Cureus,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 26, 2024
The
Spike
protein
enables
the
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
by
binding
to
multiple
receptors,
including
angiotensin-converting
enzyme
(ACE2).
Scientific
studies
also
indicate
that
is
involved
in
forms
of
disease
2019
(COVID-19),
"long-haul
COVID
diseases"
-
known
as
"long
syndromes"
or
"post-acute
sequelae
SARS-CoV-2
infection"
(PACS)
or,
recently,
adverse
reactions
lipid
nanoparticle-messenger
ribonucleic
acid
(mRNA)
vaccines
other
anti-COVID19
products.
Numerous
mutations,
notably
within
subunit
1
(S1),
prevent
neutralization
antibodies,
but
more
generally,
virus
has
developed
numerous
strategies
avoid
immune
system
surveillance,
especially
type-I
interferons
(IFN-I).
Meanwhile,
a
"hyperinflammatory"
state,
named
"cytokine
storm,"
sets
in.
However,
what
role
does
play
escape
mechanisms?
Can
its
inflammatory
activities
affect
IFN-I?
Does
block
IFN-I
hijack
them
for
benefits?
What
are
potential
consequences?
This
article
was
written
provide
an
up-to-date
and
general
overview
impact
on
innate
effectors
at
molecular
level.
BMC Research Notes,
Journal Year:
2024,
Volume and Issue:
17(1)
Published: Oct. 27, 2024
Abstract
Objective
This
study
aimed
to
evaluate
the
roles
of
galectin-3
and
irisin
as
biomarkers
in
predicting
severe
outcomes
COVID-19
patients.
Results
We
analyzed
serum
levels
59
patients
with
30
healthy
controls.
Elevated
were
associated
increased
risks
mortality,
need
for
intensive
care,
acute
respiratory
distress
syndrome.
The
optimal
cut-off
value
was
13.47
ng/ml,
a
sensitivity
72.7%
specificity
76.6%.
Irisin
did
not
differ
significantly
between
survivors
non-survivors
at
admission
or
on
3rd
day
post-admission,
but
approached
significance
7th
day.
These
findings
suggest
that
could
be
valuable
prognostic
biomarker
outcomes,
while
irisin’s
role
remains
clarified
further
studies.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(13), P. 7314 - 7314
Published: June 30, 2022
Galectin-3
binding
protein
(Gal-3BP)
is
a
multifunctional
glycoprotein
involved
in
cell–cell
and
cell–matrix
interactions
known
to
be
upregulated
cancer
various
viral
infections,
including
HIV-1,
HCV,
SARS-CoV-2,
with
key
role
regulating
the
antiviral
immune
response.
Studies
have
identified
direct
correlation
between
circulating
levels
of
Gal-3BP
severity
disease
and/or
progression
for
some
suggesting
these
processes.
Due
Gal-3BP’s
complex
biology,
molecular
mechanisms
underlying
its
diseases
been
only
partially
clarified.
induces
expression
interferons
(IFNs)
proinflammatory
cytokines,
interleukin-6
(IL-6),
mainly
interacting
galectin-3,
targeting
TNF
receptor-associated
factors
(TRAF-6
TRAF-3)
complex,
thus
having
putative
modulation
TGF-β
signaling.
In
addition,
an
activity
has
ascribed
interaction
virus
components.
this
review,
we
explored
infections
relationship
upregulation
progression,
focusing
on
SARS-CoV-2.
Augmented
knowledge
can
useful
evaluate
possible
use
as
prognostic
biomarker
target
block
or
attenuate
severe
disease.
Therapeutic Advances in Respiratory Disease,
Journal Year:
2023,
Volume and Issue:
17
Published: Jan. 1, 2023
The
central
role
of
inflammatory
progression
in
the
development
Coronavirus
disease
2019
(COVID-19),
especially
severe
cases,
is
indisputable.
However,
some
novel
biomarkers
prognosis
COVID-19
remains
controversial.
Cureus,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 26, 2024
The
Spike
protein
enables
the
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infection
by
binding
to
multiple
receptors,
including
angiotensin-converting
enzyme
(ACE2).
Scientific
studies
also
indicate
that
is
involved
in
forms
of
disease
2019
(COVID-19),
"long-haul
COVID
diseases"
-
known
as
"long
syndromes"
or
"post-acute
sequelae
SARS-CoV-2
infection"
(PACS)
or,
recently,
adverse
reactions
lipid
nanoparticle-messenger
ribonucleic
acid
(mRNA)
vaccines
other
anti-COVID19
products.
Numerous
mutations,
notably
within
subunit
1
(S1),
prevent
neutralization
antibodies,
but
more
generally,
virus
has
developed
numerous
strategies
avoid
immune
system
surveillance,
especially
type-I
interferons
(IFN-I).
Meanwhile,
a
"hyperinflammatory"
state,
named
"cytokine
storm,"
sets
in.
However,
what
role
does
play
escape
mechanisms?
Can
its
inflammatory
activities
affect
IFN-I?
Does
block
IFN-I
hijack
them
for
benefits?
What
are
potential
consequences?
This
article
was
written
provide
an
up-to-date
and
general
overview
impact
on
innate
effectors
at
molecular
level.
