Frontiers in Microbiology,
Journal Year:
2022,
Volume and Issue:
13
Published: Sept. 23, 2022
Patients
infected
with
SARS-CoV-2
at
various
severities
have
different
clinical
manifestations
and
treatments.
Mild
or
moderate
patients
usually
recover
conventional
medical
treatment,
but
severe
require
prompt
professional
treatment.
Thus,
stratifying
for
targeted
treatment
is
meaningful.
A
computational
workflow
was
designed
in
this
study
to
identify
key
blood
methylation
features
rules
that
can
distinguish
the
severity
of
infection.
First,
expression
profile
were
deeply
analyzed
by
a
Monte
Carlo
feature
selection
method.
list
generated.
Next,
ranked
fed
into
incremental
method
determine
optimal
classification
algorithms,
thereby
further
building
classifiers.
These
selected
functional
enrichment
detect
their
biofunctional
information.
Furthermore,
set
up
white-box
algorithm,
decision
tree,
uncover
patterns
on
Some
genes
(PARP9,
MX1,
IRF7),
corresponding
essential
sites,
validated
published
academic
literature.
Overall,
contributes
revealing
potential
provides
reference
patient
stratification.
The
physicians
prioritize
allocate
health
resources
COVID-19
based
predicted
outcomes.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(20), P. 12292 - 12292
Published: Oct. 14, 2022
The
highly
transmittable
and
infectious
COVID-19
remains
a
major
threat
worldwide,
with
the
elderly
comorbid
individuals
being
most
vulnerable.
While
vaccines
are
currently
available,
therapeutic
drugs
will
help
ease
viral
outbreak
prevent
serious
health
outcomes.
Epigenetic
modifications
regulate
gene
expression
through
changes
in
chromatin
structure
have
been
linked
to
pathophysiology.
Since
epigenetic
contribute
life
cycle
of
virus
host
immune
responses
infection,
promising
treatment
targets
ameliorate
COVID-19.
Deficiency
multifunctional
secosteroid
hormone
vitamin
D
is
global
threat.
Vitamin
its
receptor
function
genes
involved
immunity,
apoptosis,
proliferation,
differentiation,
inflammation.
Amassed
evidence
also
indicates
biological
relations
reduced
disease
risk,
while
can
be
modulated
by
mechanisms.
immunomodulatory
effects
suggest
role
for
as
agent.
Therefore,
this
review
highlights
on
proposing
infections.
Scandinavian Journal of Immunology,
Journal Year:
2022,
Volume and Issue:
97(3)
Published: Dec. 21, 2022
SARS-CoV-2
triggers
inflammasome-dependent
release
of
pro-inflammatory
cytokine
IL-1β
and
pyroptosis,
therefore,
contributes
to
the
huge
inflammatory
response
observed
in
severe
COVID-19
patients.
Less
is
known
about
engagement
inflammasome
neutrophils,
main
players
tissue
injury
infection.
We
studied
activation
neutrophils
from
patients
assessed
its
consequence
term
cells
contribution
disease
pathogenesis.
demonstrated
that
NLRP3
dramatically
activated
specific
inhibition
reverts
neutrophils'
activation.
Next,
stimulation
patients'
with
common
stimuli
was
not
able
further
activate
inflammasome,
possibly
due
exhaustion
or
increased
percentage
circulating
immature
neutrophils.
Collectively,
our
results
demonstrate
hyperactivated
may
be
responsible
for
susceptibility
subsequent
(and
lethal)
infections.
Our
findings
thus
include
a
novel
piece
complex
puzzle
Epigenetics,
Journal Year:
2022,
Volume and Issue:
17(13), P. 1875 - 1891
Published: June 26, 2022
A
majority
of
SARS-CoV-2
recoverees
develop
only
mild-to-moderate
symptoms,
while
some
remain
completely
asymptomatic.
Although
viruses,
including
SARS-CoV-2,
may
evade
host
immune
responses
by
epigenetic
mechanisms
DNA
methylation,
little
is
known
about
whether
these
modifications
are
important
in
defence
against
and
healthy
recovery
from
COVID-19
the
host.
To
this
end,
epigenome-wide
methylation
patterns
convalescents
were
compared
to
uninfected
controls
before
after
pandemic.
Peripheral
blood
mononuclear
cell
(PBMC)
was
extracted
controls,
convalescents,
symptom-free
individuals
with
SARS-CoV-2-specific
T
cell-responses,
as
well
PBMCs
stimulated
vitro
SARS-CoV-2.
Subsequently,
Illumina
MethylationEPIC
850K
array
performed,
statistical/bioinformatic
analyses
comprised
differential
pathway
over-representation,
module
identification
analyses.
Differential
distinguished
similar
results
an
experimental
infection
model.
SARS-CoV-2-induced
identified
vivo,
comprising
66
genes
which
six
(TP53,
INS,
HSPA4,
SP1,
ESR1,
FAS)
present
corresponding
Over-representation
revealed
involvement
Wnt,
muscarinic
acetylcholine
receptor
signalling,
gonadotropin-releasing
hormone
pathways.
Furthermore,
numerous
differentially
methylated
network
both
settings
interacted
interactome.
Altered
suggest
leaves
longstanding
traces.
Both
vivo
exposure
caused
modulation
pathways
thataffect
odour
perception.
Future
studies
should
determine
reflects
host-induced
protective
antiviral
defense
or
targeted
viral
hijacking
defence.
Epigenomics,
Journal Year:
2023,
Volume and Issue:
15(4), P. 227 - 248
Published: Feb. 1, 2023
The
COVID-19
outbreak
has
created
disaster
globally,
and
mankind
is
yet
to
come
in
terms
with
combating
this
global
menace.
Amid
turmoil,
immunocompromised
individuals
like
cancer
patients
exhibit
dismal
immune
responses
toward
such
infection.
In
order
treat
during
adverse
situations,
it
necessary
understand
the
phenomena
that
interlink
these
two
diseased
states.
Modulation
of
host
epigenetic
landscape
a
key
hallmark
both
viral
infections,
including
COVID-19.
Our
review
aims
shed
light
upon
interplay
between
cancer,
primarily
through
genetic
modulations
gene
expression
profile,
so
as
design
better
therapeutic
strategies
near
future.
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2023,
Volume and Issue:
13
Published: Dec. 13, 2023
Background
Despite
the
significant
progress
achieved
in
understanding
pathology
and
clinical
management
of
SARS-CoV-2
infection,
still
pathogenic
issues
need
to
be
clarified.
Treatment
with
modulators
epigenetic
targets,
i.e.,
epidrugs,
is
a
current
therapeutic
option
several
cancers
could
represent
an
approach
therapy
viral
diseases.
Results
Aim
this
study
was
analysis
role
histone
deacetylase
(HDAC)
inhibition
modulation
infection
mesothelial
cells
(MCs).
MeT5A
cells,
pleura
MC
line,
were
pre-treated
different
specific
class
I
IIb
HDAC
inhibitors.
Unexpectedly,
treatment
HDAC1-3
inhibitors
significantly
increased
ACE2/TMPRSS2
expression,
suggesting
favoring
infection.
We
focused
our
on
most
potent
inducer
among
analysed,
MS-275,
inhibitor.
expression
validated
by
Western
Blot
(WB)
immunofluorescence.
The
involvement
receptor
induction
confirmed
HDAC1/HDAC2
silencing.
In
accordance
data,
MS-275
replication
virus
propagation
Vero
E6
cells.
Notably,
able
increase
production,
although
lesser
extent,
also
lung
adenocarcinoma
cell
line
Calu-3
Mechanistically,
H3
H4
acetylation
at
promoters,
increasing
their
transcription.
Conclusion
This
highlights
previously
unrecognized
effect
entry,
productive
correlating
ACE2
TMPRSS2.
These
while
adding
basic
insight
into
COVID-19
pathogenesis,
warn
for
use
patients.
Journal of Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12(1), P. 9 - 9
Published: Feb. 9, 2024
Developmental
biology
is
intricately
regulated
by
epigenetics
and
metabolism
but
the
mechanisms
are
not
completely
understood.
The
situation
becomes
even
more
complicated
during
diseases
where
all
three
phenomena
dysregulated.
A
salient
example
COVID-19,
death
toll
exceeded
6.96
million
in
4
years,
while
virus
continues
to
mutate
into
different
variants
infect
people.
Early
evidence
pandemic
showed
that
host’s
immune
inflammatory
responses
COVID-19
(like
cytokine
storm)
impacted
metabolism,
causing
damage
organs
overall
physiology.
involvement
of
angiotensin-converting
enzyme
2
(ACE2),
pivotal
host
receptor
for
SARS-CoV-2
virus,
was
identified
linked
epigenetic
abnormalities
along
with
other
contributing
factors.
Recently,
studies
have
revealed
stronger
connections
between
impact
development
accelerate
aging.
Patients
manifest
systemic
toxicity,
dysfunction
multi-organ
failure.
Single-cell
multiomics
state-of-the-art
high-throughput
only
just
beginning
demonstrate
extent
dysregulation
damage.
As
directly
development,
there
a
crucial
need
research
implementing
cutting-edge
technology,
next-generation
sequencing,
bioinformatics
analysis,
identification
biomarkers
clinical
trials
help
prevention
therapeutic
interventions
against
similar
threats
future.
European Journal of Clinical Investigation,
Journal Year:
2021,
Volume and Issue:
52(2)
Published: Sept. 28, 2021
Obesity
was
consistently
associated
with
a
poor
prognosis
in
patients
COVID-19.
Epigenetic
mechanisms
were
proposed
as
the
link
between
obesity
and
comorbidities
risk.To
evaluate
methylation
levels
of
angiotensin-converting
enzyme
2
(ACE2)
gene,
main
entry
receptor
SARS-CoV-2,
different
depots
adipose
tissue
(AT)
leukocytes
(PBMCs)
after
weight
loss
therapy
based
on
very-low-calorie
ketogenic
diet
(VLCKD),
balanced
hypocaloric
(HCD)
or
bariatric
surgery
(BS).DNA
ACE2
extracted
from
our
data
sets
generated
by
hybridization
subcutaneous
(SAT)
(n
=
32)
visceral
(VAT;
n
tissue,
PBMCs
34)
samples
Infinium
HumanMethylation450
BeadChips.
Data
compared
degree
4-6
months
either
following
nutritional
surgical
treatment
correlated
transcript
levels.As
normal
weight,
VAT
showed
higher
levels.
These
differences
mirrored
but
not
SAT.
The
observed
obesity-associated
reversed
VLCKD
HCD
BS.
Among
studied
CpG
sites,
cg16734967
cg21598868,
located
at
promoter,
most
affected
BMI.
DNA
pattern
inversely
expression.Obesity-related
shows
hypermethylation
downregulation
gene
that
is
restored
reduction
therapy.
results
warrant
necessity
to
further
its
implication
for
COVID-19
pathogenesis.