RIG-I-Mediated Antiviral Signaling Is Inhibited in HIV-1 Infection by a Protease-Mediated Sequestration of RIG-I

Solis, Mayra; Nakhaei, Peyman; Jalalirad, Mohammad; Lacoste, Judith; Douville, Renée N.; Arguello, Meztli; Zhao, Tiejun; Laughrea, Michael; Wainberg, Mark A.; Hiscott, John

doi:10.1128/jvi.01635-10

Cited by 165 publications

(183 citation statements)

References 78 publications

(86 reference statements)

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“…In contrast to the typical scenario, HIV-1 infection of T-cells and macrophages does not stimulate IRF3 activation and fails to induce IFN expression, but does lead to expression of a subset of ISGs [3][4][5]. However, it has been reported that HIV-1 genomic RNA can induce IFN responses in specific cell culture systems via toll-like receptor 7 and retinoid-acid inducible gene I [6][7][8]. Moreover, it has become clear that a potent type I IFN response can be induced by HIV-1 infection under conditions where the cellular DNA exonuclease Trex-1 is depleted [9].…”

Section: Human Immunodeficiency Virus Type 1 (Hiv-1) Is the Cause Ofmentioning

confidence: 77%

Caught in translation: innate restriction of HIV mRNA translation by a schlafen family protein

2012

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Section: Human Immunodeficiency Virus Type 1 (Hiv-1) Is the Cause Ofmentioning

confidence: 77%

Caught in translation: innate restriction of HIV mRNA translation by a schlafen family protein

2012

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“…Among genes commonly modulated by ATRA in CCR6 + and CCR6 -T cells, the RIG-I is essential for sensing of viral nucleic acids and promoting antiviral immunity (66). HIV is known to subvert RIG-I-mediated antiviral mechanisms (67); this may explain robust HIV replication in RIG-I-expressing ATRA-treated CCR6 + T cells. Of particular importance, Li et al recently demonstrated that acitretin, a RA derivative, increases HIV transcription in CD4 + T cells from ART-treated HIV-infected individuals and enhances RIG-I signaling, thus leading to an antiviral response and the apoptosis of infected cells (68).…”

Section: Discussionmentioning

confidence: 99%

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

Planas¹,

Zhang²,

Monteiro³

et al. 2017

JCI Insight

161

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“…Upon recognition of foreign elements, they elicit the production of cytokines that protect noninfected cells and attract effector cells to the site of infection. HIV-1 infection perturbs innate antiviral signaling through specific disruption of both TLR and RIG-I signaling [83,84]. The determinants of this inhibition lie in the Pol polyprotein; the viral protease causes inhibition of IFN regulator factor-3 (IRF-3) phosphorylation, which results in a decrease of IFN and IFN-stimulated genes transcription [84].…”

Section: Box 2 Prrs Constitute the First Line Of Defense Against Pathmentioning

confidence: 99%

How Samhd1 changes our view of viral restriction

Laguette¹,

Benkirane²

2012

Trends in Immunology

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Recent studies have uncovered sterile alpha motif and HD domain 1 (SAMHD1) as the restriction factor that blocks HIV-1 replication in myeloid cells. In contrast to previously identified HIV-1 restriction factors, SAMHD1 does not meet a countermeasure developed by HIV-1. However, HIV-2 and certain simian immunodeficiency virus (SIV) strains express the auxiliary protein Vpx that potently blocks SAMHD1. It is therefore perplexing why this function has been lost or not acquired during the course of lentiviral evolution. This article summarizes the similarities and differences between SAMHD1 and other HIV-1 restriction factors, while highlighting the new questions that are emerging about the crosstalk between restriction factors and innate immune responses. Intrinsic cellular defenses and the viral arsenalHIV was identified as a human pathogen 28 years ago [1]. As a result of the inability of the human host to mount a coordinated immune response to the virus, infection by HIV usually results in chronic activation of the immune system that paradoxically allows for poorly controlled viral replication and immune exhaustion: the hallmark of AIDS. HIV-1 has evolved from SIVcpz, which causes AIDS in its natural chimpanzee host, whereas HIV-2 has evolved from SIVsm, which replicates to high levels in its natural simian host without causing disease [2] (Box 1). Hence, it is possible to speculate that lentiviruses and their host immune systems undergo an evolutionary co-adaptation to establish an equilibrium that will permit efficient spread without killing the host. However, tolerance to the infection is a multifactorial process that requires a fertile ground in the host as much as specific features of the virus. Here, we review the recent advances related to how host restriction factors may influence immune sensing and response against HIV. In particular, we examine the recent identification that the immune modulator SAMHD1 is the HIV restriction factor operating in myeloid cells, which are key players in the immune response during viral infection. A not so fertile ground?Upon entry into the human host, viruses are confronted with numerous blocks that oppose their replication (Figure 1). The first line of defense to be triggered is the so-called 'intrinsic' immune system. The intrinsic immune system includes proteins that detect the presence of the assailant pattern recognition receptors (PRRs), [Box 2] and which initiate a subsequent immune response, as well as proteins referred to as restriction factors that are directly devoted to arresting the replication cycle of the virus. To date, four restriction factors have been identified that specifically block HIV-1 replication: tripartite motif (TRIM)5α, apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G Europe PMC Funders Author ManuscriptsEurope PMC Funders Author Manuscripts (APOBEC3G) (A3G), bone marrow stromal cell antigen 2 (BST-2) (also known as tetherin) and SAMHD1 [3][4][5][6][7]. Host restriction factor characteristicsTRIM5α interacts with...

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RIG-I-Mediated Antiviral Signaling Is Inhibited in HIV-1 Infection by a Protease-Mediated Sequestration of RIG-I

Cited by 165 publications

References 78 publications

Caught in translation: innate restriction of HIV mRNA translation by a schlafen family protein

Caught in translation: innate restriction of HIV mRNA translation by a schlafen family protein

HIV-1 selectively targets gut-homing CCR6+CD4+ T cells via mTOR-dependent mechanisms

How Samhd1 changes our view of viral restriction

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