Frontiers in Microbiology,
Journal Year:
2021,
Volume and Issue:
12
Published: Sept. 16, 2021
Despite
the
availability
of
a
prophylactic
vaccine,
chronic
hepatitis
B
(CHB)
caused
by
virus
(HBV)
is
major
health
problem
affecting
an
estimated
292
million
people
globally.
Current
therapeutic
goals
are
to
achieve
functional
cure
characterized
HBsAg
seroclearance
and
absence
HBV-DNA
after
treatment
cessation.
However,
at
present,
thought
be
complicated
due
presence
covalently
closed
circular
DNA
(cccDNA)
integrated
HBV-DNA.
Even
if
episomal
cccDNA
silenced
or
eliminated,
it
remains
unclear
how
important
high
level
that
expressed
from
HBV
for
pathology.
To
identify
therapies
could
bring
about
rates
cure,
in-depth
knowledge
virus’
biology
imperative
pinpoint
mechanisms
novel
targets.
The
viral
proteins
considered
integral
control
maintenance
life
cycle
through
direct
interaction
with
host
proteome
they
help
create
most
optimal
environment
whilst
avoiding
immune
detection.
New
HBV-host
protein
interactions
continuously
being
identified.
Unfortunately,
compendium
recent
information
lacking
interactome
unavailable.
This
article
provides
comprehensive
review
virus-host
relationship
entry
release,
as
well
cccDNA,
HBc,
HBx.
Biomedicines,
Journal Year:
2021,
Volume and Issue:
9(11), P. 1577 - 1577
Published: Oct. 29, 2021
Hepatitis
B
virus
(HBV)
is
a
small
enveloped
DNA
which
replicates
its
tiny
3.2
kb
genome
by
reverse
transcription
inside
an
icosahedral
nucleocapsid,
formed
single
~180
amino
acid
capsid,
or
core,
protein
(Cp).
HBV
causes
chronic
hepatitis
(CHB),
severe
liver
disease
responsible
for
nearly
million
deaths
each
year.
Most
of
HBV's
only
seven
primary
gene
products
are
multifunctional.
Though
less
obvious
than
the
multi-domain
polymerase,
P
protein,
this
equally
crucial
Cp
with
multiple
roles
in
viral
life-cycle.
provides
stable
container
during
extracellular
phases,
allows
directed
intracellular
transport
and
timely
release
from
subsequent
assembly
new
nucleocapsids
around
pregenomic
(pg)
RNA,
forming
distinct
compartment
transcription.
These
opposing
features
enabled
dynamic
post-transcriptional
modifications
result
structural
alterations.
Their
perturbation
capsid
modulators
(CAMs)
promising
antiviral
concept.
CAMs
inappropriately
accelerate
and/or
distort
shell.
We
summarize
functional,
biochemical,
dynamics
Cp,
discuss
therapeutic
potential
based
on
clinical
data.
Presently,
appear
as
valuable
addition
but
not
substitute
existing
therapies.
However,
part
rational
combination
therapies
may
bring
ambitious
goal
cure
CHB
closer
to
reality.
Infection and Drug Resistance,
Journal Year:
2020,
Volume and Issue:
Volume 13, P. 3873 - 3886
Published: Oct. 1, 2020
Abstract:
Chronic
hepatitis
B
is
a
numerically
important
cause
of
cirrhosis
and
hepatocellular
carcinoma,
despite
an
effective
prophylactic
vaccine
well-tolerated
oral
antivirals.
Both
the
incapacity
immune
system
to
clear
virus
(HBV)
infection
unique
replication
strategies
adopted
by
HBV
are
considered
key
determinants
chronicity.
In
this
regard,
formation
DNA
minichromosome,
covalently
closed
circular
(cccDNA),
in
nucleus
infected
hepatocytes,
essential
not
only
for
production
all
viral
proteins
but
also
persistence
even
after
long-term
antiviral
therapy.
Licensed
polymerase
inhibitors
target
reverse
transcriptase
activity,
control
disease
with
therapy
fail
eliminate
cccDNA.
Consequently,
RNAs
proteins,
including
surface
antigen
(HBsAg),
abolished.
Novel
therapeutic
efforts
that
pipeline
early
clinical
trials
explore
novel
targets
molecules.
Such
focus
on
achieving
functional
cure,
which
defined
loss
HBsAg
undetectable
levels
serum.
Since
true
cure
requires
elimination
cccDNA
from
cells,
comprehension
mechanisms
implicated
biogenesis,
regulation
stability
appears
necessary
achieve
eradication.
review,
we
will
summarize
state
knowledge
metabolism,
focusing
insights
suggesting
potential
weak
points
may
be
development
approaches
design
aiming
at
lowering
loads
activity.
Keywords:
virus,
cccDNA,
animal
models,
human
liver
chimeric
mice,
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.
Frontiers in Microbiology,
Journal Year:
2021,
Volume and Issue:
12
Published: Sept. 16, 2021
Despite
the
availability
of
a
prophylactic
vaccine,
chronic
hepatitis
B
(CHB)
caused
by
virus
(HBV)
is
major
health
problem
affecting
an
estimated
292
million
people
globally.
Current
therapeutic
goals
are
to
achieve
functional
cure
characterized
HBsAg
seroclearance
and
absence
HBV-DNA
after
treatment
cessation.
However,
at
present,
thought
be
complicated
due
presence
covalently
closed
circular
DNA
(cccDNA)
integrated
HBV-DNA.
Even
if
episomal
cccDNA
silenced
or
eliminated,
it
remains
unclear
how
important
high
level
that
expressed
from
HBV
for
pathology.
To
identify
therapies
could
bring
about
rates
cure,
in-depth
knowledge
virus’
biology
imperative
pinpoint
mechanisms
novel
targets.
The
viral
proteins
considered
integral
control
maintenance
life
cycle
through
direct
interaction
with
host
proteome
they
help
create
most
optimal
environment
whilst
avoiding
immune
detection.
New
HBV-host
protein
interactions
continuously
being
identified.
Unfortunately,
compendium
recent
information
lacking
interactome
unavailable.
This
article
provides
comprehensive
review
virus-host
relationship
entry
release,
as
well
cccDNA,
HBc,
HBx.
