Journal of Molecular Histology,
Journal Year:
2020,
Volume and Issue:
51(6), P. 613 - 628
Published: Oct. 4, 2020
The
outbreak
of
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV2)
in
December
2019
form
Wuhan,
China
leads
to
disease
(COVID-19)
pandemic.
While
the
common
cold
symptoms
are
observed
mild
cases,
COVID-19
is
accompanied
by
multiorgan
failure
patients.
involvement
different
organs
patients
results
lengthening
hospitalization
duration
and
increasing
mortality
rate.
In
this
review,
we
aimed
investigate
patients,
particularly
cases.
Also,
tried
define
potential
underlying
mechanisms
SARS-CoV2
induced
failure.
multi-organ
dysfunction
characterized
lung
failure,
liver
kidney
injury,
cardiovascular
disease,
as
well
a
wide
spectrum
hematological
abnormalities
neurological
disorders.
most
important
related
direct
indirect
pathogenic
features
SARS-CoV2.
Although
presence
angiotensin-converting
enzyme
2,
receptor
lung,
heart,
kidney,
testis,
liver,
lymphocytes,
nervous
system
was
confirmed,
there
controversial
findings
about
observation
RNA
these
organs.
Moreover,
organ
may
be
cytokine
storm,
result
increased
levels
inflammatory
mediators,
endothelial
dysfunction,
coagulation
abnormalities,
infiltration
cells
into
Therefore,
further
investigations
needed
detect
exact
pathogenesis.
Since
several
for
clinicians,
their
knowledge
help
improve
outcomes
decrease
rate
morbidity.
Nature Medicine,
Journal Year:
2020,
Volume and Issue:
26(6), P. 842 - 844
Published: May 12, 2020
Respiratory
immune
characteristics
associated
with
Coronavirus
Disease
2019
(COVID-19)
severity
are
currently
unclear.
We
characterized
bronchoalveolar
lavage
fluid
cells
from
patients
varying
of
COVID-19
and
healthy
people
by
using
single-cell
RNA
sequencing.
Proinflammatory
monocyte-derived
macrophages
were
abundant
in
the
severe
COVID-9.
Moderate
cases
presence
highly
clonally
expanded
CD8+
T
cells.
This
atlas
microenvironment
suggests
potential
mechanisms
underlying
pathogenesis
recovery
COVID-19.
New England Journal of Medicine,
Journal Year:
2020,
Volume and Issue:
383(4), P. 334 - 346
Published: June 29, 2020
Understanding
the
epidemiology
and
clinical
course
of
multisystem
inflammatory
syndrome
in
children
(MIS-C)
its
temporal
association
with
coronavirus
disease
2019
(Covid-19)
is
important,
given
public
health
implications
syndrome.
We
conducted
targeted
surveillance
for
MIS-C
from
March
15
to
May
20,
2020,
pediatric
centers
across
United
States.
The
case
definition
included
six
criteria:
serious
illness
leading
hospitalization,
an
age
less
than
21
years,
fever
that
lasted
at
least
24
hours,
laboratory
evidence
inflammation,
organ
involvement,
infection
severe
acute
respiratory
2
(SARS-CoV-2)
based
on
reverse-transcriptase
polymerase
chain
reaction
(RT-PCR),
antibody
testing,
or
exposure
persons
Covid-19
past
month.
Clinicians
abstracted
data
onto
standardized
forms.
report
186
patients
26
states.
median
was
8.3
115
(62%)
were
male,
135
(73%)
had
previously
been
healthy,
131
(70%)
positive
SARS-CoV-2
by
RT-PCR
164
(88%)
hospitalized
after
April
16,
2020.
Organ-system
involvement
gastrointestinal
system
171
(92%),
cardiovascular
149
(80%),
hematologic
142
(76%),
mucocutaneous
137
(74%),
(70%).
duration
hospitalization
7
days
(interquartile
range,
4
10);
148
(80%)
received
intensive
care,
37
(20%)
mechanical
ventilation,
90
(48%)
vasoactive
support,
(2%)
died.
Coronary-artery
aneurysms
(z
scores
≥2.5)
documented
(8%),
Kawasaki's
disease-like
features
74
(40%).
Most
(171
[92%])
elevations
four
biomarkers
indicating
inflammation.
use
immunomodulating
therapies
common:
intravenous
immune
globulin
used
144
(77%),
glucocorticoids
91
(49%),
interleukin-6
1RA
inhibitors
38
(20%).
Multisystem
associated
led
life-threatening
healthy
adolescents.
(Funded
Centers
Disease
Control
Prevention.).
The Lancet,
Journal Year:
2020,
Volume and Issue:
395(10240), P. 1845 - 1854
Published: May 22, 2020
BackgroundA
vaccine
to
protect
against
COVID-19
is
urgently
needed.
We
aimed
assess
the
safety,
tolerability,
and
immunogenicity
of
a
recombinant
adenovirus
type-5
(Ad5)
vectored
expressing
spike
glycoprotein
severe
acute
respiratory
syndrome
coronavirus
2
(SARS-CoV-2)
strain.MethodsWe
did
dose-escalation,
single-centre,
open-label,
non-randomised,
phase
1
trial
an
Ad5
in
Wuhan,
China.
Healthy
adults
aged
between
18
60
years
were
sequentially
enrolled
allocated
one
three
dose
groups
(5
×
1010,
1011,
1·5
1011
viral
particles)
receive
intramuscular
injection
vaccine.
The
primary
outcome
was
adverse
events
7
days
post-vaccination.
Safety
assessed
over
28
Specific
antibodies
measured
with
ELISA,
neutralising
antibody
responses
induced
by
vaccination
detected
SARS-CoV-2
virus
neutralisation
pseudovirus
tests.
T-cell
enzyme-linked
immunospot
flow-cytometry
assays.
This
study
registered
ClinicalTrials.gov,
NCT04313127.FindingsBetween
March
16
27,
2020,
we
screened
195
individuals
for
eligibility.
Of
them,
108
participants
(51%
male,
49%
female;
mean
age
36·3
years)
recruited
received
low
(n=36),
middle
or
high
(n=36)
All
included
analysis.
At
least
reaction
within
first
after
reported
30
(83%)
group,
27
(75%)
group.
most
common
site
pain,
which
58
(54%)
recipients,
commonly
systematic
reactions
fever
(50
[46%]),
fatigue
(47
[44%]),
headache
(42
[39%]),
muscle
pain
(18
[17%].
Most
that
all
mild
moderate
severity.
No
serious
event
noted
ELISA
increased
significantly
at
day
14,
peaked
response
14
post-vaccination.InterpretationThe
tolerable
immunogenic
Humoral
post-vaccination
healthy
adults,
rapid
specific
from
Our
findings
suggest
warrants
further
investigation.FundingNational
Key
R&D
Program
China,
National
Science
Technology
Major
Project,
CanSino
Biologics.
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
11
Published: July 10, 2020
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS-Cov-2)
is
the
pathogen
that
causes
disease
2019
(COVID-19).
As
of
25
May
2020,
outbreak
COVID-19
has
caused
347,192
deaths
around
world.
The
current
evidence
showed
severely
ill
patients
tend
to
have
a
high
concentration
pro-inflammatory
cytokines,
such
as
interleukin
(IL)-6,
compared
those
who
are
moderately
ill.
level
cytokines
also
indicates
poor
prognosis
in
COVID-19.
Besides,
excessive
infiltration
cells,
mainly
involving
macrophages
and
T-helper
17
been
found
lung
tissues
with
by
postmortem
examination.
Recently,
increasing
studies
indicate
"cytokine
storm"
may
contribute
mortality
Here,
we
summarize
clinical
pathologic
features
cytokine
storm
Our
review
shows
SARS-Cov-2
selectively
induces
IL-6
results
exhaustion
lymphocytes.
tocilizumab,
an
inhibitor,
relatively
effective
safe.
corticosteroids,
programmed
cell
death
protein
(PD)-1/PD-L1
checkpoint
inhibition,
cytokine-adsorption
devices,
intravenous
immunoglobulin,
antimalarial
agents
could
be
potentially
useful
reliable
approaches
counteract
patients.
Nature Communications,
Journal Year:
2020,
Volume and Issue:
11(1)
Published: Sept. 17, 2020
Many
public
health
responses
and
modeled
scenarios
for
COVID-19
outbreaks
caused
by
SARS-CoV-2
assume
that
infection
results
in
an
immune
response
protects
individuals
from
future
infections
or
illness
some
amount
of
time.
The
presence
absence
protective
immunity
due
to
vaccination
(when
available)
will
affect
transmission
severity.
Here,
we
review
the
scientific
literature
on
antibody
coronaviruses,
including
as
well
related
SARS-CoV,
MERS-CoV
endemic
human
coronaviruses
(HCoVs).
We
reviewed
2,452
abstracts
identified
491
manuscripts
relevant
5
areas
focus:
1)
kinetics,
2)
correlates
protection,
3)
immunopathogenesis,
4)
antigenic
diversity
cross-reactivity,
5)
population
seroprevalence.
While
further
studies
are
necessary
determine
responses,
evidence
other
can
provide
clues
guide
research.
Signal Transduction and Targeted Therapy,
Journal Year:
2020,
Volume and Issue:
5(1)
Published: July 25, 2020
Abstract
The
recent
novel
coronavirus
disease
(COVID-19)
outbreak,
caused
by
severe
acute
respiratory
syndrome
2
(SARS-CoV-2),
is
seeing
a
rapid
increase
in
infected
patients
worldwide.
host
immune
response
to
SARS-CoV-2
appears
play
critical
role
pathogenesis
and
clinical
manifestations.
not
only
activates
antiviral
responses,
but
can
also
cause
uncontrolled
inflammatory
responses
characterized
marked
pro-inflammatory
cytokine
release
with
COVID-19,
leading
lymphopenia,
lymphocyte
dysfunction,
granulocyte
monocyte
abnormalities.
These
SARS-CoV-2-induced
abnormalities
may
lead
infections
microorganisms,
septic
shock,
multiple
organ
dysfunction.
Therefore,
mechanisms
underlying
COVID-19
must
be
elucidated
guide
management
of
the
disease.
Moreover,
rational
SARS-CoV-2,
which
includes
enhancing
anti-viral
immunity
while
inhibiting
systemic
inflammation,
key
successful
treatment.
In
this
review,
we
discuss
immunopathology
its
potential
mechanisms,
implications
aid
development
new
therapeutic
strategies
against
COVID-19.