Structural basis of Epstein-Barr virus gp350 receptor recognition and neutralization
Cong Sun,
No information about this author
Xin‐Yan Fang,
No information about this author
Guo‐Long Bu
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et al.
Cell Reports,
Journal Year:
2025,
Volume and Issue:
44(1), P. 115168 - 115168
Published: Jan. 1, 2025
Highlights•Cryo-EM
structure
of
EBV
gp350-CR2
complex
at
a
resolution
3.29
ŕDepiction
polar
and
glycan-free
contacting
interface•Key
residue
divergence
in
CR2
affects
host
tropism•Designed
CR2-Fc
neutralizes
B
cell
infection
by
targeting
72A1
epitopeSummaryEpstein-Barr
virus
(EBV)
is
an
oncogenic
associated
with
multiple
lymphoid
malignancies
autoimmune
diseases.
During
cells,
uses
its
major
glycoprotein
gp350
to
recognize
the
receptor
CR2,
initiating
viral
attachment,
process
that
has
lacked
direct
structural
evidence
for
decades.
In
this
study,
we
resolved
complex,
elucidated
their
key
interactions,
determined
site-specific
N-glycosylation
map
gp350.
Our
findings
reveal
primarily
binds
through
electrostatically
complementary
interface
diversity
residues
across
different
species
influences
selectivity
mediated
With
confirmed
binding,
constructed
antibody
analog
targets
vulnerable
site
gp350,
demonstrating
potent
neutralization
effect
against
cells.
work
provides
essential
insights
into
mechanism
tropism,
suggesting
potential
antiviral
agent.Graphical
abstract
Language: Английский
Understanding EBV Infection and EBV-Associated Lymphomas in children
Virology,
Journal Year:
2025,
Volume and Issue:
608, P. 110544 - 110544
Published: April 17, 2025
Language: Английский
The Tumor Microenvironment Remodeled by Epstein–Barr Virus: From Primary Site to Distant Metastatic Niche
Qiuyun Li,
No information about this author
Yuping Liu,
No information about this author
Yong Chen
No information about this author
et al.
Biological and Pharmaceutical Bulletin,
Journal Year:
2025,
Volume and Issue:
48(5), P. 495 - 506
Published: May 1, 2025
Epstein-Barr
virus
(EBV)
is
one
of
the
most
pervasive
viruses
worldwide,
and
EBV
infection
inextricably
linked
to
a
multitude
lymphoid
epithelial
neoplasms.
responsible
for
advancement
malignant
disease
by
modifying
tumor
microenvironment
(TME),
which
sophisticated
evolving
system
that
facilitates
growth,
invasion,
metastasis.
has
profound
impact
on
cellular
noncellular
components
constitute
TME.
Our
review
presents
summary
composition
EBV-remodeled
TME,
with
particular
focus
EBV-induced
functional
phenotypes
in
non-tumor
cells.
Furthermore,
we
discuss
potential
reversing
EBV-driven
TME
remodeling
as
therapeutic
strategy
treating
malignancies
associated
infection.
Language: Английский