Genes,
Год журнала:
2023,
Номер
14(7), С. 1420 - 1420
Опубликована: Июль 10, 2023
The
role
of
genetics
as
a
predisposing
factor
related
to
an
increased
risk
developing
long
COVID
symptomatology
is
under
debate.
aim
the
current
secondary
analysis
was
identify
association
between
Apolipoprotein
E
(ApoE)
gene,
gene
affecting
cholesterol
metabolism
and
previously
associated
with
higher
SARS-CoV-2
infection
COVID-19
severity,
development
in
cohort
individuals
who
had
been
hospitalized
by
infection.
Unstimulated
whole
saliva
samples
were
collected
from
287
survivors.
Three
genotypes
ApoE
(ApoE
ε2,
ε3,
ε4)
obtained
based
on
combination
rs429358
rs7412
polymorphisms.
Participants
asked
self-report
presence
any
post-COVID
symptom
face-to-face
interview
at
17.8
±
5.2
months
after
hospital
discharge
medical
records
obtained.
Each
participant
reported
3.0
(1.9)
symptoms.
Overall,
no
significant
differences
symptoms
observed
depending
genotype
ε4).
ε4
genotype,
albeit
did
not
appear
predispose
for
our
Viruses,
Год журнала:
2023,
Номер
15(1), С. 175 - 175
Опубликована: Янв. 7, 2023
The
clinical
course
and
outcome
of
COVID-19
are
highly
variable,
ranging
from
asymptomatic
infections
to
severe
disease
death.
Understanding
the
risk
factors
is
relevant
both
in
setting
at
epidemiological
level.
Here,
we
provide
an
overview
host,
viral
environmental
that
have
been
shown
or
(in
some
cases)
hypothesized
be
associated
with
outcomes.
considered
detail
include
age
frailty,
genetic
polymorphisms,
biological
sex
(and
pregnancy),
co-
superinfections,
non-communicable
comorbidities,
immunological
history,
microbiota,
lifestyle
patient;
variation
infecting
dose;
socioeconomic
factors;
air
pollution.
For
each
category,
compile
(sometimes
conflicting)
evidence
for
association
factor
outcomes
(including
strength
effect)
outline
possible
action
mechanisms.
We
also
discuss
complex
interactions
between
various
factors.
Infection Genetics and Evolution,
Год журнала:
2023,
Номер
110, С. 105426 - 105426
Опубликована: Март 17, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
is
the
etiologic
agent
of
disease
2019
(COVID-19)
pandemic.
Clinical
manifestations
range
from
an
asymptomatic
condition
to
life-threatening
events
and
death,
with
more
severe
courses
being
associated
age,
male
sex,
comorbidities.
Besides
these
risk
factors,
intrinsic
characteristics
virus
as
well
genetic
factors
host
are
expected
account
for
COVID-19
clinical
heterogeneity.
Genetic
studies
have
long
been
recognized
fundamental
identify
biological
mechanisms
underlying
congenital
diseases,
pinpoint
genes/proteins
responsible
susceptibility
different
inherited
conditions,
highlight
targets
therapeutic
relevance,
suggest
drug
repurposing,
even
clarify
causal
relationships
that
make
modifiable
some
environmental
factors.
Though
usually
take
time
be
concluded
and,
above
all,
translate
their
discoveries
patients'
bedside,
scientific
community
moved
really
fast
deliver
signals
phenotypes.
In
this
Review,
besides
a
concise
description
symptomatology
SARS-CoV-2
mechanism
infection,
we
aimed
recapitulate
current
literature
in
terms
specifically
associate
increased
severity
disease.
Although
advanced
age,
male
sex,
and
some
comorbidities
impact
the
clinical
course
of
COVID-19,
these
factors
only
partially
explain
inter-individual
variability
in
disease
severity.
Some
studies
have
shown
that
genetic
polymorphisms
contribute
to
COVID-19
severity;
however,
results
are
inconclusive.
Thus,
we
investigated
association
between
ACE1,
ACE2,
DPP9,
IFIH1,
IFNAR2,
IFNL4,
TLR3,
TMPRSS2,
TYK2
COVID-19.
A
total
694
patients
with
were
categorized
as:
(1)
ward
inpatients
(moderate
symptoms)
or
admitted
at
intensive
care
unit
(ICU;
severe
symptoms);
(2)
survivors
non-survivors.
In
females,
rs1990760/IFIH1
T/T
genotype
was
associated
risk
ICU
admission
death.
Moreover,
rs1799752/ACE1
Ins
rs12329760/TMPRSS2
T
alleles
admission.
non-white
patients,
rs2236757/IFNAR2
A/A
admission,
while
Ins/Ins
genotype,
allele
analyzed
interact
worse
outcomes.
conclusion,
this
study
shows
an
rs1799752/ACE1,
rs1990760/IFIH1,
rs2236757/IFNAR2,
rs12329760/TMPRSS2,
rs2304256/TYK2
outcomes,
especially
among
female
patients.
BMC Medical Genomics,
Год журнала:
2025,
Номер
18(1)
Опубликована: Фев. 7, 2025
This
study
aims
to
investigate
the
association
between
candidate
host
genetic
polymorphisms
and
COVID-19
susceptibility,
severity,
hospitalization,
hypoxia,
their
combined
effect,
measured
by
polygenic
risk
score
(PRS).
Three
hundred
seventy-six
Lebanese
participants,
comprising
151
controls
225
cases,
were
included.
Clinical
data
obtained
from
questionnaires
medical
records.
DNA
isolated
peripheral
blood
was
genotyped
for
ACE1
rs1799752,
ACE2
rs2074192,
TMPRSS2
rs75603675
OAS1
rs107746771
using
TaqMan
assays,
rs35074065
Sanger
Sequencing.
Candidate
variants
analyzed
in
with
hospitalization
univariate
multivariate
models.
PRS
constructed
weighted
sum
of
evaluated
outcomes.
In
this
study,
there
no
statistically
significant
differences
frequencies
variant
alleles
within
disease
outcomes
subgroups,
after
adjustment
confounders.
not
associated
susceptibility
it
however
significantly
predicted
severity
(P
=
0.01).
highlights
importance
testing
key
genes
involved
life
cycle
eventually
measuring
which
proves
be
an
important
tool
prognosis
assessment
vulnerable
individuals,
potentially
enhancing
patient
care.
Frontiers in Pediatrics,
Год журнала:
2025,
Номер
13
Опубликована: Фев. 24, 2025
Recent
studies
have
underscored
the
importance
of
genetic
factors
in
predicting
COVID-19
susceptibility
and
severity.
While
cytokine
storms
are
crucial
disease
severity,
predisposition
significantly
influences
immune
responses.
Our
study
examined
genes
related
to
SARS-CoV-2
invasion
(ACE2
rs2074192)
interferon-induced
immunity
(IFNAR2
rs2236757,
TYK2
rs2304256,
OAS1
rs10774671,
OAS3
rs10735079).
Additionally,
we
investigated
linked
Kawasaki
(CD40
rs4813003,
FCGR2A
rs1801274,
CASP3
rs113420705)
that
play
roles
immunogenesis.
The
pilot
study,
which
involved
75
pediatric
patients
aged
one
month
17
years
[43
with
active
COVID-19,
children
multisystem
inflammatory
syndrome
(MIS-C),
15
healthy
controls],
was
conducted
Ternopil,
Ukraine.
Gene
polymorphism
studied
for
all
patients.
ELISA
kits
were
used
interleukin
studies,
including
Human
IL-1β
(Interleukin
1
Beta),
IL-6
6),
IL-8
8),
IL-12
12),
IFN-α
(Interferon
Alpha),
TNF-α
(Tumor
Necrosis
Factor
Alpha).
Statistical
analysis
performed
using
IBM
SPSS
Statistics
21
GraphPad
Prism
8.4.3.
identified
significant
gene-cytokine
associations
ACE2
rs2074192
T
allele
correlated
increased
IL-1β,
IL-6,
IL-8,
TNF-α.
IFNAR2
rs2236757
A
elevated
levels
low
levels,
while
rs10774671
carriers
also
exhibited
lower
levels.
prognostically
determining
infected
SARS-CoV-2.
gene
rs10735079
associated
changes
precisely
a
high
level.
CD40
rs4813003
C
had
higher
IL-12.
results
our
revealed
correlation
between
rs1801274
(A/G).
rs113420705
led
an
increase
IL-6.
These
findings
enhance
understanding
may
hold
promise
developing
targeted
interventions
providing
personalized
medical
approach
each
patient.
To
examine
the
clinical
outcomes
of
systemic
lupus
erythematosus
(SLE)
patients
with
COVID-19
during
Pre-Delta/Delta
and
Omicron
periods.
A
retrospective
study
was
conducted
in
a
cohort
adult
Puerto
Ricans
SLE.
Demographic
parameters,
SLE
manifestations,
comorbidities,
pharmacologic
treatment,
exacerbations,
hospitalizations,
mortality
were
determined.
SARS
CoV-2
infection
confirmed
by
polymerase
chain
reaction
or
antigen
tests.
Variables
compared
between
Pre-delta/Delta
Also,
proportion
cases
to
general
population
Rico.
Of
entire
(n
=
347),
169
(48.7%)
had
COVID-19.
Twenty-two
period
147
period.
The
significantly
higher
when
Rico
(25.7%),
but
no
difference
found.
Overall,
favorable,
low
rates
flares
(3.0%),
hospitalizations
(3.6%),
(0.6%).
Patients
more
likely
have
oral
ulcers,
anti-Smith
antibodies,
chronic
kidney
disease,
whereas
those
symptoms
(rhinorrhea,
sore
throat,
cough).
In
summary,
is
this
group
SLE,
high
COVID-19,
disease
exacerbation,
hospitalization,
low.
Few
differences
noted
comparing
Abstract
Background
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
causes
Coronavirus
disease
2019
(COVID-19),
which
is
a
huge
global
health
threat.
Interleukin27
(IL-27)
gene
cytokine
that
produces
antiviral
proteins
in
an
IFN-independent
manner
and
stimulates
both
pro-
anti-inflammatory
responses.
Interferon
induced
transmembrane
protein
3
(IFITM3)
inhibits
SARS-CoV2
infection
by
blocking
SARSCoV-2
spike
facilitate
viral
entrance
cell-to-cell
fusion.
The
association
between
genetic
variants
COVID-19
Egyptians
still
unclear.
Hence,
we
sought
to
investigate
the
impact
of
single
nucleotide
polymorphism
IL-27P28
rs153109
IFITM3
rs12252
on
susceptibility
severity
SARS-CoV-2
Egyptian
patients.
Methods
Our
study
included
242
patients
were
recruited
from
Main
University
Hospital,
Alexandria
University,
Egypt,
187
healthy
controls.
We
subdivided
patient
group
into
two
subgroups:
A
comprised
mild/moderate
cases
(N
=
42)
(17.4%),
B
severe/critical
200)
(82.6%).
Genomic
DNA
was
extracted
blood
samples
using
QIAamp
Blood
Mini
kit,
then
PCR
products
IL27
cut
FastDigest
XhoI
MScI,
respectively,
for
detection
SNPs
(-964A/G)
(T>C).
Results
present
found
significant
after
adjusting
risk
factor
(advanced
age),
AG
genotype
(OR
2.791,
95%
CI:
1.237–6.295,
P
0.013),
AA
2.385,
1.075–5.291,
0.033),
(AG+AA
vs.
GG)
genotypes
2.558,
1.186–5.517,
0.017).
On
other
hand,
rs12252(T>C)
CT
1.419,
0.843–2.391,
0.188),
CC
2.132,
0.436–10.415,
0.350),
(C/T+C/C
TT)
1.466,
0.884–2.432,
0.138)
did
not
show
statistically
with
either
or
SARS-CoV-2.
Conclusion
IL27P28
may
be
associated
but
severity.
Concerning
SNP,
could
confirm
its
influence
this
population.
Journal of Clinical Medicine,
Год журнала:
2025,
Номер
14(6), С. 1931 - 1931
Опубликована: Март 13, 2025
Background/Objectives:
To
elucidate
the
factors
that
contribute
to
individual
variability
in
progression
of
COVID-19,
experiments
on
endothelial
nitric
oxide
synthase
polymorphisms
have
been
reported.
Nitric
(NOS3)
is
located
endothelium
and
involved
regulation
inflammation
vascular
homeostasis.
In
this
study,
we
investigated
association
between
COVID-19
severity
NOS3
G894T
27-bp
VNTR
4b/a
genetic
polymorphisms.
Methods:
Patients
with
(n
=
178)
were
divided
into
Group
1
(mild
disease)
2
(severe
based
oxygen
saturation
levels
room
air
(Group
1,
SpO2
≥
93%,
n
107;
2,
<
73)
hospitalization
requirements.
Genotyping
was
performed
using
polymerase
chain
reaction-restriction
fragment
length
polymorphism
analysis.
Results:
Overall,
genotype
allele
frequencies
similar
across
two
study
groups
(p
>
0.05).
However,
subgroup
analysis
showed
a
notable
trend
for
4b/4a
distribution
Groups
2.
younger
patients
(≤50
years
old)
without
chronic
obstructive
pulmonary
disease,
tended
higher
frequency
4b
than
(97.4%
vs.
85.4%
p
0.06)
occurrence
4b/4b
(94.7%
74.0%,
Additionally,
rarely
observed
4c
detected
only
subjects
within
but
not
1.
Conclusions:
These
findings
suggest
polymorphism.
Genetic
may
reveal
patient
susceptibility
prognosis
risk
factors,
drug
responsiveness.
SCRIPTA MEDICA,
Год журнала:
2025,
Номер
56(1), С. 105 - 115
Опубликована: Янв. 1, 2025
Background/Aim:
Numerous
reports
have
been
published
on
the
association
of
chemokine
receptor
5
D32
genetic
variation
(rs333)
with
risk
multiple
sclerosis
(MS),
results
that
are
inconsistent.
The
relationship
between
rs333
and
susceptibility
to
MS
was
evaluated
in
this
study.
Methods:
PRISMA
guidelines
were
followed
current
Twelve
databases
used
find
eligible
articles.
investigators
extracted
necessary
information.
associations
alleles
genotypes
different
models
inheritance:
co-dominant,
dominant
recessive
genotype
allele
model.
Results:
analysis
included
14
articles
reporting
16
studies
involving
3265
patients
3735
healthy
controls.
There
no
substantial
heterogeneity
for
any
comparisons.
significance
level
not
reached
susceptibility.
Conclusion:
findings
study
could
confirm
sclerosis.