Viruses,
Journal Year:
2025,
Volume and Issue:
17(3), P. 349 - 349
Published: Feb. 28, 2025
Studies
on
human
respiratory
viral
infections
and
pathogenesis
have
historically
been
conducted
using
immortalized
cells
animal
models.
However,
these
models
are
limited
in
their
ability
to
recapitulate
the
complex
structure
of
airway
or
full
spectrum
disease
symptoms
observed
humans.
Recently,
nose
lung
organoids
revolutionized
culture
complexity
infection
biology
demonstrated
potential
for
research
virus
In
this
opinion,
we
review
how
advances
organoid
models,
which
able
express
all
cell
types
epithelia,
i.e.,
Club,
basal,
goblet,
ciliated
cells,
provided
novel
insight
into
pathogenesis,
age-dependent
susceptibility,
attenuation
signature,
immune
mechanisms
viruses
such
as
SARS-CoV-2,
syncytial
virus,
influenza
virus.
The
also
studying
hitherto
uncultivable
be
useful
studies
zoonotic
risk.
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: July 7, 2022
Abstract
COVID-19,
caused
by
SARS-CoV-2,
is
the
most
consequential
pandemic
of
this
century.
Since
outbreak
in
late
2019,
animal
models
have
been
playing
crucial
roles
aiding
rapid
development
vaccines/drugs
for
prevention
and
therapy,
as
well
understanding
pathogenesis
SARS-CoV-2
infection
immune
responses
hosts.
However,
current
some
deficits
there
an
urgent
need
novel
to
evaluate
virulence
variants
concerns
(VOC),
antibody-dependent
enhancement
(ADE),
various
comorbidities
COVID-19.
This
review
summarizes
clinical
features
COVID-19
different
populations,
characteristics
major
including
those
naturally
susceptible
animals,
such
non-human
primates,
Syrian
hamster,
ferret,
minks,
poultry,
livestock,
mouse
sensitized
genetically
modified,
AAV/adenoviral
transduced,
mouse-adapted
strain
engraftment
human
tissues
or
cells.
host
receptors
proteases
essential
designing
advanced
modified
models,
successful
studies
on
are
also
reviewed.
Several
improved
alternatives
future
proposed,
reselection
alternative
receptor
genes
multiple
gene
combinations,
use
transgenic
knock-in
method,
strains
establishing
next
generation
mice.
Cell,
Journal Year:
2023,
Volume and Issue:
186(11), P. 2392 - 2409.e21
Published: April 13, 2023
T
cell
responses
play
an
important
role
in
protection
against
beta-coronavirus
infections,
including
SARS-CoV-2,
where
they
associate
with
decreased
COVID-19
disease
severity
and
duration.
To
enhance
immunity
across
epitopes
infrequently
altered
SARS-CoV-2
variants,
we
designed
BNT162b4,
mRNA
vaccine
component
that
is
intended
to
be
combined
BNT162b2,
the
spike-protein-encoding
vaccine.
BNT162b4
encodes
variant-conserved,
immunogenic
segments
of
nucleocapsid,
membrane,
ORF1ab
proteins,
targeting
diverse
HLA
alleles.
elicits
polyfunctional
CD4+
CD8+
animal
models,
alone
or
when
co-administered
BNT162b2
while
preserving
spike-specific
immunity.
Importantly,
demonstrate
protects
hamsters
from
severe
reduces
viral
titers
following
challenge
variants.
These
data
suggest
a
combination
could
reduce
duration
caused
by
circulating
future
currently
being
clinically
evaluated
BA.4/BA.5
Omicron-updated
bivalent
(NCT05541861).
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: April 4, 2022
Vaccine-associated
enhanced
disease
(VAED)
is
a
difficult
phenomenon
to
define
and
can
be
confused
with
vaccine
failure.
Using
studies
on
respiratory
syncytial
virus
(RSV)
vaccination
dengue
infection,
we
highlight
known
theoretical
mechanisms
of
VAED,
including
antibody-dependent
enhancement
(ADE),
antibody-enhanced
(AED)
Th2-mediated
pathology.
We
also
critically
review
the
literature
surrounding
this
in
pathogenic
human
coronaviruses,
MERS-CoV,
SARS-CoV-1
SARS-CoV-2.
Poor
quality
histopathological
data
lack
consistency
defining
severe
pathology
VAED
preclinical
MERS-CoV
vaccines
particular
make
it
interrogate
potential
cases
VAED.
Fortuitously,
there
have
been
only
few
reports
mild
SARS-CoV-2
models
no
observations
their
clinical
use.
describe
problem
areas
discuss
methods
improve
characterisation
future.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Jan. 16, 2024
Abstract
Improved
therapies
are
needed
against
snakebite
envenoming,
which
kills
and
permanently
disables
thousands
of
people
each
year.
Recently
developed
neutralizing
monoclonal
antibodies
several
snake
toxins
have
shown
promise
in
preclinical
rodent
models.
Here,
we
use
phage
display
technology
to
discover
a
human
antibody
show
that
this
causes
antibody-dependent
enhancement
toxicity
(ADET)
myotoxin
II
from
the
venomous
pit
viper,
Bothrops
asper
,
mouse
model
envenoming
mimics
snakebite.
While
clinical
ADET
related
venom
has
not
yet
been
reported
humans,
report
toxin
animal
kingdom
highlights
necessity
assessing
even
well-known
formats
representative
models
evaluate
their
therapeutic
utility
or
venoms.
This
is
essential
avoid
potential
deleterious
effects
as
exemplified
present
study.
Journal of Clinical Investigation,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 7, 2025
Neutrophils,
particularly
low-density
neutrophils
(LDNs),
are
believed
to
contribute
acute
COVID-19
severity.
Here,
we
showed
that
neutrophilia
can
be
detected
acutely
and
even
months
after
SARS-CoV-2
infection
in
patients
mice,
while
neutrophil
depletion
reduced
disease
severity
mice.
A
key
factor
severe
infected
mice
was
traced
the
chemokine
CXCL12
secreted
by
bone
marrow
cells
unexpectedly,
endothelial
cells.
levels
were
negatively
correlated
with
LDN
numbers
longitudinal
analyses
of
patient
blood
samples.
blockade
SARS-CoV-2-infected
increased
blood/lung
thereby
accelerating
progression
without
changing
lung
virus
titers.
The
exaggerated
mortality
caused
reversed
depletion.
In
addition,
blocking
interactions
between
Angiotensin-Converting
Enzyme
2
(ACE2)
levels,
suggesting
a
signal
transduction
from
virus-mediated
ACE2
ligation
secretion.
Collectively,
these
results
demonstrate
previously
unappreciated
role
diminishing
neutrophilia,
including
low
density
its
deleterious
effects
infections.
also
support
involvement
SARS-CoV-2-endothelial
cell
viral
pathogenesis.