TRAF6 and IRF7 control HIV replication in macrophages
TRAF6 and IRF7 control HIV replication in macrophages
The innate immune system recognizes virus infection and evokes antiviral responses which include producing type I interferons (IFNs). The induction of IFN provides a crucial mechanism of antiviral defense by upregulating interferon-stimulated genes (ISGs) that restrict viral replication. ISGs inhibit the replication of many viruses by acting at different steps of their viral cycle. Specifically, IFN treatment prior to in vitro human immunodeficiency virus (HIV) infection stops or significantly delays HIV-1 production indicating that potent inhibitory factors are generated. We report that HIV-1 infection of primary human macrophages decreases tumor necrosis factor receptor-associated factor 6 (TRAF6) and virus-induced signaling adaptor (VISA) expression, which are both components of the IFN signaling pathway controlling viral replication. Knocking down the expression of TRAF6 in macrophages increased HIV-1 replication and augmented the expression of IRF7 but not IRF3. Suppressing VISA had no impact on viral replication. Overexpression of IRF7 resulted in enhanced viral replication while knocking down IRF7 expression in macrophages significantly reduced viral output. These findings are the first demonstration that TRAF6 can regulate HIV-1 production and furthermore that expression of IRF7 promotes HIV-1 replication.
e28125
Sirois, M.
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Robitaille, L.
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Allary, R.
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Shah, M.
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Woelk, C.H.
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Estaquier, J.
9a486fdf-5e17-426f-b7e0-26fb46984faf
Corbeil, J.C.
493a211d-6d39-4b08-9d99-236e1ab6fb94
28 November 2011
Sirois, M.
c412412e-18bc-4287-8a57-c49ca763fbb3
Robitaille, L.
3a878bef-6ed0-4091-870a-5061b4f9230c
Allary, R.
c6f78624-8a77-451e-8bd9-c8bd5143f0b5
Shah, M.
c89fdf39-3923-475c-9365-d51d86888d6c
Woelk, C.H.
4d3af0fd-658f-4626-b3b5-49a6192bcf7d
Estaquier, J.
9a486fdf-5e17-426f-b7e0-26fb46984faf
Corbeil, J.C.
493a211d-6d39-4b08-9d99-236e1ab6fb94
Sirois, M., Robitaille, L., Allary, R., Shah, M., Woelk, C.H., Estaquier, J. and Corbeil, J.C.
(2011)
TRAF6 and IRF7 control HIV replication in macrophages.
PLoS ONE, 6 (11), .
(doi:10.1371/journal.pone.0028125).
(PMID:22140520)
Abstract
The innate immune system recognizes virus infection and evokes antiviral responses which include producing type I interferons (IFNs). The induction of IFN provides a crucial mechanism of antiviral defense by upregulating interferon-stimulated genes (ISGs) that restrict viral replication. ISGs inhibit the replication of many viruses by acting at different steps of their viral cycle. Specifically, IFN treatment prior to in vitro human immunodeficiency virus (HIV) infection stops or significantly delays HIV-1 production indicating that potent inhibitory factors are generated. We report that HIV-1 infection of primary human macrophages decreases tumor necrosis factor receptor-associated factor 6 (TRAF6) and virus-induced signaling adaptor (VISA) expression, which are both components of the IFN signaling pathway controlling viral replication. Knocking down the expression of TRAF6 in macrophages increased HIV-1 replication and augmented the expression of IRF7 but not IRF3. Suppressing VISA had no impact on viral replication. Overexpression of IRF7 resulted in enhanced viral replication while knocking down IRF7 expression in macrophages significantly reduced viral output. These findings are the first demonstration that TRAF6 can regulate HIV-1 production and furthermore that expression of IRF7 promotes HIV-1 replication.
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Published date: 28 November 2011
Organisations:
Clinical & Experimental Sciences
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Local EPrints ID: 352895
URI: http://eprints.soton.ac.uk/id/eprint/352895
ISSN: 1932-6203
PURE UUID: 88cf7b02-3edf-4f3e-b89d-e522136b9807
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Date deposited: 23 May 2013 14:12
Last modified: 14 Mar 2024 13:57
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Contributors
Author:
M. Sirois
Author:
L. Robitaille
Author:
R. Allary
Author:
M. Shah
Author:
C.H. Woelk
Author:
J. Estaquier
Author:
J.C. Corbeil
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