Antioxidants,
Journal Year:
2021,
Volume and Issue:
10(7), P. 1152 - 1152
Published: July 20, 2021
Viral
infections
constitute
a
tectonic
convulsion
in
the
normophysiology
of
hosts.
The
current
coronavirus
disease
2019
(COVID-19)
pandemic
is
not
an
exception,
and
therefore
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
infection,
like
any
other
invading
microbe,
enacts
generalized
immune
response
once
virus
contacts
body.
Melatonin
systemic
dealer
that
does
overlook
homeostasis
disturbance,
which
consequently
brings
into
play
its
cooperative
triad,
antioxidant,
anti-inflammatory,
immune-stimulant
backbone,
to
stop
infective
cycle
SARS-CoV-2
or
endogenous
exogenous
threat.
In
COVID-19,
corporal
propagation
involves
exacerbated
oxidative
activity
overproduction
great
amounts
reactive
oxygen
nitrogen
species
(RONS).
endorsement
melatonin
as
possible
protective
agent
against
indirectly
supported
by
widely
demonstrated
beneficial
role
preclinical
clinical
studies
diseases.
addition,
focusing
therapeutic
action
on
strengthening
host
protection
responses
critical
phases
makes
it
likely
multi-tasking
will
provide
multi-protection,
maintaining
efficacy
variants
are
already
emerging
emerge
long
continues
circulate
among
us.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(4), P. 2108 - 2108
Published: Feb. 20, 2021
Severe
COVID-19
is
characterized
by
a
"cytokine
storm",
the
mechanism
of
which
not
yet
understood.
I
propose
that
cytokine
storms
result
from
synergistic
interactions
among
Toll-like
receptors
(TLR)
and
nucleotide-binding
oligomerization
domain-like
(NLR)
due
to
combined
infections
SARS-CoV-2
with
other
microbes,
mainly
bacterial
fungal.
This
proposition
based
on
eight
linked
types
evidence
their
logical
connections.
(1)
cases
differ
healthy
controls
mild
patients
in
exhibiting
increased
TLR4,
TLR7,
TLR9
NLRP3
activity.
(2)
related
coronaviruses
activate
TLR3,
RIG1
NLRP3.
(3)
cannot,
therefore,
account
for
innate
receptor
activation
pattern
(IRAP)
found
severe
patients.
(4)
also
differs
its
form
being
fungal
infections.
(5)
Respiratory
TLR2,
(6)
A
combination
bacterial/fungal
coinfections
accounts
IRAP
why
it
cases.
(7)
Notably,
TLR7
(viral)
TLR4
(bacterial/fungal)
synergize,
(both
bacterial/fungal)
synergize
TLR2
(viral
bacterial).
(8)
Thus,
SARS-CoV-2-bacterium/fungus
coinfection
produces
activation,
resulting
hyperinflammation
characteristic
storm.
Unique
clinical,
experimental
therapeutic
predictions
(such
as
melatonin
effective
treating
COVID-19)
are
discussed,
broader
implications
outlined
understanding
syndromes
such
acute
lung
injury,
respiratory
distress
syndrome
sepsis
display
varied
storm
symptoms.
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2021,
Volume and Issue:
11
Published: May 26, 2021
COVID-19
is
a
zoonotic
disease
with
devastating
economic
and
public
health
impacts
globally.
Being
novel
disease,
current
research
focused
on
clearer
understanding
of
the
mechanisms
involved
in
its
pathogenesis
viable
therapeutic
strategies.
Oxidative
stress
inflammation
are
intertwined
processes
that
play
roles
progression
response
to
therapy
via
interference
multiple
signaling
pathways.
The
redox
status
host
cell
an
important
factor
viral
entry
due
unique
conditions
required
for
conformational
changes
ensure
binding
virus
into
cell.
Upon
airways,
replication
occurs
innate
immune
system
responds
by
activating
macrophage
dendritic
cells
which
contribute
inflammation.
This
review
examines
available
literature
proposes
oxidative
could
pathogenesis.
Further,
certain
antioxidants
currently
undergoing
some
form
trial
patients
corresponding
gaps
highlighted
show
how
targeting
ameliorate
severity.
Diseases,
Journal Year:
2020,
Volume and Issue:
8(4), P. 44 - 44
Published: Nov. 26, 2020
The
therapeutic
potential
of
melatonin
as
a
chronobiotic
cytoprotective
agent
to
counteract
the
consequences
COVID-19
infections
has
been
advocated.
Because
its
wide-ranging
effects
an
antioxidant,
anti-inflammatory,
and
immunomodulatory
compound,
could
be
unique
in
impairing
SARS-CoV-2
infection.
Moreover,
indirect
evidence
points
out
possible
antiviral
action
by
interfering
with
SARS-CoV-2/angiotensin-converting
enzyme
2
association.
Melatonin
is
also
effective
reverse
circadian
disruption
social
isolation
control
delirium
severely
affected
patients.
As
cytoprotector,
serves
combat
several
comorbidities
such
diabetes,
metabolic
syndrome,
ischemic
non-ischemic
cardiovascular
diseases,
which
aggravate
disease.
In
view
on
occurrence
neurological
sequels
COVID-19-infected
patients,
another
putative
application
emerges
based
neuroprotective
properties.
Since
means
cognitive
decay
minimal
impairment,
significance
for
infection
should
considered.
Finally,
yet
importantly,
exogenous
can
adjuvant
capable
augmenting
efficacy
anti-SARS-CoV-2
vaccines.
We
discuss
this
review
experimental
suggesting
that
“silver
bullet”
COVID
19
pandemic.
Journal of Medical Virology,
Journal Year:
2021,
Volume and Issue:
94(1), P. 263 - 271
Published: Aug. 30, 2021
Abstract
This
trial
aims
to
evaluate
the
effectiveness
of
adding
melatonin
treatment
protocol
hospitalized
coronavirus
disease
2019
(COVID‐19)
patients.
was
an
open‐label,
randomized
controlled
clinical
in
COVID‐19
Patients
were
into
a
arm
receiving
plus
standard
care
or
control
alone.
The
trial's
primary
endpoint
sleep
quality
examined
by
Leeds
Sleep
Evaluation
Questionnaire
(LSEQ).
secondary
endpoints
symptoms
alleviation
Day
7,
intensive
unit
admission,
10‐day
mortality,
white
blood
cell
count,
lymphocyte
C‐reactive
protein
status,
and
peripheral
capillary
oxygen
saturation.
Ninety‐six
patients
recruited
allocated
either
(
n
=
48)
48).
Baseline
characteristics
similar
across
arms.
There
no
significant
difference
on
7.
mean
LSEQ
scores
significantly
higher
group
p
<
0.001).
laboratory
data,
except
for
saturation,
which
has
improved
compared
with
(95.81%
vs.
93.65%
respectively,
0.003).
study
showed
that
combination
oral
tablets
could
substantially
improve
saturation
Frontiers in Neurology,
Journal Year:
2021,
Volume and Issue:
11
Published: Jan. 28, 2021
Clinical
reports
of
neurological
manifestations
associated
with
severe
coronavirus
disease
2019
(COVID-19),
such
as
acute
ischemic
stroke
(AIS),
encephalopathy,
seizures,
headaches,
necrotizing
encephalitis,
cerebral
microbleeds,
posterior
reversible
leukoencephalopathy
syndrome,
hemophagocytic
lymphohistiocytosis,
peripheral
neuropathy,
cranial
nerve
palsies,
transverse
myelitis,
and
demyelinating
disorders,
are
increasing
rapidly.
However,
there
comparatively
few
studies
investigating
the
potential
impact
immunological
responses
secondary
to
hypoxia,
oxidative
stress,
excessive
platelet-induced
aggregation
on
brain.
This
scoping
review
has
focused
pathophysiological
mechanisms
consequential
neural
(central)
inflammation
leading
COVID-19-related
strokes.
It
also
highlights
common
biological
processes
shared
between
AIS
COVID-19
infection
importance
recognition
that
respiratory
dysfunction
impairments
COVID
chronic
[post-COVID-19
syndrome
(PCNS)]
may
significantly
recovery
ability
benefit
from
neurorehabilitation.
study
provides
a
comprehensive
pathobiology
stroke.
affirms
contribution
pathophysiology
is
predictive
sequelae
particularly
stroke,
which
makes
it
expectation
rather
than
exception.
work
fundamental
significance
neurorehabilitation
community
given
number
COVID-related
strokes,
current
limited
knowledge
regarding
risk
reinfection,
recent
PCNS.
further
need
for
global
collaboration
research
into
new
pathobiology-based
treatment
strategies
more
integrated
evidence-based
care.
Molecules,
Journal Year:
2020,
Volume and Issue:
25(19), P. 4410 - 4410
Published: Sept. 25, 2020
Fighting
infectious
diseases,
particularly
viral
infections,
is
a
demanding
task
for
human
health.
Targeting
the
pathogens
or
targeting
host
are
different
strategies,
but
with
an
identical
purpose,
i.e.,
to
curb
pathogen’s
spreading
and
cure
illness.
It
appears
that
increase
tolerance
against
can
be
of
substantial
advantage
strategy
used
in
evolution.
Practically,
it
has
broader
protective
spectrum
than
only
specific
pathogens,
which
differ
terms
susceptibility.
Methods
applied
one
pandemic
even
effective
upcoming
pandemics
pathogens.
This
more
urgent
if
we
consider
possible
concomitance
two
respiratory
diseases
potential
multi-organ
afflictions
such
as
Coronavirus
disease
2019
(COVID-19)
seasonal
flu.
Melatonin
molecule
enhance
host’s
pathogen
invasions.
Due
its
antioxidant,
anti-inflammatory,
immunoregulatory
activities,
melatonin
capacity
reduce
severity
mortality
deadly
virus
infections
including
COVID-19.
synthesized
functions
mitochondria,
play
critical
role
infections.
Not
surprisingly,
synthesis
become
target
strategies
manipulate
mitochondrial
status.
For
example,
infection
switch
energy
metabolism
from
respiration
widely
anaerobic
glycolysis
plenty
oxygen
available
(the
Warburg
effect)
when
cell
cannot
generate
acetyl-coenzyme
A,
metabolite
required
biosynthesis.
Under
some
conditions,
aging,
gender,
predisposed
health
already
compromised
exposed
further
challenges,
lose
their
producing
sufficient
amounts
melatonin.
leads
reduced
support
makes
these
individuals
vulnerable
diseases.
Thus,
maintenance
function
by
supplementation
expected
beneficial
effects
on
outcome