Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: Dec. 22, 2023
Acute
brain
injury
(ABI)
and
neuroinflammation
is
reported
in
COVID-19
acute
respiratory
distress
syndrome
(ARDS).
It
remains
unclear
if
plays
an
independent
role
development
of
ABI
compared
to
those
with
non-COVID-19
ARDS.
We
aimed
evaluate
ARDS
associated
higher
risk
specific
patterns
conducted
age
sex
matched
case-control
autopsy
study
at
a
tertiary
academic
center.
Ten
patients
were
20
patients.
Baseline
demographics
comparable
between
the
two
groups
including
severity
(
p
=
0.3).
The
frequency
overall
(70
vs.
60%),
infratentorial
(40
25%),
ischemic
infarct
intracranial
hemorrhage
(30
35%),
hypoxic-ischemic
35%)
was
similar
patients,
respectively
>
0.05).
Intracapillary
megakaryocytes
exclusively
seen
30%
Overall,
pattern
non-COVID-19.
Russian Journal of Archive of Pathology,
Journal Year:
2025,
Volume and Issue:
87(1), P. 5 - 5
Published: Feb. 12, 2025
There
is
no
consolidated
opinion
on
the
pathogenesis
of
neurological
manifestations
COVID-19,
especially
after
infection.
A
significant
contribution
to
understanding
mechanisms
neuropathology
in
COVID-19
can
be
made
by
detailed
morphologic
studies
brain
with
assessment
changes
different
regions
during
periods
infection
process.
Objective.
Clarification
nature
and
intracerebral
virus
invasion
postinfection.
Material
methods.
The
study
included
15
patients
who
died
acute
phase
(11
people)
or
an
(4
without
a
history
focal
diseases.
In
each
case,
9
areas
were
assessed,
including
cortex,
hippocampus,
brainstem
(pons
medulla
oblongata),
cerebellum,
basal
ganglia,
central
parts
olfactory
system.
addition
histological
study,
immunohistochemical
was
performed
using
antibodies
against
CD8,
Iba1,
as
well
SARS-CoV-2
proteins
(S1
N)
semi-quantitative
circulatory
disorders,
microglial
reaction
expression
S1
protein
brain.
Results.
neuropathological
picture
similar
post-infectious
phases
COVID-19:
microcirculatory
diffuse
cerebral
edema,
ischemic-hypoxic
neuronal
changes,
accumulations
corpora
amylacea,
gliosis,
small
mainly
perivascular
lymphocytic
infiltrates
predominance
CD8+
T
cells,
moderate
reaction,
accumulation
N
not
detected
most
pronounced
observed
brainstem,
oblongata,
cerebellum.
severity
structural
did
correlate
disease
duration.
response
Conclusion.
identified
are
nonspecific
vascular
disorders
stem
accumulate
neurons
year
more
PLOS Global Public Health,
Journal Year:
2025,
Volume and Issue:
5(4), P. e0004420 - e0004420
Published: April 8, 2025
This
study
explores
the
linkage
between
acute
SARS-CoV-2
and
car
crashes
across
U.S.
states,
correlating
with
COVID-19
mitigation
strategies,
vaccination
rates,
Long
COVID
prevalence.
investigation
analyzed
aggregate
crash
data
spanning
2020–2023,
collection
occurring
March
May
2024.
Analysis
was
done
via
a
Poisson
regression
model,
adjusted
for
population.
Key
variables
included
status,
month-specific
effects
relating
to
initial
pandemic
shutdowns,
rates.
Results
demonstrated
significant
association
infections
an
increase
in
crashes,
independent
of
status
tune
OR
1.25
[1.23-1.26].
observed
despite
varying
efforts
rates
states.
The
found
no
protective
effect
against
challenging
prior
assumptions
about
benefits
vaccination.
Notably,
risk
associated
be
analogous
driving
impairments
seen
alcohol
consumption
at
legal
limits.
Findings
suggest
implications
public
health
policies,
especially
assessing
readiness
individuals
recovering
from
engage
high-risk
activities
such
as
pilots
or
nuclear
plant
employees.
Further
research
is
necessary
establish
causation
explore
exact
within
CNS
affecting
cognition
behavior.
During
the
past
decade
(and
beyond),
neurologists
have
become
aware
of
emergence,
persistence,
and
consequences
some
familiar
new
infections
affecting
nervous
system.
Even
among
CNS
infections,
such
as
herpes
virus,
polyoma
virus/JC,
influenza,
arbovirus,
hepatitis,
challenges
remain
in
developing
effective
antiviral
treatments
postinfection
sequelae.
With
changing
environment
increased
global
travel,
arthropod
vectors
that
mediate
zoonotic
disease
transmission
spread
unfamiliar
viruses
West
Nile
dengue,
chikungunya,
equine
encephalitis,
Zika,
others.
Although
health
impact
these
diseases
has
not
risen
to
COVID-19
HIV,
it
is
likely
dramatically
increase
with
continued
emergence
animal-to-human
mediated
by
those
vectors.
Furthermore,
specific
virus-targeting
or
vaccines
for
arboviral
are
yet
available,
this
represents
a
major
challenge
limiting
morbidity
infections.
By
contrast,
HIV-1,
originated
direct
from
nonhuman
primates
humans
(as
early
1930s),
after
many
years
intense
study,
now
targeted
highly
drugs
can
limit
infection
extend
human
life
all
populations.
dramatic
therapeutic
effects
suppressing
HIV
replication,
neurologic
dysfunction
(primarily
cognitive
impairment)
affects
significant
numbers
persons
living
HIV.
This
emphasizes
only
importance
treating
underlying
but
also
legacy
initial
even
therapy.
Notably,
rapid
SARS-CoV-2
was
met
implementation
therapies.
resulted
lowering
mortality
infection.
Nonetheless,
postinfectious
complications
(long
COVID)
more
costly
emerging
worldwide.
Developing
therapies
penetrate
CNS,
vaccines,
target
host
immune
responses
metabolic
will
be
necessary
management
infectious
established
Frontiers in Cellular Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: Nov. 30, 2023
Intracranial
(i.c.)
inoculation
of
susceptible
mice
with
a
glial-tropic
strain
mouse
hepatitis
virus
(JHMV),
murine
coronavirus,
results
in
an
acute
encephalomyelitis
followed
by
viral
persistence
white
matter
tracts
accompanied
chronic
neuroinflammation
and
demyelination.
Microglia
serve
numerous
functions
including
maintenance
the
healthy
central
nervous
system
(CNS)
are
among
first
responders
to
injury
or
infection.
More
recently,
studies
have
demonstrated
that
microglia
aid
tailoring
innate
adaptive
immune
responses
following
infection
neurotropic
viruses
flaviviruses,
herpesviruses,
picornaviruses.
These
findings
emphasized
important
role
for
host
defense
against
these
pathogens.
In
addition,
also
critical
optimizing
immune-mediated
control
JHMV
replication
within
CNS
while
restricting
severity
demyelination
enhancing
remyelination.
This
review
will
highlight
our
current
understanding
molecular
cellular
mechanisms
which
defense,
limit
neurologic
disease,
promote
repair
coronavirus.
Viral Immunology,
Journal Year:
2024,
Volume and Issue:
37(2), P. 61 - 78
Published: Feb. 5, 2024
COVID-19,
caused
by
the
SARS-CoV-2
virus,
can
have
neurological
effects,
including
cognitive
symptoms
like
brain
fog
and
memory
problems.
Research
on
effects
of
COVID-19
is
ongoing,
factors
such
as
inflammation,
disrupted
blood
flow,
damage
to
vessels
may
contribute
symptoms.
Notably,
some
authors
existing
evidence
suggest
that
virus
enter
central
nervous
system
through
different
routes,
olfactory
nerve
bloodstream.
infection
has
been
associated
with
altered
consciousness,
headaches,
dizziness,
mental
disorders.
The
exact
mechanisms
impact
formation
shrinkage
are
still
being
studied.
This
review
will
focus
pathways
blood–brain
barrier
disruption,
it
then
highlight
interactions
cell
types
in
brain,
namely
neurons,
astrocytes,
oligodendrocytes,
microglia.
Human
immunodeficiency
virus
(HIV)
and
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
cause
significant
neurologic
disease.
Central
nervous
system
(CNS)
involvement
of
HIV
has
been
extensively
studied,
with
well-documented
invasion
into
the
brain
in
initial
stage
infection,
while
effects
SARS-CoV-2
are
unclear.
Neuropathologic
features
active
infection
well
characterized
whereas
neuropathologic
findings
COVID-19
largely
non-specific.
On
other
hand,
substrates
chronic
dysfunction
both
infections,
as
HIV-associated
neurocognitive
disorders
(HAND)
post-COVID
conditions
(PCC)/long
COVID
unknown.
Thus
far,
studies
on
patients
HAND
era
combined
antiretroviral
therapy
have
inconclusive,
autopsy
diagnosed
PCC
yet
to
be
published.
Further
longitudinal,
multidisciplinary
comparison
controls
warranted
help
elucidate
mechanisms
CNS
conditions.
Frontiers in Microbiology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 24, 2024
COVID-19
presents
with
a
plethora
of
neurological
signs
and
symptoms
despite
being
characterized
as
respiratory
disease,
including
seizures,
anxiety,
depression,
amnesia,
attention
deficits,
alterations
in
consciousness.
The
olfactory
nerve
is
widely
accepted
the
neuroinvasive
route
by
which
etiological
agent
SARS-CoV-2
enters
brain,
but
trigeminal
an
often-overlooked
additional
route.
Based
on
this
consensus,
we
initially
conducted
pilot
experiment
investigating
neuroinvasion
via
intranasal
inoculation
AC70
human
ACE2
transgenic
mice.
Notably,
found
that
ganglion
early
highly
efficient
site
viral
replication,
then
rapidly
spread
throughout
brain
where
neurons
were
primarily
targeted.
Despite
extensive
infection
across
obvious
evidence
tissue
pathology
inflammatory
infiltration,
glial
activation,
apoptotic
cell
deaths
not
consistently
observed,
albeit
cytokines
significantly
induced.
However,
expression
levels
different
genes
related
to
neuronal
function,
neurotransmitter
dopamine
pathway
well
synaptic
markers
damage
altered
compared
mock-infected
Our
findings
suggest
may
serve
complementary
ensuing
presented
unique
neuropathological
profile.
This
study
provides
insights
into
potential
neuropathogenic
mechanisms
utilized
coronaviruses.
Acta Virologica,
Journal Year:
2024,
Volume and Issue:
68
Published: Oct. 15, 2024
The
global
pandemic
of
COVID-19
caused
by
SARS-CoV-2
has
had
a
devastating
impact.
Although
many
survived
the
acute
effects
pandemic,
significant
number
survivors,
including
those
with
only
mild
symptoms,
are
now
experiencing
prolonged
and
debilitating
post-viral
syndrome
known
as
LC/PASC
(long
COVID/post-acute
sequelae
SARS-CoV-2).
Typical
symptoms
include
fatigue,
breathlessness,
chest
pain,
impaired
cognition,
difficulty
sleeping,
fever
gastrointestinal
symptoms.
Anxiety
depression
can
also
last
for
weeks
to
months
range
from
disabling.
association
between
neuropsychiatric
infection
raises
questions
about
possible
routes
entry
central
nervous
system
(CNS)
long-term
virus
on
CNS,
their
molecular
basis,
potential
risk
neuronal
damage
associated
subsequent
development
neurodegenerative
diseases.