Deletion of the Human Cytomegalovirus US2 to US11 Gene Family Members Impairs the Type-I Interferon Response
Inessa Penner,
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Nadine Krämer,
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J Hirsch
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et al.
Viruses,
Journal Year:
2025,
Volume and Issue:
17(3), P. 426 - 426
Published: March 15, 2025
Infection
of
cells
with
the
human
cytomegalovirus
(HCMV)
triggers
expression
interferon-stimulated
genes
(ISGs).
ISGs
encode
proteins
antiviral
functions,
such
as
inhibiting
viral
replication,
promoting
cell
death
infected
and
enhancing
immune
responses.
HCMV
has
evolved
mechanisms
to
evade
effects
ISGs.
The
encoded
by
US7,
US8,
US9
have
been
shown
interfere
interferon
induction.
US7
are
embedded
in
a
cluster
genes,
termed
US2
US11.
individual
members
this
gene
family
on
multiple
levels
innate
adaptive
responses
infection.
Using
mutants
different
deletions
US11,
we
addressed
question
if
other
than
would
also
influence
IFN
Surprisingly,
deletion
complete
US11
region
led
reduced
selected
Cells
viruses
which
were
deleted
showed
less
pronounced
reduction
experiments
including
RNA-seq
analyses
indicate
that
complex
interaction
IFN-ISG
response
is
likely
regulated
level
ISG
protein
stability.
As
US2–US11
dispensable
for
replication
culture,
genomic
was
frequently
used
insertion
bacterial
artificial
chromosome
vectors
process
cloning
genome.
results
here
must
be
considered
when
derived
from
BACs
whether
appropriate
controls
applied.
Language: Английский
Cytomegalovirus Biology Viewed Through a Cell Death Suppression Lens
Viruses,
Journal Year:
2024,
Volume and Issue:
16(12), P. 1820 - 1820
Published: Nov. 23, 2024
Cytomegaloviruses,
species-specific
members
of
the
betaherpesviruses,
encode
an
impressive
array
immune
evasion
strategies
committed
to
manipulation
host
system
enabling
these
viruses
remain
for
life
in
a
stand-off
with
innate
and
adaptive
mechanisms.
Even
though
they
are
species-restricted,
cytomegaloviruses
distributed
across
wide
range
different
mammalian
species
which
cause
systemic
infection
involving
many
cell
types.
Regulated,
or
programmed
death
has
recognized
potential
eliminate
infected
cells
prior
completion
viral
replication
release
progeny.
Cell
also
naturally
terminates
during
final
stages
replication.
Over
past
two
decades,
defense
known
pathways
(apoptosis,
necroptosis,
pyroptosis),
as
well
novel
mitochondrial
serine
protease
pathway
have
been
defined
through
studies
cytomegalovirus-encoded
suppressors.
Such
virus-encoded
inhibitors
prevent
virus-induced,
cytokine-induced,
stress-induced
while
moderating
inflammation.
By
evading
consequent
inflammation
clearance,
represent
successful
pathogens
that
become
critical
disease
threat
when
is
compromised.
This
review
will
discuss
programs
acquired
against
enumerate
modulatory
this
type
virus
employs
balance
favor
lifelong
persistence.
Language: Английский
A Better Understanding of the Clinical and Pathological Changes in Viral Retinitis: Steps to Improve Visual Outcomes
Microorganisms,
Journal Year:
2024,
Volume and Issue:
12(12), P. 2513 - 2513
Published: Dec. 5, 2024
Infectious
retinitis,
though
rare,
poses
a
significant
threat
to
vision,
often
leading
severe
and
irreversible
damage.
Various
pathogens,
including
viruses,
bacteria,
tick-borne
agents,
parasites,
fungi,
can
cause
this
condition.
Among
these,
necrotizing
herpetic
retinitis
represents
critical
spectrum
of
retinal
infections
primarily
caused
by
herpes
viruses
such
as
varicella-zoster
virus
(VZV),
simplex
(HSV),
cytomegalovirus
(CMV).
This
review
underscores
the
retina’s
susceptibility
viral
infections,
focusing
on
molecular
mechanisms
through
which
invade
damage
tissue,
supported
clinical
preclinical
evidence.
We
also
identify
existing
knowledge
gaps
propose
future
research
directions
deepen
our
understanding
improve
therapeutic
outcomes.
Language: Английский