Journal of Medical Virology,
Год журнала:
2024,
Номер
96(6)
Опубликована: Май 24, 2024
Human
papillomaviruses
(HPVs)
are
double-stranded
DNA
(dsDNA)
tumor
viruses
causally
associated
with
5%
of
human
cancers,
comprising
both
anogenital
and
upper
aerodigestive
tract
carcinomas.
Despite
the
availability
prophylactic
vaccines,
HPVs
continue
to
pose
a
significant
global
health
challenge,
primarily
due
inadequate
vaccine
access
coverage.
These
can
establish
persistent
infections
by
evading
intrinsic
defenses
infected
tissues
extrinsic
provided
professional
innate
immune
cells.
Crucial
for
their
evasion
strategies
is
unique
intraepithelial
life
cycle,
which
effectively
shields
them
from
host
detection.
Thus,
aimed
at
reactivating
response
within
or
transformed
epithelial
cells,
particularly
through
production
type
I
interferons
(IFNs)
lymphocyte-recruiting
chemokines,
considered
viable
solutions
counteract
adverse
effects
these
oncogenic
viruses.
This
review
focuses
on
complex
interplay
between
high-risk
HPV
oncoproteins
E6
E7
in
cells
HPV-associated
cancers.
In
particular,
it
details
molecular
mechanisms
modulate
response,
highlighting
progress
our
comprehension
processes.
It
also
examines
forward-looking
that
exploit
system
ameliorate
existing
anticancer
therapies,
thereby
providing
crucial
insights
into
future
therapeutic
developments.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(10), С. 8493 - 8493
Опубликована: Май 9, 2023
Human
papillomavirus
(HPV)
is
a
group
of
alpha
papillomaviruses
that
cause
various
illnesses,
including
cancer.
There
are
more
than
160
types
HPV,
with
many
being
"high-risk"
have
been
clinically
linked
to
cervical
and
other
"Low-risk"
HPV
less
severe
conditions,
such
as
genital
warts.
Over
the
past
few
decades,
numerous
studies
shed
light
on
how
induces
carcinogenesis.
The
genome
circular
double-stranded
DNA
molecule
approximately
8
kilobases
in
size.
Replication
this
strictly
regulated
requires
two
virus-encoded
proteins,
E1
E2.
helicase
necessary
for
replisome
assembly
replication
genome.
On
hand,
E2
responsible
initiating
regulating
transcription
HPV-encoded
genes,
most
importantly
E6
E7
oncogenes.
This
article
explores
genetic
characteristics
high-risk
types,
roles
proteins
replication,
regulation
oncogenes,
development
oncogenesis.
Pathogens,
Год журнала:
2023,
Номер
12(12), С. 1380 - 1380
Опубликована: Ноя. 23, 2023
Human
papillomavirus
(HPV)
is
implicated
in
over
90%
of
cervical
cancer
cases,
with
factors
like
regional
variability,
HPV
genotype,
the
population
studied,
vaccination
status,
and
anatomical
sample
collection
location
influencing
prevalence
pathology
HPV-induced
cancer.
HPV-16
-18
are
mainly
responsible
for
progression
several
cancers,
including
cervix,
anus,
vagina,
penis,
vulva,
oropharynx.
The
oncogenic
ability
not
only
sufficient
malignancy,
but
also
other
tumor-generating
steps
required
production
invasive
cancer,
such
as
coinfection
viruses,
lifestyle
high
parity,
smoking,
tobacco
chewing,
use
contraceptives
a
long
time,
immune
responses
stimulation
chronic
stromal
inflammation
deviation
tumor
microenvironment.
Viral
evasion
from
immunosurveillance
supports
viral
persistence,
virus-like
particle-based
prophylactic
vaccines
have
been
licensed,
which
effective
against
high-risk
types.
In
addition,
awareness
programs
preventive
strategies
could
help
reduce
rate
incidence
infection.
this
review,
we
emphasize
infection
its
role
progression,
molecular
immunopathogenesis,
host
response,
by
HPV,
vaccination,
schemes
battling
HPV-related
cancers.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(9), С. 7803 - 7803
Опубликована: Апрель 25, 2023
Some
viruses
are
known
to
be
associated
with
the
onset
of
specific
cancers.
These
microorganisms,
oncogenic
or
oncoviruses,
can
convert
normal
cells
into
cancer
by
modulating
central
metabolic
pathways
hampering
genomic
integrity
mechanisms,
consequently
inhibiting
apoptotic
machinery
and/or
enhancing
cell
proliferation.
Seven
promote
tumorigenesis
in
humans:
human
papillomavirus
(HPV),
hepatitis
B
and
C
(HBV,
HCV),
Epstein-Barr
virus
(EBV),
T-cell
leukemia
1
(HTLV-1),
Kaposi
sarcoma-associated
herpesvirus
(KSHV),
Merkel
polyomavirus
(MCPyV).
Recent
research
indicates
that
SARS-CoV-2
infection
COVID-19
progression
may
predispose
recovered
patients
accelerate
development.
This
hypothesis
is
based
on
growing
evidence
regarding
ability
modulate
pathways,
promoting
chronic
low-grade
inflammation
causing
tissue
damage.
Herein,
we
summarize
main
relationships
date
between
cancer,
providing
a
summary
proposed
biochemical
mechanisms
behind
cellular
transformation.
Mechanistically,
DNA
(such
as
HPV,
HBV,
EBV,
MCPyV)
encode
their
oncogenes.
In
contrast,
RNA
(like
HCV,
HTLV-1)
oncogenes
trigger
host
through
cis-/-trans
activation
leading
different
types
cancer.
As
for
SARS-CoV-2,
its
role
an
seems
occur
inhibition
oncosuppressors
controlling
autophagy
infected
cells.
However,
these
effects
could
significant
particular
scenarios
like
those
linked
severe
long
COVID.
On
other
hand,
looking
at
SARS-CoV-2─cancer
relationship
from
opposite
perspective,
oncolytic
anti-tumor
immune
response
were
triggered
some
cases.
summary,
our
work
aims
recall
comprehensive
attention
scientific
community
elucidate
and,
more
general,
β-coronavirus
susceptibility
prevention
supporting
therapeutic
approaches.
Journal of Medical Virology,
Год журнала:
2024,
Номер
96(6)
Опубликована: Май 24, 2024
Human
papillomaviruses
(HPVs)
are
double-stranded
DNA
(dsDNA)
tumor
viruses
causally
associated
with
5%
of
human
cancers,
comprising
both
anogenital
and
upper
aerodigestive
tract
carcinomas.
Despite
the
availability
prophylactic
vaccines,
HPVs
continue
to
pose
a
significant
global
health
challenge,
primarily
due
inadequate
vaccine
access
coverage.
These
can
establish
persistent
infections
by
evading
intrinsic
defenses
infected
tissues
extrinsic
provided
professional
innate
immune
cells.
Crucial
for
their
evasion
strategies
is
unique
intraepithelial
life
cycle,
which
effectively
shields
them
from
host
detection.
Thus,
aimed
at
reactivating
response
within
or
transformed
epithelial
cells,
particularly
through
production
type
I
interferons
(IFNs)
lymphocyte-recruiting
chemokines,
considered
viable
solutions
counteract
adverse
effects
these
oncogenic
viruses.
This
review
focuses
on
complex
interplay
between
high-risk
HPV
oncoproteins
E6
E7
in
cells
HPV-associated
cancers.
In
particular,
it
details
molecular
mechanisms
modulate
response,
highlighting
progress
our
comprehension
processes.
It
also
examines
forward-looking
that
exploit
system
ameliorate
existing
anticancer
therapies,
thereby
providing
crucial
insights
into
future
therapeutic
developments.