Viruses,
Journal Year:
2021,
Volume and Issue:
13(9), P. 1725 - 1725
Published: Aug. 30, 2021
Respiratory
tract
infections
constitute
a
significant
public
health
problem,
with
therapeutic
arsenal
that
remains
relatively
limited
and
is
threatened
by
the
emergence
of
antiviral
and/or
antibiotic
resistance.
Viral-bacterial
co-infections
are
very
often
associated
severity
these
respiratory
have
been
explored
mainly
in
context
bacterial
superinfections
following
primary
influenza
infection.
This
review
summarizes
our
current
knowledge
mechanisms
underlying
between
viruses
(influenza
viruses,
RSV,
SARS-CoV-2)
bacteria,
at
both
physiological
immunological
levels.
also
explores
importance
microbiome
pathological
evolution
presents
different
vitro
vivo
experimental
models
available.
A
better
understanding
complex
functional
interactions
viruses/bacteria
host
cells
will
allow
development
new,
specific,
more
effective
diagnostic
approaches.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Jan. 26, 2023
The
emergence
of
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
caused
a
pandemic
named
disease
2019
(COVID-19)
that
has
become
the
greatest
worldwide
public
health
threat
this
century.
Recent
studies
have
unraveled
numerous
mysteries
SARS-CoV-2
pathogenesis
and
thus
largely
improved
COVID-19
vaccines
therapeutic
strategies.
However,
important
questions
remain
regarding
its
therapy.
In
review,
recent
research
advances
on
mechanism
are
quickly
summarized.
We
mainly
discuss
current
therapy
strategies
for
COVID-19,
with
an
emphasis
antiviral
agents,
neutralizing
antibody
therapies,
Janus
kinase
inhibitors,
steroids.
When
necessary,
specific
mechanisms
history
present,
representative
described
in
detail.
Finally,
we
key
outstanding
future
directions
development
treatment.
Science Immunology,
Journal Year:
2022,
Volume and Issue:
7(67)
Published: Jan. 7, 2022
Coronavirus
disease
2019
(COVID-19)
is
a
characterized
by
profound
dysregulation
of
the
innate
immune
system.
This
knowledge
has
emerged
from
large
body
single-cell
omics
studies
patients
with
COVID-19,
which
have
provided
one
most
detailed
cellular
atlases
human
ever.
However,
we
are
only
beginning
to
understand
immunological
pathways
that
govern
host
defense
and
immunopathology
in
COVID-19.
In
this
review,
discuss
emerging
understanding
how
SARS-CoV-2
host-derived
molecules
activate
specific
pattern
recognition
receptors
elicit
protective
interferon
responses
pathological
cytokine
responses,
particular
focus
on
acute
infection
lung
pathophysiology
critical
addition,
these
modulated
virus-host
interactions
stress-sensing
pathways.
In-depth
mechanisms
will
likely
uncover
molecular
targets
for
treatment
COVID-19
other
viral
infections.
it
reveal
fine
balance
between
beneficial
versus
causing
responses.
Thrombotic
and
microvascular
complications
are
frequently
seen
in
deceased
COVID-19
patients.
However,
whether
this
is
caused
by
direct
viral
infection
of
the
endothelium
or
inflammation-induced
endothelial
activation
remains
highly
contentious.Here,
we
use
patient
autopsy
samples,
primary
human
cells
an
vitro
model
pulmonary
epithelial-endothelial
cell
barrier.We
show
that
express
very
low
levels
SARS-CoV-2
receptor
ACE2
protease
TMPRSS2,
which
blocks
their
capacity
for
productive
infection,
limits
to
produce
infectious
virus.
Accordingly,
can
only
be
infected
when
they
overexpress
ACE2,
exposed
high
concentrations
SARS-CoV-2.
We
also
does
not
infect
3D
vessels
under
flow
conditions.
further
demonstrate
a
co-culture
with
Endothelial
do
however
sense
respond
adjacent
epithelial
cells,
increasing
ICAM-1
expression
releasing
pro-inflammatory
cytokines.Taken
together,
these
data
suggest
vivo,
unlikely
may
occur
if
epithelium
denuded
(basolateral
infection)
load
present
blood
(apical
infection).
In
such
scenario,
whilst
occur,
it
contribute
amplification.
still
play
key
role
pathogenesis
sensing
mounting
response
Scientific Reports,
Journal Year:
2021,
Volume and Issue:
11(1)
Published: July 1, 2021
Abstract
Human
cells
respond
to
infection
by
SARS-CoV-2,
the
virus
that
causes
COVID-19,
producing
cytokines
including
type
I
and
III
interferons
(IFNs)
proinflammatory
factors
such
as
IL6
TNF.
IFNs
can
limit
SARS-CoV-2
replication
but
cytokine
imbalance
contributes
severe
COVID-19.
We
studied
how
detect
infection.
report
cytosolic
RNA
sensor
MDA5
was
required
for
IFN
induction
in
lung
cancer
cell
line
Calu-3
upon
Type
further
MAVS
IRF3.
In
contrast,
of
TNF
independent
MDA5-MAVS-IRF3
axis
this
setting.
found
inhibited
ability
IFNs.
sum,
we
identified
a
cellular
induced
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2021,
Volume and Issue:
unknown
Published: June 7, 2021
Abstract
Emergence
of
SARS-CoV-2
variants,
including
the
globally
successful
B.1.1.7
lineage,
suggests
viral
adaptations
to
host
selective
pressures
resulting
in
more
efficient
transmission.
Although
much
effort
has
focused
on
Spike
adaptation
for
entry
and
adaptive
immune
escape,
mutations
outside
likely
contribute
enhance
Here
we
used
unbiased
abundance
proteomics,
phosphoproteomics,
mRNA
sequencing
replication
assays
show
that
isolates
effectively
suppress
innate
responses
airway
epithelial
cells.
We
found
have
dramatically
increased
subgenomic
RNA
protein
levels
Orf9b
Orf6,
both
known
antagonists.
Expression
alone
suppressed
response
through
interaction
with
TOM70,
a
mitochondrial
required
sensing
adaptor
MAVS
activation,
binding
activity
was
regulated
via
phosphorylation.
conclude
evolved
beyond
coding
region
antagonise
upregulation
specific
synthesis
expression
key
propose
effective
antagonism
increases
likelihood
transmission,
may
increase
vivo
duration
infection.
