Cells,
Год журнала:
2024,
Номер
13(11), С. 898 - 898
Опубликована: Май 23, 2024
NeuroHIV
affects
approximately
30-60%
of
people
living
with
HIV-1
(PLWH)
and
is
characterized
by
varying
degrees
cognitive
impairments,
presenting
a
multifaceted
challenge,
the
underlying
cause
which
chronic,
low-level
neuroinflammation.
Such
smoldering
neuroinflammation
likely
an
outcome
lifelong
reliance
on
antiretrovirals
coupled
residual
virus
replication
in
brains
PLWH.
Despite
advancements
antiretroviral
therapeutics,
our
understanding
molecular
mechanism(s)
driving
inflammatory
processes
brain
remains
limited.
Recent
times
have
seen
emergence
non-coding
RNAs
(ncRNAs)
as
critical
regulators
gene
expression,
neuroinflammatory
HIV
infection,
NeuroHIV,
their
associated
comorbidities.
This
review
explores
role
various
classes
ncRNAs
regulatory
functions
implicated
neuropathogenesis,
related
conditions.
The
dysregulated
expression
known
to
exacerbate
responses,
thus
contributing
neurocognitive
impairments
also
discusses
diagnostic
therapeutic
potential
infection
its
comorbidities,
suggesting
utility
non-invasive
biomarkers
targets
for
modulating
pathways.
Understanding
these
roles
could
pave
way
novel
strategies
interventions
context
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Окт. 28, 2024
Human
immunodeficiency
virus
(HIV-1)
remains
a
persistent
global
health
crisis.
Even
while
successfully
virologically
suppressed,
people
with
HIV
(PWH)
experience
higher
risk
for
inflammatory
disorders
such
as
HIV-associated
neurocognitive
disorder
(HAND).
Tobacco
use
puts
PWH
at
symptoms
resulting
from
neuroinflammation.
The
NLR
Family
Pyrin
Domain
Containing
3
(NLRP3)
inflammasome
has
been
implicated
driver
of
inflammation,
including
HAND.
Nicotine,
the
psychoactive
component
tobacco
smoke,
also
shown
to
signal
through
NLRP3
and
modulate
signaling
in
CNS.
Here,
we
explore
impacts
nicotine
on
complex
neurobiology
HAND,
effects
cognition,
viral
latency,
blood-brain
barrier
integrity.
We
outline
nicotine’s
role
establishment
active
latent
infection
brain
posit
common
pathway
by
which
HIV-1
promote
neuroinflammation
PWH.
Revista Contemporânea,
Год журнала:
2024,
Номер
4(1), С. 350 - 368
Опубликована: Янв. 4, 2024
Objetivo:
Descrever
os
distúrbios
neurológicos
associados
ao
HIV/AIDS.
Metodologia:
Trata-se
de
um
estudo
analítico,
que
utiliza
como
técnica
a
Revisão
Integrativa
da
Literatura.
A
busca
foi
realizada
dentro
das
bases
dados
SCIELO
e
PUBMED,
por
meio
três
descritores:
“Distúrbios
Neurológicos”
AND
“HIV”
‘’ENFERMAGEM”.
Foram
encontrados
100
artigos
na
totalidade
nas
dados.
Ao
adicionar
critérios,
números
reduziram
para
51.
Após
análise
pesquisas,
15
publicações
foram
selecionadas
compor
esta
pesquisa.
Resultados:
As
manifestações
neurológicas
se
dão
meios
primários
secundários
sendo
as
infecções
oportunistas
principais
fatores
acometimento
do
sistema
nervoso.
Os
profissionais
saúde
trabalham
com
pessoas
vivem
HIV
(PVHIV)
devem
ser
regidos
práticas
fundamentais
rastreio
à
essas
complicações
associadas
HIV.
Conclusão:
O
decorrer
assunto
levanta
importância
implementação
processo
enfermagem,
sistematização
intervenções
voltadas
especificidades
doença
em
seu
curso.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Фев. 12, 2024
Abstract
Human
Immunodeficiency
Virus
(HIV)
latency
regulation
in
monocytes
and
macrophages
can
vary
according
to
signals
directing
differentiation,
polarization,
function.
To
investigate
these
processes,
we
generated
an
HIV
model
THP-1
showed
differential
levels
of
reactivation
among
clonal
populations.
Monocyte-to-macrophage
differentiation
HIV-infected
primary
human
CD14+
cells
induced
that
virus
production
increased
concomitant
with
macrophage
differentiation.
We
applied
the
monocyte-to-
(MLat)
assess
biological
mechanisms
regulating
dynamics
during
monocyte-to-macrophage
pinpointed
PKC
signaling
pathway
activation
Cyclin
T1
upregulation
as
inherent
regulate
reactivation.
Macrophage
polarization
regulated
latency,
revealing
pro-inflammatory
M1
suppressed
while
M2
promoted
Because
rely
on
reactive-
oxygen
species
(ROS)
exert
numerous
cellular
functions,
disrupted
redox
pathways
discovered
inhibitors
thioredoxin
(Trx)
system
acted
promoting
agents
(LPAs)
T-cells
monocytes,
but
opposingly
reversing
(LRAs)
macrophages.
explored
this
mechanism
Auranofin,
a
clinical
candidate
for
reducing
reservoirs,
demonstrated
Trx
reductase
(TrxR)
inhibition
led
ROS
NF-κB
activity,
which
macrophages,
not
monocytes.
Collectively,
cell
type-specific
differences
could
pose
barrier
eradication
strategies.
Neurotherapeutics,
Год журнала:
2024,
Номер
21(2), С. e00329 - e00329
Опубликована: Фев. 22, 2024
Cognitive
impairment
remains
a
persistent
challenge
in
people
living
with
HIV
(PWLH)
despite
antiretroviral
therapy
(ART)
due
to
ART's
inability
eliminate
brain
HIV.
HIV-induced
cognitive
dysfunction
results
from
immune
dysregulation,
ongoing
neuroinflammation,
and
the
continuous
virus
presence,
collectively
contributing
deficits.
Therefore,
adjunctive
therapies
are
needed
reduce
cerebral
reservoirs,
mitigate
impede
progression.
Our
study
focused
on
Honokiol,
known
for
its
anti-inflammatory
neuroprotective
properties,
an
experimental
mouse
model
simulating
dysfunction.
Using
Honokiol
Hexafluoro
(HH),
synthetic
analogue,
we
comprehensively
evaluated
potential
ameliorate
pathology
HIV-associated
findings
showed
that
HH
treatment
effectively
reversed
dysfunction,
concurrently
suppressing
astrocyte
activation,
restoring
neuronal
dendritic
arborization,
reducing
microglial
activation.
Furthermore,
remodeled
metabolic
profile
of
HIV-infected
human
monocyte-derived
macrophages,
resulting
decreased
activation
promotion
quiescent
state
vitro.
Cells,
Год журнала:
2024,
Номер
13(11), С. 898 - 898
Опубликована: Май 23, 2024
NeuroHIV
affects
approximately
30-60%
of
people
living
with
HIV-1
(PLWH)
and
is
characterized
by
varying
degrees
cognitive
impairments,
presenting
a
multifaceted
challenge,
the
underlying
cause
which
chronic,
low-level
neuroinflammation.
Such
smoldering
neuroinflammation
likely
an
outcome
lifelong
reliance
on
antiretrovirals
coupled
residual
virus
replication
in
brains
PLWH.
Despite
advancements
antiretroviral
therapeutics,
our
understanding
molecular
mechanism(s)
driving
inflammatory
processes
brain
remains
limited.
Recent
times
have
seen
emergence
non-coding
RNAs
(ncRNAs)
as
critical
regulators
gene
expression,
neuroinflammatory
HIV
infection,
NeuroHIV,
their
associated
comorbidities.
This
review
explores
role
various
classes
ncRNAs
regulatory
functions
implicated
neuropathogenesis,
related
conditions.
The
dysregulated
expression
known
to
exacerbate
responses,
thus
contributing
neurocognitive
impairments
also
discusses
diagnostic
therapeutic
potential
infection
its
comorbidities,
suggesting
utility
non-invasive
biomarkers
targets
for
modulating
pathways.
Understanding
these
roles
could
pave
way
novel
strategies
interventions
context
