Rev Activity Determines Sensitivity of HIV-1-Infected Primary T Cells to CTL Killing

Bobbitt, Kevin; Addo, Marylyn M.; Altfeld, Marcus; Filzen, Tracey; Onafuwa, Adewunmi A.; Walker, Bruce D.; Collins, Kathleen L.

doi:10.1016/s1074-7613(03)00031-1

Cited by 42 publications

(35 citation statements)

References 46 publications

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“…Furthermore, HIV-1 Rev has recently been shown to influence MHC class I Ag presentation by an indirect mechanism (56). The Rev protein assists in the transport of certain other HIV-1 mRNAs, and so it is necessary for the expression of these other HIV-1 proteins (Gag, Pol, and Env).…”

Section: Hiv-1: Nef Tat and Now Revmentioning

confidence: 99%

Virus Evasion of MHC Class I Molecule Presentation

Petersen¹,

Morris²,

Solheim

2003

The Journal of Immunology

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Section: Hiv-1: Nef Tat and Now Revmentioning

confidence: 99%

Virus Evasion of MHC Class I Molecule Presentation

Petersen¹,

Morris²,

Solheim

2003

The Journal of Immunology

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“…NiV is in the genus Henipavirus, whose members are a source of public health and agricultural concern due to their ability to spread between species and to transmit through highly mobile reservoir species, specifically, the fruit-eating bats of the genus Pteropus (15,19,45,63). NiV is thought to be transmitted via a respiratory route; it presents as acute febrile encephalitis, causes high mortality, and can manifest a dangerous secondary spread to contacts (8,15,19,35). Like all viruses that are pathogenic for humans, NiV has evolved immune-antagonist proteins that suppress the human innate immune response and facilitate virus replication.…”

mentioning

confidence: 99%

Novel Nipah Virus Immune-Antagonism Strategy Revealed by Experimental and Computational Study

Seto

Qiao

Guenzel

et al. 2010

J Virol

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Nipah virus is an emerging pathogen that causes severe disease in humans. It expresses several antagonist proteins that subvert the immune response and that may contribute to its pathogenicity. Studies of its biology are difficult due to its high pathogenicity and requirement for biosafety level 4 containment. We integrated experimental and computational methods to elucidate the effects of Nipah virus immune antagonists. Individual Nipah virus immune antagonists (phosphoprotein and V and W proteins) were expressed from recombinant Newcastle disease viruses, and the responses of infected human monocyte-derived dendritic cells were determined. We developed an ordinary differential equation model of the infectious process that that produced results with a high degree of correlation with these experimental results. In order to simulate the effects of wild-type virus, the model was extended to incorporate published experimental data on the time trajectories of immune-antagonist production. These data showed that the RNA-editing mechanism utilized by the wild-type Nipah virus to produce immune antagonists leads to a delay in the production of the most effective immune antagonists, V and W. Model simulations indicated that this delay caused a disconnection between attenuation of the antiviral response and suppression of inflammation. While the antiviral cytokines were efficiently suppressed at early time points, some early inflammatory cytokine production occurred, which would be expected to increase vascular permeability and promote virus spread and pathogenesis. These results suggest that Nipah virus has evolved a unique immune-antagonist strategy that benefits from controlled expression of multiple antagonist proteins with various potencies.

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“…HIV-1 employs numerous mechanisms in order to evade the cell-mediated arm of the host immune response. These mechanisms include infection and elimination of HIV-specific CD4 ϩ -T-helper cells, viral mutational escape from immunodominant CTL epitopes, and downregulation of class I major histocompatibility complex molecules by Nef (12,31,37,38,42).…”

mentioning

confidence: 99%

Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120

Brainard

Tharp

Granado

et al. 2004

J Virol

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Cell-mediated immunity depends in part on appropriate migration and localization of cytotoxic T lymphocytes (CTL), a process regulated by chemokines and adhesion molecules. Many viruses, including human immunodeficiency virus type 1 (HIV-1), encode chemotactically active proteins, suggesting that dysregulation of immune cell trafficking may be a strategy for immune evasion. HIV-1 gp120, a retroviral envelope protein, has been shown to act as a T-cell chemoattractant via binding to the chemokine receptor and HIV-1 coreceptor CXCR4. We have previously shown that T cells move away from the chemokine stromal cell-derived factor 1 (SDF-1) in a concentration-dependent and CXCR4 receptor-mediated manner. Here, we demonstrate that CXCR4-binding HIV-1 X4 gp120 causes the movement of T cells, including HIV-specific CTL, away from high concentrations of the viral protein. This migratory response is CD4 independent and inhibited by anti-CXCR4 antibodies and pertussis toxin. Additionally, the expression of X4 gp120 by target cells reduces CTL efficacy in an in vitro system designed to account for the effect of cell migration on the ability of CTL to kill their target cells. Recombinant X4 gp120 also significantly reduced antigen-specific T-cell infiltration at a site of antigen challenge in vivo. The repellant activity of HIV-1 gp120 on immune cells in vitro and in vivo was shown to be dependent on the V2 and V3 loops of HIV-1 gp120. These data suggest that the active movement of T cells away from CXCR4-binding HIV-1 gp120, which we previously termed fugetaxis, may provide a novel mechanism by which HIV-1 evades challenge by immune effector cells in vivo.

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Rev Activity Determines Sensitivity of HIV-1-Infected Primary T Cells to CTL Killing

Cited by 42 publications

References 46 publications

Virus Evasion of MHC Class I Molecule Presentation

Virus Evasion of MHC Class I Molecule Presentation

Novel Nipah Virus Immune-Antagonism Strategy Revealed by Experimental and Computational Study

Migration ofAntigen-Specific T Cells Away from CXCR4-Binding Human ImmunodeficiencyVirus Type 1gp120

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