Non-coding RNA Research,
Journal Year:
2020,
Volume and Issue:
5(4), P. 222 - 231
Published: Nov. 21, 2020
Coronavirus
disease
2019
(COVID-19)
caused
by
a
novel
betacoronavirus
named
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
has
attracted
top
health
concerns
worldwide
within
few
months
after
its
appearance.
Since
viruses
are
highly
dependent
on
the
host
small
RNAs
(microRNAs)
for
their
replication
and
propagation,
in
this
study,
miRNAs
targeting
SARS-CoV-2
genome
differentially
expressed
genes
(DEGs)
lungs
of
patients
infected
with
SARS-CoV-2,
were
predicted.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: July 7, 2021
There
are
still
many
unanswered
questions
concerning
viral
SARS-CoV-2
pathogenesis
in
COVID-19.
Accessory
proteins
consist
of
eleven
whose
roles
during
infection
not
completely
understood.
Here,
a
review
on
the
current
knowledge
accessory
is
summarized
updating
new
research
that
could
be
critical
understanding
interaction
with
host.
Some
such
as
ORF3b,
ORF6,
ORF7a
and
ORF8
have
been
shown
to
important
IFN-I
antagonists
inducing
an
impairment
host
immune
response.
In
addition,
ORF3a
involved
apoptosis
whereas
others
like
ORF9b
ORF9c
interact
cellular
organelles
leading
suppression
antiviral
response
infected
cells.
However,
possible
ORF7b
ORF10
awaiting
described.
Also,
ORF3d
has
reassigned.
Relevant
information
knowns
unknowns
these
analyzed,
which
crucial
for
further
design
strategies
counteracting
their
actions
evading
responses
Journal of Virology,
Journal Year:
2020,
Volume and Issue:
94(23)
Published: Sept. 16, 2020
Coronaviruses
(CoVs)
stand
out
for
their
large
RNA
genome
and
complex
RNA-synthesizing
machinery
comprising
16
nonstructural
proteins
(nsps).
The
bifunctional
nsp14
contains
3'-to-5'
exoribonuclease
(ExoN)
guanine-N7-methyltransferase
(N7-MTase)
domains.
While
the
latter
presumably
supports
mRNA
capping,
ExoN
is
thought
to
mediate
proofreading
during
replication.
In
line
with
such
a
role,
knockout
mutants
of
mouse
hepatitis
virus
(MHV)
severe
acute
respiratory
syndrome
coronavirus
(SARS-CoV)
were
previously
reported
have
crippled
but
viable
hypermutation
phenotypes.
Remarkably,
using
reverse
genetics,
set
corresponding
mutations
has
now
been
found
be
lethal
another
betacoronavirus,
Middle
East
(MERS-CoV).
For
13
mutants,
viral
progeny
could
not
recovered,
unless-as
happened
occasionally-reversion
had
first
occurred.
Only
single
mutant
was
viable,
likely
because
its
E191D
substitution
highly
conservative.
SARS-CoV-2
unable
replicate,
resembling
observations
made
alpha-
gammacoronaviruses,
starkly
contrasting
documented
phenotype
closely
related
SARS-CoV.
Subsequently,
we
established
Cell & Bioscience,
Journal Year:
2021,
Volume and Issue:
11(1)
Published: July 19, 2021
Abstract
SARS-CoV-2
is
an
extremely
contagious
respiratory
virus
causing
adult
atypical
pneumonia
COVID-19
with
severe
acute
syndrome
(SARS).
has
a
single-stranded,
positive-sense
RNA
(+RNA)
genome
of
~
29.9
kb
and
exhibits
significant
genetic
shift
from
different
isolates.
After
entering
the
susceptible
cells
expressing
both
ACE2
TMPRSS2,
directly
functions
as
mRNA
to
translate
two
polyproteins
ORF1a
ORF1b
region,
which
are
cleaved
by
viral
proteases
into
sixteen
non-structural
proteins
(nsp1-16)
initiate
replication
transcription.
The
also
encodes
four
structural
(S,
E,
M
N)
up
six
accessory
(3a,
6,
7a,
7b,
8,
9b)
proteins,
but
their
translation
requires
newly
synthesized
individual
subgenomic
RNAs
(sgRNA)
in
infected
cells.
Synthesis
full-length
genomic
(gRNA)
sgRNAs
conducted
inside
double-membrane
vesicles
(DMVs)
transcription
complex
(RTC),
comprises
nsp7,
nsp8,
nsp9,
nsp12,
nsp13
short
primer.
To
produce
sgRNAs,
RTC
starts
synthesis
highly
structured
gRNA
3'
end
switches
template
at
various
regulatory
sequence
(TRS
B
)
sites
along
body
probably
mediated
long-distance
RNA–RNA
interaction.
TRS
motif
5'
leader
L
responsible
for
interaction
upstream
each
ORF
skipping
between
them
sgRNAs.
Abundance
depend
on
location
read-through
efficiency
.
Although
more
studies
needed,
unprecedented
pandemic
taught
world
painful
lesson
that
invest
proactively
prepare
future
emergence
other
types
coronaviruses
any
possible
biological
horrors.
Biomedicine & Pharmacotherapy,
Journal Year:
2020,
Volume and Issue:
129, P. 110493 - 110493
Published: July 3, 2020
Despite
intense
research
there
is
currently
no
effective
vaccine
available
against
the
new
severe
acute
respiratory
syndrome
coronavirus-2
(SARS-CoV-2)
emerged
in
later
2019
and
responsible
for
COVID-19
pandemic.
This
infectious
communicable
disease
has
become
one
of
major
public
health
challenges
world.
The
clinical
management
been
limited
to
infection
prevention
control
measures
associated
with
supportive
care
such
as
supplemental
oxygen
mechanical
ventilation.
Meanwhile
efforts
find
an
treatment
inhibit
virus
replication,
mitigate
symptoms,
increase
survival
decrease
mortality
rate
are
ongoing.
Several
classes
drugs,
many
them
already
use
other
diseases,
being
evaluated
based
on
body
knowledge
obtained
from
infected
patients
regarding
natural
history
evolution
infection.
Herein
we
will
provide
updated
overview
current
drugs
therapeutic
agents
tested
COVID-19.
These
include
different
antiviral
(chloroquine,
ivermectin,
nitazoxanide,
hydroxychloroquine,
lopinavir,
remdesivir,
tocilizumab),
supporting
(Vitamin
C,
Vitamin
D,
azithromycin,
corticosteroids)
promising
investigational
vaccines.
Considering
controversies
excessive
number
compounds
reported
literature
hope
that
this
review
can
useful
consolidated
information
potential
used
prevent,
treat
worldwide.
Cell Research,
Journal Year:
2021,
Volume and Issue:
31(8), P. 847 - 860
Published: June 10, 2021
Cytokine
storm
and
multi-organ
failure
are
the
main
causes
of
SARS-CoV-2-related
death.
However,
origin
excessive
damages
caused
by
SARS-CoV-2
remains
largely
unknown.
Here
we
show
that
envelope
(2-E)
protein
alone
is
able
to
cause
acute
respiratory
distress
syndrome
(ARDS)-like
in
vitro
vivo.
2-E
proteins
were
found
form
a
type
pH-sensitive
cation
channels
bilayer
lipid
membranes.
As
observed
SARS-CoV-2-infected
cells,
heterologous
expression
induced
rapid
cell
death
various
susceptible
types
robust
secretion
cytokines
chemokines
macrophages.
Intravenous
administration
purified
into
mice
ARDS-like
pathological
lung
spleen.
A
dominant
negative
mutation
lowering
channel
activity
attenuated
production.
Newly
identified
inhibitors
exhibited
potent
anti-SARS-CoV-2
excellent
protective
these
activities
positively
correlated
with
inhibition
channel.
Importantly,
prophylactic
therapeutic
inhibitor
effectively
reduced
both
viral
load
inflammation
lungs
transgenic
expressing
human
angiotensin-converting
enzyme
2
(hACE-2).
Our
study
supports
promising
drug
target
against
SARS-CoV-2.