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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Virol
2015 ; 89
(9
): 4880-93
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Oncogenic human T-cell lymphotropic virus type 1 tax suppression of primary
innate immune signaling pathways
#MMPMID25694597
Hyun J
; Ramos JC
; Toomey N
; Balachandran S
; Lavorgna A
; Harhaj E
; Barber GN
J Virol
2015[May]; 89
(9
): 4880-93
PMID25694597
show ga
Human T-cell lymphotropic virus type I (HTLV-1) is an oncogenic retrovirus
considered to be the etiological agent of adult T-cell leukemia (ATL). The viral
transactivator Tax is regarded as the oncoprotein responsible for contributing
toward the transformation process. Here, we demonstrate that Tax potently
inhibits the activity of DEx(D/H) box helicases RIG-I and MDA5 as well as
Toll-dependent TIR-domain-containing adapter-inducing interferon-? (TRIF), which
function as cellular sensors or mediators of viral RNA and facilitate innate
immune responses, including the production of type I IFN. Tax manifested this
function by binding to the RIP homotypic interaction motif (RHIM) domains of TRIF
and RIP1 to disrupt interferon regulatory factor 7 (IRF7) activity, a critical
type I IFN transcription factor. These data provide further mechanistic insight
into HTLV-1-mediated subversion of cellular host defense responses, which may
help explain HTLV-1-related pathogenesis and oncogenesis. IMPORTANCE: It is
predicted that up to 15% of all human cancers may involve virus infection. For
example, human T-cell lymphotropic virus type 1 (HTLV-1) has been reported to
infect up to 25 million people worldwide and is the causative agent of adult
T-cell leukemia (ATL). We show here that HTLV-1 may be able to successfully
infect the T cells and remain latent due to the virally encoded product Tax
inhibiting a key host defense pathway. Understanding the mechanisms by which Tax
subverts the immune system may lead to the development of a therapeutic treatment
for HTLV-1-mediated disease.
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