The Htlv-1 P8 Protein Inhibits Antigen Presentation And Promotes Viral Transmission Via Dangerous Liasons.

Overview

Recent studies demonstrate that over-expressing Bap31 increases the major histocompatibility complex (MHC) I cell surface levels and stability 1. The goals of the present study were to further explore Bap31's role in MHC I traffic and quality control. We used fluorescence resonance energy transfer (FRET) and quantitative fluorescence imaging in HeLa cells to show clustering between Bap31 and an endoplasmic reticulum Golgi intermediate compartment (ERGIC) marker. Feeding cells high affinity peptide increased the ...
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Overview

Recent studies demonstrate that over-expressing Bap31 increases the major histocompatibility complex (MHC) I cell surface levels and stability 1. The goals of the present study were to further explore Bap31's role in MHC I traffic and quality control. We used fluorescence resonance energy transfer (FRET) and quantitative fluorescence imaging in HeLa cells to show clustering between Bap31 and an endoplasmic reticulum Golgi intermediate compartment (ERGIC) marker. Feeding cells high affinity peptide increased the amount of both Bap31 and MHC I in the ERGIC. Interestingly, the anterograde traffic of Bap31 can be blocked in cells over-expressing Bap29. We identified Bap31 coatomer protein (COP) I and COP II binding mutants. Finally, we show that neutralizing compartmental pH increased the amount of MHC I on the cell surface, but decreased overall stability. The pH neutralization treatment does not affect MHC I stability in Bap31 deficient cells, suggesting that pH is an important factor for normal Bap31 function. Human T-cell Leukemia/Lymphoma Virus Type I (HTLV-1) causes a persistent infection in T-cells that can culminate with leukemia. HTLV-1 is transmitted through cell-to-cell contact upon the formation of the virological synapse. However, the nature of the intercellular connections in HTLV-1 transmission remains unknown. HTLV-1 encodes a 12kD (p12I) protein that increases T-cell proliferation and the truncated form, p8I, that induces T-cell anergy. Here we reconcile this apparent paradox and found that the p8I increases T-cell contact and the number and length of tunneling nanotubes (TNTs), cellular conduits that establish a physical communication network among dendritic cells and T-cells, both targets of HTLV-I infection. Strikingly, p8I is rapidly transferred to neighboring cells through direct cell-cell contacts and TNT, which may prime surrounding T-cells for viral acquisition. The increase of cell-cell contact is explained in part by the clustering of LFA-1 adhesion molecule on the cell surface. Quantitative analysis revealed that HTLV-1 p8I significantly increases transmission of the HTLV-1 virus to neighboring cells. The core (Gag) and Envelope proteins of HTLV-I and p8I were visualized in the TNTs by confocal microscopy and live imaging. Electron microscopy demonstrated virus particles are associated with TNT formed following p8I expression. The ability of p8I to simultaneously induce T-cell anergy and cluster T-cells by TNT formation represents a novel and elegant example of virus adaptation in an immune competent host. This model identifies a novel viral target for intervention in HTLV-I infection.
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Product Details

  • ISBN-13: 9781243765833
  • Publisher: BiblioLabsII
  • Publication date: 9/9/2011
  • Pages: 232
  • Product dimensions: 7.44 (w) x 9.69 (h) x 0.49 (d)

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