
identified
labelled
long
COVID.
Since
then,
great
effort
been
made
by
clinicians
scientific
community
understand
underlying
mechanisms
develop
preventive
measures
treatment.
role
autoimmunity
induced
infection
development
COVID
is
discussed
review.
We
aim
deliver
description
several
conditions
an
autoimmune
background
observed
COVID-19
convalescents,
including
Guillain-Barré
syndrome,
antiphospholipid
syndrome
related
thrombosis,
Kawasaki
disease
highlighting
relationship
between
autoimmunity.
However,
further
studies
are
required
determine
its
true
clinical
significance.