Vesicular Stomatitis Virus

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Richard Vile - One of the best experts on this subject based on the ideXlab platform.

  • Interference of CD40L-Mediated Tumor Immunotherapy by Oncolytic Vesicular Stomatitis Virus
    Human Gene Therapy, 2010
    Co-Authors: Feorillo Galivo, Rosa Maria Diaz, Timothy Kottke, Phonphimon Wongthida, Jill Thompson, Glen N Barber, Uma Thanarajasingam, Dragan Jevremovic, Alan Melcher, Richard Vile
    Abstract:

    Galivo and colleagues examine the efficacy of two different vector platforms in tumor immunotherapy. The authors report that replication-defective adenoVirus (Ad)- and Vesicular Stomatitis Virus (VSV)-based vectors induce antitumor immunity via different therapeutic effector mechanisms.

  • oncolytic immunovirotherapy for melanoma using Vesicular Stomatitis Virus
    Cancer Research, 2007
    Co-Authors: Rosa Maria Diaz, Feorillo Galivo, Timothy Kottke, Phonphimon Wongthida, Jian Qiao, Jill Thompson, Mikael Valdes, Glen N Barber, Richard Vile
    Abstract:

    Relatively little attention has been paid to the role of virotherapy in promoting antitumor immune responses. Here, we show that CD8+ T cells are critical for the efficacy of intratumoral Vesicular Stomatitis Virus virotherapy and are induced against both virally encoded and tumor-associated immunodominant epitopes. We tested three separate immune interventions to increase the frequency/activity of activated antitumoral T cells. Depletion of Treg had a negative therapeutic effect because it relieved suppression of the antiviral immune response, leading to early viral clearance. In contrast, increasing the circulating levels of tumor antigen–specific T cells using adoptive T cell transfer therapy, in combination with intratumoral virotherapy, generated significantly improved therapy over either adoptive therapy or virotherapy alone. Moreover, the incorporation of a tumor-associated antigen within the oncolytic Vesicular Stomatitis Virus increased the levels of activation of naive T cells against the antigen, which translated into increased antitumor therapy. Therefore, our results show that strategies which enhance immune activation against tumor-associated antigens can also be used to enhance the efficacy of virotherapy. [Cancer Res 2007;67(6):2840–7]

Dekai Zhang - One of the best experts on this subject based on the ideXlab platform.

  • a novel toll like receptor that recognizes Vesicular Stomatitis Virus
    Journal of Biological Chemistry, 2011
    Co-Authors: Amir Sanchez, Tingting Zhang, Jun Wang, Jianhua Yang, Songbin Fu, Dekai Zhang
    Abstract:

    Toll-like receptors (TLRs) are the key molecular sensors used by the mammalian innate immune system to detect various types of pathogens. Tlr13 is a novel and uncharacterized member of the mammalian TLR family. Here we report the cloning and characterization of tlr13. Tlr13 is predominantly expressed in the spleen, particularly in dendritic cells and macrophages. Tlr13 appears to activate a MyD88- and TAK1-dependent TLR signaling pathway, inducing the activation of NF-κB. This receptor can also activate type 1 interferon through IRF7. Furthermore, Tlr13 seems to be another intracellular TLR. Remarkably, cells expressing tlr13 fail to respond to known TLR ligands but instead respond specifically to Vesicular Stomatitis Virus. Cells with the knockdown of tlr13 are highly susceptible to Vesicular Stomatitis Virus infection. Thus, these results provide an important insight into the potential role of the novel Toll-like receptor tlr13 in the recognition of viral infection.

Amir Sanchez - One of the best experts on this subject based on the ideXlab platform.

  • a novel toll like receptor that recognizes Vesicular Stomatitis Virus
    Journal of Biological Chemistry, 2011
    Co-Authors: Amir Sanchez, Tingting Zhang, Jun Wang, Jianhua Yang, Songbin Fu, Dekai Zhang
    Abstract:

    Toll-like receptors (TLRs) are the key molecular sensors used by the mammalian innate immune system to detect various types of pathogens. Tlr13 is a novel and uncharacterized member of the mammalian TLR family. Here we report the cloning and characterization of tlr13. Tlr13 is predominantly expressed in the spleen, particularly in dendritic cells and macrophages. Tlr13 appears to activate a MyD88- and TAK1-dependent TLR signaling pathway, inducing the activation of NF-κB. This receptor can also activate type 1 interferon through IRF7. Furthermore, Tlr13 seems to be another intracellular TLR. Remarkably, cells expressing tlr13 fail to respond to known TLR ligands but instead respond specifically to Vesicular Stomatitis Virus. Cells with the knockdown of tlr13 are highly susceptible to Vesicular Stomatitis Virus infection. Thus, these results provide an important insight into the potential role of the novel Toll-like receptor tlr13 in the recognition of viral infection.

G W Wertz - One of the best experts on this subject based on the ideXlab platform.

  • structure of the Vesicular Stomatitis Virus nucleoprotein rna complex
    Science, 2006
    Co-Authors: Todd Green, Xin Zhang, G W Wertz
    Abstract:

    Vesicular Stomatitis Virus is a negative-stranded RNA Virus. Its nucleoprotein (N) binds the viral genomic RNA and is involved in multiple functions including transcription, replication, and assembly. We have determined a 2.9 angstrom structure of a complex containing 10 molecules of the N protein and 90 bases of RNA. The RNA is tightly sequestered in a cavity at the interface between two lobes of the N protein. This serves to protect the RNA in the absence of polynucleotide synthesis. For the RNA to be accessed, some conformational change in the N protein should be necessary.

Glen N Barber - One of the best experts on this subject based on the ideXlab platform.

  • Interference of CD40L-Mediated Tumor Immunotherapy by Oncolytic Vesicular Stomatitis Virus
    Human Gene Therapy, 2010
    Co-Authors: Feorillo Galivo, Rosa Maria Diaz, Timothy Kottke, Phonphimon Wongthida, Jill Thompson, Glen N Barber, Uma Thanarajasingam, Dragan Jevremovic, Alan Melcher, Richard Vile
    Abstract:

    Galivo and colleagues examine the efficacy of two different vector platforms in tumor immunotherapy. The authors report that replication-defective adenoVirus (Ad)- and Vesicular Stomatitis Virus (VSV)-based vectors induce antitumor immunity via different therapeutic effector mechanisms.

  • oncolytic immunovirotherapy for melanoma using Vesicular Stomatitis Virus
    Cancer Research, 2007
    Co-Authors: Rosa Maria Diaz, Feorillo Galivo, Timothy Kottke, Phonphimon Wongthida, Jian Qiao, Jill Thompson, Mikael Valdes, Glen N Barber, Richard Vile
    Abstract:

    Relatively little attention has been paid to the role of virotherapy in promoting antitumor immune responses. Here, we show that CD8+ T cells are critical for the efficacy of intratumoral Vesicular Stomatitis Virus virotherapy and are induced against both virally encoded and tumor-associated immunodominant epitopes. We tested three separate immune interventions to increase the frequency/activity of activated antitumoral T cells. Depletion of Treg had a negative therapeutic effect because it relieved suppression of the antiviral immune response, leading to early viral clearance. In contrast, increasing the circulating levels of tumor antigen–specific T cells using adoptive T cell transfer therapy, in combination with intratumoral virotherapy, generated significantly improved therapy over either adoptive therapy or virotherapy alone. Moreover, the incorporation of a tumor-associated antigen within the oncolytic Vesicular Stomatitis Virus increased the levels of activation of naive T cells against the antigen, which translated into increased antitumor therapy. Therefore, our results show that strategies which enhance immune activation against tumor-associated antigens can also be used to enhance the efficacy of virotherapy. [Cancer Res 2007;67(6):2840–7]

  • defective translational control facilitates Vesicular Stomatitis Virus oncolysis
    Cancer Cell, 2004
    Co-Authors: Siddharth Balachandran, Glen N Barber
    Abstract:

    Abstract Vesicular Stomatitis Virus (VSV) exerts potent antitumor activity, although the molecular mechanisms underlying its oncolytic properties remain to be fully clarified. Here, we demonstrate that normally resistant murine embryonic fibroblasts are rendered highly permissive to VSV replication following cellular transformation, a progression that appears to compromise the antiviral effects of interferon (IFN). Subsequent studies revealed normal dsRNA-dependent protein kinase (PKR) activation and phosphorylation of eukaryotic initiation factor 2 (eIF2) α. Nevertheless, eIF2B-mediated guanine nucleotide exchange activity downstream of eIF2 was frequently aberrant in transformed cells, neutralizing eIF2α phosphorylation and permitting VSV mRNA translation. Thus, defects in translational regulation can cooperate with impaired IFN signaling to facilitate VSV replication, and may represent a common hallmark of tumorigenesis.