Viruses,
Journal Year:
2023,
Volume and Issue:
15(2), P. 352 - 352
Published: Jan. 26, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
is
the
causative
agent
of
disease
2019
(COVID-19)
pandemic
that
has
caused
disastrous
effects
on
society
and
human
health
globally.
SARS-CoV-2
a
sarbecovirus
in
Coronaviridae
family
with
positive-sense
single-stranded
RNA
genome.
It
mainly
replicates
cytoplasm
viral
components
including
RNAs
proteins
can
be
sensed
by
pattern
recognition
receptors
toll-like
(TLRs),
RIG-I-like
(RLRs),
NOD-like
(NLRs)
regulate
host
innate
adaptive
immune
responses.
On
other
hand,
genome
encodes
multiple
antagonize
response
to
facilitate
replication.
In
this
review,
we
discuss
current
knowledge
sensors
countermeasures
against
provide
insights
virus–host
interactions
novel
approaches
modulate
inflammation
antiviral
Science,
Journal Year:
2022,
Volume and Issue:
375(6585), P. 1122 - 1127
Published: March 10, 2022
Considerable
research
effort
has
been
made
worldwide
to
decipher
the
immune
response
triggered
upon
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
infections,
identify
drivers
of
and
fatal
COVID-19,
understand
what
leads
prolongation
symptoms
after
disease
resolution.
We
review
results
almost
years
COVID-19
immunology
discuss
definitive
findings
remaining
questions
regarding
our
understanding
pathophysiology.
emerging
differences
in
responses
seen
those
with
without
Long
Covid
syndrome,
also
known
as
post-acute
sequelae
SARS-CoV-2.
hope
that
knowledge
gained
from
this
will
be
applied
studies
inflammatory
processes
involved
critical
chronic
illnesses,
which
remain
a
major
unmet
need.
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: Dec. 5, 2022
Abstract
The
outbreak
of
COVID-19
has
become
a
global
crisis,
and
brought
severe
disruptions
to
societies
economies.
Until
now,
effective
therapeutics
against
are
in
high
demand.
Along
with
our
improved
understanding
the
structure,
function,
pathogenic
process
SARS-CoV-2,
many
small
molecules
potential
anti-COVID-19
effects
have
been
developed.
So
far,
several
antiviral
strategies
were
explored.
Besides
directly
inhibition
viral
proteins
such
as
RdRp
M
pro
,
interference
host
enzymes
including
ACE2
proteases,
blocking
relevant
immunoregulatory
pathways
represented
by
JAK/STAT,
BTK,
NF-κB,
NLRP3
pathways,
regarded
feasible
drug
development.
development
treat
achieved
strategies,
computer-aided
lead
compound
design
screening,
natural
product
discovery,
repurposing,
combination
therapy.
Several
representative
remdesivir
paxlovid
proved
or
authorized
emergency
use
countries.
And
candidates
entered
clinical-trial
stage.
Nevertheless,
due
epidemiological
features
variability
issues
it
is
necessary
continue
exploring
novel
COVID-19.
This
review
discusses
current
findings
for
treatment.
Moreover,
their
detailed
mechanism
action,
chemical
structures,
preclinical
clinical
efficacies
discussed.
Immunological Reviews,
Journal Year:
2022,
Volume and Issue:
310(1), P. 76 - 92
Published: May 22, 2022
Abstract
The
COVID‐19
pandemic
has
caused
an
unprecedented
health
crisis
and
economic
burden
worldwide.
Its
etiological
agent
SARS‐CoV‐2,
a
new
virus
in
the
coronavirus
family,
infected
hundreds
of
millions
people
SARS‐CoV‐2
evolved
over
past
2
years
to
increase
its
transmissibility
as
well
evade
immunity
established
by
previous
infection
vaccination.
Nevertheless,
strong
immune
responses
can
be
elicited
viral
vaccination,
which
have
proved
protective
against
emergence
variants,
particularly
with
respect
hospitalization
or
severe
disease.
Here,
we
review
our
current
understanding
how
enters
host
cell
system
is
able
defend
entry
infection.
Neutralizing
antibodies
are
major
component
defense
been
extensively
studied
for
variants.
Structures
these
neutralizing
provided
valuable
insights
into
epitopes
that
original
ancestral
variants
emerged.
molecular
characterization
epitope
conservation
resistance
important
design
next‐generation
vaccines
antibody
therapeutics.
Molecular Cell,
Journal Year:
2022,
Volume and Issue:
82(21), P. 4131 - 4144.e6
Published: Oct. 21, 2022
RIG-I
is
an
essential
innate
immune
receptor
for
detecting
and
responding
to
infection
by
RNA
viruses.
specifically
recognizes
the
unique
molecular
features
of
viral
molecules
selectively
distinguishes
them
from
closely
related
RNAs
abundant
in
host
cells.
The
physical
basis
this
exquisite
selectivity
revealed
through
a
series
high-resolution
cryo-EM
structures
complex
with
ligands.
These
studies
demonstrate
that
actively
samples
double-stranded
cytoplasm
adopting
two
different
types
protein
folds.
Upon
binding
RNA,
adopts
high-affinity
conformation
conducive
signaling,
while
induces
autoinhibited
stimulates
release.
By
coupling
folding
selectivity,
differ
as
little
one
phosphate
group,
thereby
explaining
selective
antiviral
sensing
induction
autoimmunity
upon
dysregulation.
Vaccines,
Journal Year:
2023,
Volume and Issue:
11(1), P. 101 - 101
Published: Jan. 1, 2023
The
emergence
of
novel
variants
SARS-CoV-2
and
their
abilities
to
evade
the
immune
response
elicited
through
presently
available
vaccination
makes
it
essential
recognize
mechanisms
which
interacts
with
human
response.
It
is
not
only
comprehend
infection
mechanism
but
also
for
generation
effective
reliable
vaccines
against
COVID-19.
effectiveness
vaccine
supported
by
adaptive
response,
mainly
consists
B
T
cells,
play
a
critical
role
in
deciding
prognosis
COVID-19
disease.
cells
are
reducing
viral
load
containing
infection.
A
plethora
proteins
can
be
recognized
provide
broad
range
protection,
especially
amid
SARS-CoV-2.
However,
hyperactivation
effector
reduced
number
lymphocytes
have
been
found
key
characteristics
severe
Notably,
excessive
cell
activation
may
cause
acute
respiratory
distress
syndrome
(ARDS)
producing
unwarranted
amounts
cytokines
chemokines.
Nevertheless,
still
unknown
how
T-cell-mediated
responses
function
determining
Additionally,
functional
perturbations
lead
form
disease
protection
many
other
infections.
Hence,
an
updated
review
has
developed
understand
involvement
mechanism,
turn
determines
Importantly,
we
focused
on
cells’
exhaustion
under
certain
conditions
these
modulated
therapeutic
strategies
discussed
that
elevate
cell-mediated
either
directly
or
indirectly.
Immunity & Ageing,
Journal Year:
2023,
Volume and Issue:
20(1)
Published: April 12, 2023
Advanced
age
is
one
of
the
significant
risk
determinants
for
coronavirus
disease
2019
(COVID-19)-related
mortality
and
long
COVID
complications.
The
contributing
factors
may
include
age-related
dynamical
remodeling
immune
system,
known
as
immunosenescence
chronic
low-grade
systemic
inflammation.
Both
these
induce
an
inflammatory
milieu
in
aged
brain
drive
changes
microenvironment
neurons
microglia,
which
are
characterized
by
a
general
condition
inflammation,
so-called
neuroinflammation.
Emerging
evidence
reveals
that
privilege
aging
be
compromised.
Resident
cells,
such
astrocytes,
neurons,
oligodendrocytes
but
also
infiltrating
monocytes,
T
cells
macrophages
participate
complex
intercellular
networks
multiple
reciprocal
interactions.
Especially
microglia
playing
regulatory
role
contribute
to
disturbing
homeostasis
impairments
neuroimmune
responses.
Neuroinflammation
trigger
structural
damage,
diminish
regeneration,
neuronal
cell
death,
modulate
synaptic
this
manner
negatively
interfere
with
functions.In
review
article,
we
give
insights
into
interactions
highlight
impact
COVID-19
on
functional
systems
already
modulated
We
discuss
potential
ways
severe
acute
respiratory
syndrome
2
(SARS-CoV-2)
proposed
mechanisms
biological
development
persisting
conditions.
summarize
responsible
COVID,
including
autoimmunity,
direct
virus-mediated
cytotoxicity,
hypercoagulation,
mitochondrial
failure,
dysbiosis,
reactivation
other
viruses,
Cytomegalovirus
(CMV).
Finally,
effects
various
interventional
options
can
decrease
propagation
biological,
physiological,
psychosocial
stressors
activation
inhibit
triggering
unbalanced
modulatory
bioactive
nutritional
compounds
along
multimodal
benefits
behavioral
interventions
moderate
exercise,
applied
postinfectious
order
improve
health.
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(3), P. 564 - 564
Published: March 2, 2024
Memory
T
cells
form
from
the
adaptive
immune
response
to
historic
infections
or
vaccinations.
Some
memory
have
potential
recognise
unrelated
pathogens
like
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
and
generate
cross-reactive
responses.
Notably,
such
cell
cross-reactivity
has
been
observed
between
SARS-CoV-2
other
human
coronaviruses.
also
variants
microbes
vaccinations
against
influenza
A,
tuberculosis
measles,
mumps
rubella.
Extensive
research
debate
is
underway
understand
mechanism
role
of
how
it
relates
Coronavirus
disease
2019
(COVID-19)
outcomes.
Here,
we
review
evidence
for
ability
pre-existing
cross-react
with
SARS-CoV-2.
We
discuss
latest
findings
on
impact
extent
which
can
cross-protect
COVID-19.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Sept. 27, 2023
SARS-CoV-2
and
Mycobacterium
tuberculosis
(
Mtb
)
are
major
infectious
causes
of
death,
with
meta-analyses
population-based
studies
finding
increased
mortality
in
co-infected
patients
simultaneously
diagnosed
COVID-19
(TB).
There
is
a
need
to
understand
the
immune
interaction
between
which
impacts
poor
outcomes
for
those
co-infected.
We
performed
PubMed
preprint
search
using
keywords
[SARS-CoV-2]
AND
[tuberculosis]
[Immune
response],
including
publications
after
January
2020,
excluding
reviews
or
opinions.
Abstracts
were
evaluated
by
authors
inclusion
data
specifically
investigating
innate
and/or
acquired
responses
humans
animal
models,
immunopathological
co-infection
both
trials
investigations
potential
protection
against
Bacille
Calmette
Guérin
(BCG).
Of
248
articles
identified,
39
included.
Incidence
discussed,
considering
areas
high
burden
TB,
where
reported
likely
underestimated.
evidence
clinical
association
discuss
differences
similarities
murine
studies,
implications
co-infection.
have
been
shown
modulate
responses,
particularly
monocytes,
macrophages,
neutrophils,
T
cells.
Co-infection
may
result
impaired
immunity
SARS-CoV-2,
an
exacerbated
inflammatory
response,
while
cell
be
modulated
SARS-CoV-2.
Furthermore,
there
has
no
proven
benefit
BCG
despite
numerous
large-scale
trials.