Viruses,
Journal Year:
2021,
Volume and Issue:
13(6), P. 1161 - 1161
Published: June 17, 2021
In
recent
years,
major
advances
in
research
and
experimental
approaches
have
significantly
increased
our
knowledge
on
the
role
of
HIV-1
capsid
virus
life
cycle,
from
reverse
transcription
to
integration
gene
expression.
This
makes
protein
a
good
pharmacological
target
inhibit
replication.
review
covers
current
understanding
viral
cycle
its
interaction
with
different
host
factors
that
enable
transcription,
trafficking
towards
nucleus,
nuclear
import
into
chromosomes.
It
also
describes
promising
small
molecules,
some
them
clinical
trials,
as
potential
targets
for
therapy.
Cells,
Journal Year:
2020,
Volume and Issue:
9(1), P. 254 - 254
Published: Jan. 20, 2020
Innate
immunity
represents
the
human
immune
system's
first
line
of
defense
against
a
pathogenic
intruder
and
is
initiated
by
recognition
conserved
molecular
structures
known
as
pathogen-associated
patterns
(PAMPs)
specialized
cellular
sensors,
called
pattern
receptors
(PRRs).
Human
immunodeficiency
virus
type
1
(HIV-1)
unique
RNA
that
causes
acquired
syndrome
(AIDS)
in
infected
individuals.
During
replication
cycle,
HIV-1
undergoes
reverse
transcription
its
genome
integrates
resulting
DNA
into
genome.
Subsequently,
integrated
provirus
results
production
new
virions
spreading
infection
virus.
Throughout
viral
numerous
nucleic
acid
derived
PAMPs
can
be
recognized
diverse
set
innate
sensors
cells.
However,
has
evolved
efficient
strategies
to
evade
or
counteract
this
surveillance
downstream
responses.
Understanding
underpinnings
concerted
actions
system,
well
corresponding
evasion
mechanisms
during
infection,
critical
understanding
transmission
pathogenesis,
may
provide
important
guidance
for
design
appropriate
adjuvant
vaccine
strategies.
Here,
we
summarize
current
knowledge
basis
sensing
cells,
including
CD4+
T
dendritic
macrophages.
Furthermore,
discuss
underlying
which
regulated,
describe
developed
Genes,
Journal Year:
2021,
Volume and Issue:
12(10), P. 1562 - 1562
Published: Sept. 30, 2021
LINE-1
(L1)
is
a
class
of
autonomous
mobile
genetic
elements
that
form
somatic
mosaicisms
in
various
tissues
the
organism.
The
activity
L1
retrotransposons
strictly
controlled
by
many
factors
and
germ
cells
at
all
stages
ontogenesis.
Alteration
was
noted
number
diseases:
neuropsychiatric
autoimmune
diseases,
as
well
forms
cancer.
Altered
for
some
pathologies
associated
with
epigenetic
changes
defects
genes
involved
their
repression.
This
review
discusses
molecular
mechanisms
retrotransposition
regulation
elements.
contribution
controlling
expression
distribution
genome
occurs
retrotransposition.
transcriptional,
post-transcriptional
integration
into
described
detail.
Finally,
this
also
focuses
on
evolutionary
aspects
accumulation
interplay
host
system.
Oncogene,
Journal Year:
2023,
Volume and Issue:
42(22), P. 1843 - 1856
Published: April 20, 2023
Abstract
Oncogenic
stress
induces
DNA
damage
repair
(DDR)
that
permits
escape
from
mitotic
catastrophe
and
allows
early
precursor
lesions
during
the
evolution
of
cancer.
SAMHD1,
a
dNTPase
protecting
cells
viral
infections,
has
been
recently
found
to
participate
in
process.
However,
its
role
tumorigenesis
remains
largely
unknown.
Here,
we
show
SAMHD1
is
up-regulated
early-stage
human
carcinoma
tissues
cell
lines
under
oxidative
or
genotoxic
insults.
We
further
demonstrate
de-ubiquitinating
enzyme
USP7
interacts
with
de-ubiquitinates
it
at
lysine
421,
thus
stabilizing
protein
expression
for
interaction
CtIP
DDR,
which
promotes
tumor
survival
stress.
Furthermore,
levels
positively
correlates
various
carcinomas,
associated
an
unfavorable
outcome
patients
who
underwent
chemotherapy.
Moreover,
inhibitor
sensitizes
chemotherapeutic
agents
by
decreasing
vitro
vivo.
These
findings
suggest
de-ubiquitination
DDR
overcome
oncogenic
affect
chemotherapy
sensitivity.
Molecules,
Journal Year:
2019,
Volume and Issue:
24(3), P. 481 - 481
Published: Jan. 29, 2019
The
replication
of
a
virus
within
its
host
cell
involves
numerous
interactions
between
viral
and
cellular
factors,
which
have
to
be
tightly
controlled
in
space
time.
intricate
interplay
exploitation
pathways
the
intrinsic
defense
mechanisms
is
difficult
unravel
by
traditional
bulk
approaches.
In
recent
years,
novel
fluorescence
microscopy
techniques
single
tracking
transformed
investigation
dynamic
virus-host
interactions.
A
prerequisite
for
application
these
imaging-based
methods
attachment
fluorescent
label
structure
interest.
However,
their
small
size,
limited
coding
capacity
multifunctional
proteins
render
viruses
particularly
challenging
targets
labeling
Click
chemistry
conjunction
with
genetic
code
expansion
provides
virologists
toolbox
site-specific,
minimally
invasive
virion
components,
whose
potential
has
just
recently
begun
exploited.
Here,
we
summarize
achievements,
current
developments
future
challenges
nucleic
acids,
proteins,
glycoproteins
or
lipids
using
click
order
study
processes
virus-cell
Frontiers in Microbiology,
Journal Year:
2020,
Volume and Issue:
11
Published: Dec. 4, 2020
HIV-1
employs
a
rich
arsenal
of
viral
factors
throughout
its
life
cycle
and
co-opts
intracellular
trafficking
pathways.
This
exquisitely
coordinated
process
requires
precise
manipulation
the
host
microenvironment,
most
often
within
defined
subcellular
compartments.
The
virus
capitalizes
on
by
modulating
cell-surface
proteins
cleverly
exploiting
nuclear
import
pathways
for
post
entry
events,
among
other
key
processes.
Successful
virus-cell
interactions
are
indeed
crucial
in
determining
extent
infection.
By
evolving
defenses
against
restriction
factors,
while
simultaneously
dependency
presents
fascinating
montage
an
ongoing
host-virus
arms
race.
Herein,
we
provide
overview
how
exploits
native
functions
cell
discuss
recent
findings
that
fundamentally
change
our
understanding
post-entry
replication
events.
Cells,
Journal Year:
2020,
Volume and Issue:
9(11), P. 2430 - 2430
Published: Nov. 6, 2020
The
chronic
factor
of
the
Hepatitis
B
Virus
(HBV),
specifically
covalently
closed
circular
DNA
(cccDNA),
is
a
highly
stable
and
active
viral
episomal
genome
established
in
livers
hepatitis
patients
as
constant
source
disease.
Being
able
to
target
eliminate
cccDNA
end
goal
for
genuine
cure
HBV.
Yet
how
HBV
formed
from
genomic
relaxed
(rcDNA)
by
what
host
factors
had
been
long-standing
research
questions.
It
generally
acknowledged
that
hijacks
cellular
functions
turn
open
conformation
rcDNA
into
through
repair
mechanisms.
With
great
efforts
community,
there
have
several
recent
leaps
our
understanding
formation.
this
review
analyze
reports
showing
evidence
factor's
involvement
molecular
pathway
biosynthesis.
mSphere,
Journal Year:
2019,
Volume and Issue:
4(4)
Published: Aug. 6, 2019
HPVs
are
causative
agents
in
human
cancers
and
responsible
for
around
of
5%
all
cancers.
A
better
understanding
the
viral
life
cycle
keratinocytes
will
facilitate
development
novel
therapeutics
to
combat
HPV-positive
Here,
we
present
a
unique
keratinocyte
model
identify
host
proteins
that
specifically
interact
with
HPV16.
Using
this
system,
report
cellular
gene,
SAMHD1,
is
regulated
by
HPV16
at
RNA
protein
levels
keratinocytes.
Elimination
SAMHD1
from
these
cells
using
CRISPR/Cas9
editing
promotes
enhanced
proliferation
elevated
replication
but
not
do
have
Our
study
demonstrates
specific
intricate
interplay
between
during
establishes
system
assist
exploring
factors
critical
HPV
pathogenesis.