Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases

@article{Kinoh2004GenerationOA,
  title={Generation of a recombinant Sendai virus that is selectively activated and lyses human tumor cells expressing matrix metalloproteinases},
  author={Hiroaki Kinoh and Makoto Inoue and Kentaro Washizawa and T. Yamamoto and S Fujikawa and Yumiko Tokusumi and Akihiro Iida and Yoshiyuki Nagai and Mamoru Hasegawa},
  journal={Gene Therapy},
  year={2004},
  volume={11},
  pages={1137-1145}
}
Malignant tumor cells often express matrix metalloproteinases (MMPs) at a high level to enable their dissemination and metastasis. Sendai virus (SeV), a nonsegmented negative strand RNA virus, spreads in the target tissues in vivo via cleavage activation of the viral fusion glycoprotein by a tissue-specific, trypsin-like enzyme. By deleting the viral matrix protein, we previously generated a recombinant SeV that does not bud to mature virions, but is highly fusogenic and spreads extensively… 
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References

SHOWING 1-10 OF 52 REFERENCES
A New Sendai Virus Vector Deficient in the Matrix Gene Does Not Form Virus Particles and Shows Extensive Cell-to-Cell Spreading
TLDR
SeV/ΔM is a novel type of vector with the characteristic features of loss of virus particle formation and gain of cell-to-cell spreading via a mechanism dependent on the activation of the fusion protein.
A Cytoplasmic RNA Vector Derived from Nontransmissible Sendai Virus with Efficient Gene Transfer and Expression
TLDR
A virion from defective cDNA of Sendai virus (SeV) that is capable of self-replication but incapable of transmissible-virion production is recovered and it is suggested that this vector has great potential for use in human gene therapy and vaccine delivery systems.
An oncolytic measles virus engineered to enter cells through the CD20 antigen.
TLDR
It is demonstrated that the entry of a replicating oncolytic virus can be mediated through an interaction between a highly clinically relevant single-chain antibody and its target antigen, and it is shown that this interaction enhances in vivo on colytic activity.
Targeting the cytotoxicity of fusogenic membrane glycoproteins in gliomas through protease–substrate interaction
TLDR
The use of matrix metalloproteinase (MMP) cleavable linkers to target cytotoxicity of FMGs against gliomas is reported on and data indicate that GALV-induced cytotoxic in glioma cell lines can be blocked by display of the CD40 ligand.
Oncolytic measles viruses displaying a single-chain antibody against CD38, a myeloma cell marker.
TLDR
A new specificity domain against the plasma cell marker CD38 was constructed in the form of a single-chain antibody (scFv) and display of that scFv on the measles viral envelope glycoprotein successfully redirected virus entry through CD38 expressed on target cells devoid of the natural MV receptors.
An endoprotease homologous to the blood clotting factor X as a determinant of viral tropism in chick embryo.
TLDR
An endoprotease from chick embryo is isolated, that activates para‐ and orthomyxovirus fusion glycoproteins by cleaving their precursor proteins at a specific, single arginine site and was found to be highly homologous, if not identical, to the blood clotting factor X(FX), a member of the prothrombin family.
Trypsin action on the growth of Sendai virus in tissue culture cells. I. Restoration of the infectivity for L cells by direct action of tyrpsin on L cell-borne Sendai virus.
  • M. Homma
  • Biology, Medicine
    Journal of virology
  • 1971
TLDR
Recovery of the infectivity of L Sendai for L cells due to a direct enzymatic action of trypsin was demonstrated, showing that variations of Sendai virus in theinfectivity for L Cells and in the density are independent types of host-controlled modification.
Cytolytic viruses as potential anti-cancer agents.
  • C. Ring
  • Biology, Medicine
    The Journal of general virology
  • 2002
TLDR
Increasing knowledge of the pathogenesis of virus disease and the ability to manipulate specific regions of viral genomes have allowed the construction of viruses that are attenuated in normal cells but retain their ability to lyse tumour cells.
Viral oncolysis.
TLDR
The paradoxical roles of the immune response are addressed with respect to oncolytic viral therapy, as it, on one hand, impedes the spread of viral infection, and on the other, augments tumor cell destruction through the recruitment of T cells "vaccinated" against tumor antigens.
Metastatic and non-metastatic colorectal cancer (CRC) cells induce host metalloproteinase production in vivo
TLDR
Enhanced host MMP-9 production in metastatic CRC cell-derived subcutaneous and cecal tumors suggests that metastatic colon cells may acquire the expression of important MMP regulating factor(s) in vivo.
...
1
2
3
4
5
...