Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 19, 2024
Combination
antiretroviral
therapy
(cART)
has
dramatically
reduced
mortality
in
people
with
human
immunodeficiency
virus
(HIV),
but
it
does
not
completely
eradicate
the
from
brain.
Patients
long-term
HIV-1
infection
often
show
neurocognitive
impairment,
which
severely
affects
quality
of
life
those
infected.
Methamphetamine
(METH)
users
are
at
a
significantly
higher
risk
contracting
through
behaviors
such
as
engaging
high-risk
sex
or
sharing
needles,
can
lead
to
transmission
virus.
In
addition,
HIV-1-infected
individuals
who
abuse
METH
exhibit
viral
loads
and
more
severe
cognitive
dysfunction,
suggesting
that
exacerbates
neurotoxicity
associated
HIV-1.
Therefore,
this
review
focuses
on
various
mechanisms
underlying
co-induced
existing
interventions
targeting
sigma
1
receptor,
dopamine
transporter
protein,
other
relevant
targets
explored.
The
findings
envisaged
systematically
establish
theoretical
framework
for
neurotoxicity,
suggest
novel
clinical
treatment
targets.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: May 8, 2025
Introduction
HIV
proteins,
such
as
the
Transactivator
of
transcription
(Tat),
mediate
neuroinflammation
in
central
nervous
system
by
promoting
release
pro-inflammatory
cytokines
and
chemokines.
Long
noncoding
RNAs
(lncRNAs)
regulate
gene
expression
sponging
microRNAs
(miRs),
but
their
role
Tat-mediated
microglial
activation
remains
poorly
understood.
This
study
aimed
to
investigate
involvement
lncRNA
Xist–miR-124–CCL2
axis
Tat-exposed
cells.
Methods
Mouse
primary
cells
were
exposed
Tat,
Xist,
miR-124,
CCL2
was
evaluated
using
qPCR,
Western
blotting,
ELISA.
Dual-luciferase
reporter
Argonaute
immunoprecipitation
assays
used
confirm
molecular
interactions.
Functional
experiments
involved
Xist
silencing
miR-124
overexpression.
In
vivo
validation
performed
doxycycline-inducible
Tat
transgenic
mice.
Results
significantly
upregulated
downregulated
mouse
identified
a
direct
target
3′-UTR
CCL2.
Silencing
or
overexpressing
reduced
Tat-induced
activation.
studies
corroborated
these
findings,
with
doxycycline-fed
iTat
mice
showing
elevated
levels
frontal
cortex.
Discussion
Our
findings
identify
novel
regulatory
whereby
upregulation
sponges
leading
overexpression
Targeting
pathway
may
represent
promising
therapeutic
strategy
mitigate
associated
NeuroHIV.
Viruses,
Journal Year:
2023,
Volume and Issue:
15(12), P. 2373 - 2373
Published: Dec. 1, 2023
Ferroptosis
is
a
novelty
form
of
regulated
cell
death,
and
it
mainly
characterized
by
iron
accumulation
lipid
peroxidation
in
the
cells.
Its
underlying
mechanism
related
to
amino
acid,
iron,
metabolisms.
During
viral
infection,
pathogenic
microorganisms
have
evolved
interfere
with
ferroptosis,
ferroptosis
often
manipulated
viruses
regulate
host
servicing
for
reproduction.
Therefore,
this
review
provides
comprehensive
overview
mechanisms
elucidates
intricate
signaling
pathways
involved,
explores
pivotal
role
pathogenesis
infections.
By
enhancing
our
understanding
novel
therapeutic
strategies
can
be
devised
effectively
prevent
treat
diseases
associated
process.
Furthermore,
unraveling
developmental
through
which
infections
exploit
will
facilitate
development
innovative
antiviral
agents.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Aug. 19, 2024
Combination
antiretroviral
therapy
(cART)
has
dramatically
reduced
mortality
in
people
with
human
immunodeficiency
virus
(HIV),
but
it
does
not
completely
eradicate
the
from
brain.
Patients
long-term
HIV-1
infection
often
show
neurocognitive
impairment,
which
severely
affects
quality
of
life
those
infected.
Methamphetamine
(METH)
users
are
at
a
significantly
higher
risk
contracting
through
behaviors
such
as
engaging
high-risk
sex
or
sharing
needles,
can
lead
to
transmission
virus.
In
addition,
HIV-1-infected
individuals
who
abuse
METH
exhibit
viral
loads
and
more
severe
cognitive
dysfunction,
suggesting
that
exacerbates
neurotoxicity
associated
HIV-1.
Therefore,
this
review
focuses
on
various
mechanisms
underlying
co-induced
existing
interventions
targeting
sigma
1
receptor,
dopamine
transporter
protein,
other
relevant
targets
explored.
The
findings
envisaged
systematically
establish
theoretical
framework
for
neurotoxicity,
suggest
novel
clinical
treatment
targets.