Viral Immunology,
Journal Year:
2017,
Volume and Issue:
30(5), P. 315 - 329
Published: April 28, 2017
Poxviruses
have
evolved
numerous
mechanisms
to
avoid
the
immune
response
of
infected
host,
and
many
these
not
been
fully
described.
Here,
we
studied
transcriptional
innate
genes
in
BALB/c
C57BL/6
peritoneal
macrophages
following
infection
with
Moscow
strain
ectromelia
virus
(ECTV-Mos)
aim
delineating
that
contribute
difference
between
susceptibility
resistance
lethal
infection.
We
show
a
generalized
downregulation
four
categories
(toll-like
receptor
signaling,
NOD-like
RIG-I-like
type
I
interferon
signaling)
antiviral
receptors,
downstream
signaling
pathways,
responsive
components.
Two
important
observations
were
made.
First,
14
differentially
expressed
fold
change
upregulation
two
above
occurring
mice,
known
be
resistant
ECTV-Mos
infection,
whereas
same
downregulated
mice
below.
Second,
cathepsin
group
was
both
strains
but
profound
changes
17,
38,
62
for
CtsL,
CtsB,
CtsS,
respectively,
mice.
poxvirus
profoundly
downregulates
mRNA
protein
expression
three
cathepsins
this
appears
support
replication.
Based
on
data
propose
variations
gene
observed
may
resistance/susceptibility
by
ECTV-Mos.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2020,
Volume and Issue:
unknown
Published: March 7, 2020
ABSTRACT
A
novel
coronavirus
(SARS-CoV-2)
is
the
causative
agent
of
an
emergent
severe
respiratory
disease
(COVID-19)
in
humans
that
threatening
to
result
a
global
health
crisis.
By
using
genomic,
sequence,
structural
and
evolutionary
analysis,
we
show
Alpha-
Beta-CoVs
possess
several
families
immunoglobulin
(Ig)
domain
proteins,
including
ORF8
ORF7a
from
SARS-related
coronaviruses
two
protein
groups
certain
Alpha-CoVs.
Among
them,
distinguished
being
rapidly
evolving,
possessing
unique
insert
hypervariable
position
among
SARS-CoV-2
genomes
its
predicted
ligand-binding
groove.
We
also
uncover
many
Ig
proteins
metazoan
viruses
which
are
distinct
sequence
structure
but
share
architecture
comparable
CoV
proteins.
Hence,
propose
deployment
widely-used
strategy
by
viruses,
potential
pathogenicity
factor
evolves
counter
immune
response
facilitate
transmission
between
hosts.
PLoS ONE,
Journal Year:
2016,
Volume and Issue:
11(6), P. e0156898 - e0156898
Published: June 13, 2016
Norovirus
infection
is
the
main
cause
of
epidemic
non-bacterial
gastroenteritis
in
humans.
Although
human
norovirus
(HuNoV)
self-limiting,
it
can
persist
for
extended
periods
time
immune
deficient
patients.
Due
to
lack
robust
cell
culture
and
small
animal
systems,
little
known
about
HuNoV
pathogenicity.
However,
murine
(MNV)
be
propagated
used
as
a
model
study
infection.
Several
MNV
are
mice.
In
this
study,
we
show
that
strain
MNV-S99
persists
wild
type
inbred
(C57BL/6J)
mice
over
period
at
least
5
weeks
post
Viral
RNA
was
detectable
jejunum,
ileum,
cecum,
colon,
with
highest
titers
colon
cecum.
To
characterize
effect
on
innate
response,
Stat1
phosphorylation
IFN-β
production
were
analyzed
compared
non-persistent
MNV-1.CW3.
While
MNV-1.CW3
showed
comparable
growth
characteristics
vitro,
release
strongly
decreased
after
conclusion,
our
results
unlike
MNV-1.CW3,
establishes
persistent
mice,
possibly
due
interfering
response.
F1000Research,
Journal Year:
2018,
Volume and Issue:
7, P. 719 - 719
Published: June 11, 2018
Poxviruses
encode
a
set
of
secreted
proteins
that
bind
cytokines
and
chemokines
as
strategy
to
modulate
host
defense
mechanisms.
These
viral
mimic
the
activity
cytokine
decoy
receptors
but
have
unique
properties
may
enhance
their
activity.
Here,
we
describe
ability
poxvirus
attach
cell
surface
after
secretion
from
infected
cells,
discuss
advantages
this
property
confer
these
immunomodulatory
proteins.
Viral Immunology,
Journal Year:
2017,
Volume and Issue:
30(5), P. 315 - 329
Published: April 28, 2017
Poxviruses
have
evolved
numerous
mechanisms
to
avoid
the
immune
response
of
infected
host,
and
many
these
not
been
fully
described.
Here,
we
studied
transcriptional
innate
genes
in
BALB/c
C57BL/6
peritoneal
macrophages
following
infection
with
Moscow
strain
ectromelia
virus
(ECTV-Mos)
aim
delineating
that
contribute
difference
between
susceptibility
resistance
lethal
infection.
We
show
a
generalized
downregulation
four
categories
(toll-like
receptor
signaling,
NOD-like
RIG-I-like
type
I
interferon
signaling)
antiviral
receptors,
downstream
signaling
pathways,
responsive
components.
Two
important
observations
were
made.
First,
14
differentially
expressed
fold
change
upregulation
two
above
occurring
mice,
known
be
resistant
ECTV-Mos
infection,
whereas
same
downregulated
mice
below.
Second,
cathepsin
group
was
both
strains
but
profound
changes
17,
38,
62
for
CtsL,
CtsB,
CtsS,
respectively,
mice.
poxvirus
profoundly
downregulates
mRNA
protein
expression
three
cathepsins
this
appears
support
replication.
Based
on
data
propose
variations
gene
observed
may
resistance/susceptibility
by
ECTV-Mos.