Viruses,
Год журнала:
2022,
Номер
14(10), С. 2270 - 2270
Опубликована: Окт. 16, 2022
Coronavirus
Disease
2019
(COVID-19)
is
associated
with
increased
incidence
of
neurological
diseases
and
neuropsychiatric
disorders
after
infection,
but
how
it
contributes
to
their
development
remains
under
investigation.
Here,
we
investigate
the
possible
relationship
between
COVID-19
ten
three
by
exploring
two
pathological
mechanisms:
(i)
dysregulation
host
biological
processes
via
virus–host
protein–protein
interactions
(PPIs),
(ii)
autoreactivity
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
epitopes
“self”
proteins
molecular
mimicry.
We
also
identify
potential
genetic
risk
factors
which
in
combination
SARS-CoV-2
infection
might
lead
disease
development.
Our
analysis
indicated
that
neurodegenerative
(NDs)
have
a
higher
number
disease-associated
can
be
modulated
PPIs
than
disorders.
The
sequence
similarity
presence
several
matching
5-mer
and/or
6-mer
linear
motifs
autoreactive
found
Alzheimer’s
(AD),
Parkinson’s
(PD),
Myasthenia
Gravis
(MG)
Multiple
Sclerosis
(MS).
results
include
recognize
amyloid-beta
precursor
protein
(APP),
microtubule-associated
tau
(MAPT),
acetylcholine
receptors,
glial
fibrillary
acidic
(GFAP),
neurofilament
light
polypeptide
(NfL)
major
myelin
proteins.
Altogether,
our
suggest
there
an
for
NDs
both
PPIs.
The
ability
of
a
virus
to
spread
between
individuals,
its
replication
capacity
and
the
clinical
course
infection
are
macroscopic
consequences
multifaceted
molecular
interaction
viral
components
with
host
cell.
heavy
impact
COVID-19
on
world
population,
economics
sanitary
systems
calls
for
therapeutic
prophylactic
solutions
that
require
deep
characterization
interactions
occurring
cells.
Unveiling
how
SARS-CoV-2
engages
factors
throughout
life
cycle
is
therefore
fundamental
understand
pathogenic
mechanisms
underlying
design
antiviral
therapies
strategies.
Two
years
into
pandemic,
this
review
provides
an
overview
interplay
cell,
focus
machinery
compartments
pivotal
cellular
response.
Starting
cell
surface,
following
replicative
through
entry
pathways,
survival
in
cytoplasm,
egress
from
infected
unravels
complex
network
highlighting
knowledge
has
potential
set
basis
development
innovative
The
outcome
of
infection
is
dependent
on
the
ability
viruses
to
manipulate
infected
cell
evade
immunity,
and
immune
response
overcome
this
evasion.
Understanding
process
key
understanding
pathogenesis,
genetic
risk
factors,
both
natural
vaccine-induced
immunity.
SARS-CoV-2
antagonises
innate
interferon
response,
but
whether
it
manipulates
cellular
immunity
unclear.
An
unbiased
proteomic
analysis
determined
how
surface
protein
expression
altered
SARS-CoV-2-infected
lung
epithelial
cells,
showing
downregulation
activating
NK
ligands
B7-H6,
MICA,
ULBP2,
Nectin1,
with
minimal
effects
MHC-I.
This
occurred
at
level
synthesis,
could
be
mediated
by
Nsp1
Nsp14,
correlated
a
reduction
in
activation.
identifies
novel
mechanism
which
host-shutoff
Later
disease
process,
strong
antibody-dependent
activation
(ADNKA)
developed.
These
responses
were
sustained
for
least
6
months
most
patients,
led
high
levels
pro-inflammatory
cytokine
production.
Depletion
spike-specific
antibodies
confirmed
their
dominant
role
neutralisation,
these
played
only
minor
ADNKA
compared
other
proteins,
including
ORF3a,
Membrane,
Nucleocapsid.
In
contrast,
induced
following
vaccination
was
focussed
solely
spike,
weaker
than
infection,
not
boosted
second
dose.
insights
have
important
implications
progression,
vaccine
efficacy,
design.
Frontiers in Cellular and Infection Microbiology,
Год журнала:
2024,
Номер
14
Опубликована: Фев. 5, 2024
Following
virus
recognition
of
host
cell
receptors
and
viral
particle/genome
internalization,
viruses
replicate
in
the
via
hijacking
essential
machinery
components
to
evade
provoked
antiviral
innate
immunity
against
invading
pathogen.
Respiratory
infections
are
usually
acute
with
ability
activate
pattern
(PRRs)
in/on
cells,
resulting
production
release
interferons
(IFNs),
proinflammatory
cytokines,
chemokines,
IFN-stimulated
genes
(ISGs)
reduce
fitness
mitigate
infection.
Nevertheless,
game
between
is
a
complicated
dynamic
process,
which
they
restrict
each
other
specific
factors
maintain
their
own
advantages
win
this
game.
The
primary
role
non-structural
protein
1
(NS1
Nsp1)
influenza
A
(IAV)
pandemic
severe
respiratory
syndrome
coronavirus
2
(SARS-CoV-2),
respectively,
control
host-induced
immune
responses.
This
review
provides
comprehensive
overview
genesis,
spatial
structure,
cellular
interactors,
mechanisms
underlying
unique
biological
functions
IAV
NS1
SARS-CoV-2
Nsp1
infected
cells.
We
also
highlight
both
proteins
modulating
replication
pathogenicity.
Eventually,
because
important
during
infection,
we
describe
promising
potential
as
targets
for
therapy
development
live
attenuated
vaccines
(LAV).
Conclusively,
play
an
virus–host
interactions,
replication,
pathogenesis,
pave
way
develop
novel
prophylactic
and/or
therapeutic
interventions
treatment
these
human
pathogens.
Vaccines,
Год журнала:
2021,
Номер
9(11), С. 1317 - 1317
Опубликована: Ноя. 12, 2021
Respiratory
viruses
represent
a
major
public
health
concern,
as
they
are
highly
mutated,
resulting
in
new
strains
emerging
with
high
pathogenicity.
Currently,
the
world
is
suffering
from
newly
evolving
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2).
This
virus
cause
of
disease
2019
(COVID-19),
mild-to-severe
tract
infection
frequent
ability
to
give
rise
fatal
pneumonia
humans.
The
overwhelming
outbreak
SARS-CoV-2
continues
unfold
all
over
world,
urging
scientists
put
an
end
this
global
pandemic
through
biological
and
pharmaceutical
interventions.
there
no
specific
treatment
option
that
capable
COVID-19
eradication,
so
several
repurposed
drugs
conditionally
approved
vaccines
use
heavily
applied
control
pandemic.
emergence
variants
partially
or
totally
escape
immune
response
elicited
by
requires
continuous
monitoring
update
content
developed
modify
them
match
variants.
Herein,
we
discuss
potential
therapeutic
prophylactic
interventions
including
developed/approved
vaccines,
highlighting
impact
evolution
on
evasion
currently
licensed
for
COVID-19.
Journal of Clinical Medicine,
Год журнала:
2023,
Номер
12(17), С. 5501 - 5501
Опубликована: Авг. 24, 2023
Several
studies
have
reported
that
viral
infection
is
closely
associated
with
the
onset,
progression,
and
exacerbation
of
asthma.
The
purpose
this
review
to
summarize
role
infections
in
pathogenesis
asthma
onset
exacerbations,
as
well
discuss
interrelated
protective
risk
factors
current
treatment
options.
Furthermore,
we
present
knowledge
innate
immunological
pathways
driving
host
defense,
including
changes
epithelial
barrier.
In
addition,
highlight
importance
genetics
epigenetics
virus
susceptibility.
Moreover,
involvement
etiology
from
bronchiolitis
childhood
wheezing
described.
characterization
mechanisms
action
respiratory
viruses
most
frequently
related
are
mentioned.
Frontiers in Veterinary Science,
Год журнала:
2022,
Номер
9
Опубликована: Апрель 8, 2022
Infectious
bronchitis
virus
(IBV)
is
the
first
coronavirus
discovered
in
world,
which
also
prototype
of
gamma-coronaviruses.
Nowadays,
IBV
widespread
all
over
world
and
has
become
one
causative
agent
causing
severe
economic
losses
poultry
industry.
Generally,
it
believed
that
viral
replication
immune
evasion
functions
were
modulated
by
non-structural
accessory
proteins,
considered
as
causes
for
its
pathogenicity.
In
this
study,
we
summarized
current
knowledge
about
proteins.
Some
proteins
such
nsp2,
nsp3,
nsp15
have
been
shown
to
antagonize
host
innate
response.
Also,
nsp7
nsp16
can
block
antigen
presentation
inhibit
adapted
addition,
nsp13,
nsp14,
are
participating
formation
mRNA
cap
limit
recognition
system.
conclusion,
vital
importance
understand
could
help
us
further
explore
pathogenesis
provide
new
horizons
prevention
treatment
future.
