Frontiers in Microbiology,
Год журнала:
2024,
Номер
15
Опубликована: Дек. 5, 2024
Epstein-Barr
virus
(EBV)
infects
more
than
90%
of
the
human
population
worldwide
and
establishes
lifelong
infection
in
hosts
by
switching
between
latent
lytic
infection.
EBV
latency
can
be
reactivated
under
appropriate
conditions,
leading
to
expression
viral
genes
production
infectious
progeny
viruses.
reactivation
involves
crosstalk
various
factors
signaling
pathways,
subsequent
complicated
virus-host
interplays
determine
whether
continues
propagate.
However,
detailed
mechanisms
underlying
these
processes
remain
unclear.
In
this
review,
we
summarize
critical
regulating
associated
mechanisms.
This
encompasses
transcription
post-transcriptional
regulation
immediate-early
(IE)
genes,
functions
on
DNA
replication
production,
through
which
proteins
disrupt
inhibit
host's
innate
immune
response,
host
that
modulate
reactivation.
Finally,
explore
potential
applications
novel
technologies
studying
reactivation,
providing
insights
into
investigation
governing
development
anti-EBV
therapeutic
strategies.
Abstract
Epstein-Barr
virus
(EBV)
infection
has
long
been
associated
with
the
development
of
multiple
sclerosis
(MS).
Patients
MS
have
elevated
titres
EBV-specific
antibodies
in
serum
and
show
signs
CNS
damage
only
after
EBV
infection.
Regarding
CD8+
T
cells,
an
but
ineffective
response
to
was
suggested
patients,
who
present
a
broader
MHC-I-restricted
T-cell
receptor
beta
chain
(TRB)
repertoire
compared
controls.
It
is
not
known
whether
this
altered
could
be
subject
dynamic
changes,
e.g.
by
approved
therapies,
it
specific
for
MS.
Peripheral
blood
TRB
samples
(n
=
1317)
healthy
donors
409),
patients
710)
before
treatment,
neuromyelitis
optica
spectrum
disorder
87),
MOG
antibody-associated
disease
(MOGAD)
64)
Susac’s
syndrome
47)
were
analysed.
Apart
from
MS,
none
evaluated
diseases
presented
anti-EBV
repertoire.
In
undergoing
autologous
haematopoietic
stem-cell
transplantation,
reactivation
coincided
sequence
matches.
Therapy
ocrelizumab,
teriflunomide
or
dimethyl
fumarate
reduced
EBV-specific,
CMV-specific
Together,
these
data
suggest
that
aberrant
directed
against
regard
optica,
MOGAD
specifically
modified
treatments
interfering
host
cells
activated
lymphocytes.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(15), С. 8160 - 8160
Опубликована: Июль 26, 2024
Epstein-Barr
virus
(EBV),
a
member
of
the
γ-herpesvirus
family,
is
one
most
prevalent
and
persistent
human
viruses,
infecting
up
to
90%
adult
population
globally.
EBV's
life
cycle
includes
primary
infection,
latency,
lytic
reactivation,
with
primarily
B
cells
epithelial
cells.
This
has
evolved
sophisticated
strategies
evade
both
innate
adaptive
immune
responses,
thereby
maintaining
lifelong
presence
within
host.
persistence
facilitated
by
expression
latent
genes
such
as
EBV
nuclear
antigens
(EBNAs)
membrane
proteins
(LMPs),
which
play
crucial
roles
in
viral
latency
oncogenesis.
In
addition
their
well-known
several
types
cancer,
including
nasopharyngeal
carcinoma
B-cell
lymphomas,
recent
studies
have
identified
pathogenic
autoimmune
diseases
multiple
sclerosis,
rheumatoid
arthritis,
systemic
lupus
erythematosus.
review
highlights
intricate
interactions
between
host
system,
underscoring
need
for
further
research
develop
effective
therapeutic
preventive
against
EBV-associated
diseases.
The
Epstein-Barr
virus
(EBV)
infects
nearly
90%
of
adults
globally
and
is
linked
to
over
200,000
annual
cancer
cases.
Immunocompromised
individuals
from
conditions
such
as
primary
immune
disorders,
HIV,
or
posttransplant
immunosuppressive
therapies
are
particularly
vulnerable
because
EBV’s
transformative
capability.
EBV
remodels
B
cell
metabolism
support
energy,
biosynthetic
precursors,
redox
equivalents
necessary
for
transformation.
Most
EBV-driven
metabolic
pathways
center
on
mitochondria.
However,
how
regulates
mitochondrial
function
fluxes
remains
unclear.
Here,
we
show
that
boosts
cardiolipin
(CL)
biosynthesis,
essential
cristae
biogenesis,
via
nuclear
antigen
2/MYC-induced
CL
enzyme
transactivation.
Pharmacological
CRISPR
genetic
analyses
underscore
the
essentiality
biosynthesis
in
EBV-transformed
cells.
Metabolomic
isotopic
tracing
highlight
CL’s
role
sustaining
respiration,
one-carbon
metabolism,
aspartate
synthesis.
Disrupting
destabilizes
matrix
enzymes
pivotal
these
pathways.
We
demonstrate
EBV-induced
a
therapeutic
target,
offering
synthetic
lethal
strategies
against
EBV-associated
malignancies.
Journal of Medical Virology,
Год журнала:
2025,
Номер
97(2)
Опубликована: Фев. 1, 2025
ABSTRACT
Epstein–Barr
virus
(EBV)
is
the
first
human
cancer‐causing
viral
pathogen
to
be
discovered;
it
has
been
epidemiologically
associated
with
a
wide
range
of
diseases,
including
cancers,
autoimmunity,
and
hyperinflammatory
disorders.
Its
evolutionary
success
underpinned
by
coordinated
expression
transcription
factors
(EBV
nuclear
antigens),
signaling
proteins
latent
membrane
proteins),
noncoding
RNAs,
which
orchestrate
cell
transformation,
immune
evasion,
dissemination.
Each
those
activities
entails
significant
metabolic
rewiring,
achieved
subversion
key
host
regulators
such
as
mammalian
target
rapamycin
(mTOR),
MYC,
hypoxia‐inducible
factor
(HIF).
In
this
review,
we
systemically
discuss
how
EBV‐encoded
regulate
metabolism
achieve
persistence
propagation,
well
potential
research
questions
directions
in
EBV‐driven
metabolism.
Microorganisms,
Год журнала:
2025,
Номер
13(4), С. 702 - 702
Опубликована: Март 21, 2025
Long
COVID
following
SARS-CoV-2
and
Myalgic
Encephalomyelitis/Chronic
Fatigue
Syndrome
(ME/CFS)
infectious
mononucleosis
(IM)
are
two
examples
of
post-viral
syndromes.
The
identification
risk
factors
predisposing
patients
to
developing
maintaining
post-infectious
syndromes
may
help
uncover
their
underlying
mechanisms.
majority
with
ME/CFS
report
illnesses
before
the
onset
ME/CFS,
30%
cases
due
IM
caused
by
Epstein–Barr
virus.
After
IM,
one
study
found
11%
adults
had
at
6
months
9%
1
year.
Another
adolescents
13%
7%
12
respectively.
However,
it
is
unclear
which
variables
potential
contributing
development
maintenance
because
few
prospective
studies
have
collected
baseline
data
triggering
illness.
current
article
provides
an
overview
a
that
included
pre-illness
predictors
in
diverse
group
college
students
who
were
enrolled
IM.
Our
set
ethnically
sociodemographically
young
adult
students,
we
able
longitudinally
follow
these
youths
over
time
better
understand
associated
pathophysiology
ME/CFS.
General
screens
health
psychological
well-being,
as
well
blood
samples,
obtained
three
stages
(Stage
1—Baseline—when
well,
least
weeks
student
developed
IM;
Stage
2—within
diagnosis
3—six
after
when
they
either
or
recovered).
We
focused
on
for
new
both
1)
2)
predicted
nonrecovery.
now
collecting
seven-year
follow-up
this
sample,
including
long
COVID.
lessons
learned
reviewed.
