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Antiviral properties of BST-2 and Kaposi's sarcoma-associated herpesvirus countermeasures.
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Antiviral properties of BST-2 and Kaposi's sarcoma-associated herpesvirus countermeasures.
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http://www.ohsu.edu/xd/education/library/services/theses-dissertations/rights-statement.cfm
Title
Antiviral
properties
of
BST-2
and
Kaposi's
sarcoma-associated
herpesvirus
countermeasures
.
Creator.PersonalName
Hines
,
Jennie
Lyn
Thesis.Degree
M.S.
Thesis.Major
Biochemistry and Molecular Biology
Thesis.DateDegreeAwarded
June
2010
Institution
Oregon Health & Science University
School
School of Medicine
Department
Dept. of Science & Engineering
Division
Div. of Environmental & Biomolecular Systems
Thesis.Committee
Früeh, Klaus J.
Whittaker, James W.
Zuber, Peter A.
Subject.LCSH
Herpesvirus diseases
Subject.Keyword
Viral
egress
;
Innate
immune
response
Subject.MeSH
Herpesvirus 8, Human
Immune Evasion
Virus Release
Membrane Glycoproteins
Call Number
Q 183.5.OGISE H664 2010
Description.Abstract
Upon
infection
a
virus
elicits
a
great
number
of
responses
from the
host
cell
, and in
order
for a
successful
infection
to
occur
, the
virus
must
employ
various
mechanisms
to
evade
these
immune
responses
.
One
such
immune
evasion
method
of
Kaposi’s
sarcoma-associated
herpesvirus
(KSHV)
is
the
viral
E3
ubiquitin
ligase
,
K5
.
K5
is
known
to
downregulate
the
major
histocompatability
complex
(MHC)
class
one
,
which
is
part
of the
immune
response
.
Another
possible
target
for
downregulation
by
K5
,
BST-2
, had been
suggested
.
BST-2
has been
shown
to
inhibit
viral
egress
of
some
enveloped
viruses
by
tethering
nascent
virions
to the
surface
of the
cell
. Here the
relationship
of
K5
and
BST-2
, and that of
BST-2
and
KSHV
infection
,
is
examined
.
It
is
determined
that
K5
has the
ability
to
downregulate
BST-2
,
alone
or in the
context
of
KSHV
infection
. The
lysines
on the
cytoplasmic
N-terminal
tail
of
BST-2
are
ubiquitinated
by
K5
after
BST-2
leaves
the
ER
,
after
which
,
BST-2
is
then
destined
for the
lysosome
for
degradation
. In
addition
to this,
it
is
demonstrated
that
BST-2
has the
ability
to
restrict
KSHV
viral
release
in the
absence
of
K5
. By
showing
that
BST-2
is
a
bona
fide
substrate
of
K5
, the
importance
of
K5
in
overcoming
the
innate
immune
response
is
further
elucidated
.
Language
eng
Type
Text
Format.Use
Needs Adobe Acrobat to view
Format.FileSize
779889 Bytes
OCLC number
696374507
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