Vesicular stomatitis virus as an oncolytic vector

被引:109
作者
Barber, GN [1 ]
机构
[1] Miami Univ, Sch Med, Sylvester Comprehens Canc Ctr, Dept Microbiol & Immunol, Miami, FL 33136 USA
关键词
D O I
10.1089/vim.2004.17.516
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent data has shown that viruses such as vesicular stomatitis virus (VSV), a relatively non-pathogenic, negative-stranded RNA virus, can preferentially replicate in malignant cells and less so in normal cells. VSV appears able to carry out this function in transformed cells since these hosts exhibit the hallmarks of flawed host defense, probably involving the interferon system, which is essential for preventing virus replication. The simple genetic constitution of VSV, lack of any known transforming, integrating or reassortment properties, extensive knowledge relating to its interaction with the immune system and the ability to genetically manipulate this agent affords an ideal opportunity to exploit the oncolytic and gene targeting potential of this innocuous virus. Thus, aside from preferentially targeting malignant cells VSV recombinants could be generated that could increase a tumor's susceptibility to chemotherapeutic agents and/ or importantly, the host immune response. Collectively, our data and others demonstrate that VSV as well as other RNA viruses could provide a promising and exciting approach to cancer therapy.
引用
收藏
页码:516 / 527
页数:12
相关论文
共 96 条
[1]   Characterization of transgenic mice with targeted disruption of the catalytic domain of the double-stranded RNA-dependent protein kinase, PKR [J].
Abraham, N ;
Stojdl, DF ;
Duncan, PI ;
Méthot, N ;
Ishii, T ;
Dubé, M ;
Vanderhyden, BC ;
Atkins, HL ;
Gray, DA ;
McBurney, MW ;
Koromilas, AE ;
Brown, EG ;
Sonenberg, N ;
Bell, JC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (09) :5953-5962
[2]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[3]  
Ansardi DC, 2001, CANCER RES, V61, P8470
[4]   Defective translational control facilitates vesicular stomatitis virus oncolysis [J].
Balachandran, S ;
Barber, GN .
CANCER CELL, 2004, 5 (01) :51-65
[5]   Alpha/beta interferons potentiate virus-induced apoptosis through activation of the FADD/caspase-8 death signaling pathway [J].
Balachandran, S ;
Roberts, PC ;
Kipperman, T ;
Bhalla, KN ;
Compans, RW ;
Archer, DR ;
Barber, GN .
JOURNAL OF VIROLOGY, 2000, 74 (03) :1513-1523
[6]   Oncolytic activity of vesicular stomatitis virus is effective against tumors exhibiting aberrant p53, Ras, or Myc function and involves the induction of apoptosis [J].
Balachandran, S ;
Porosnicu, M ;
Barber, GN .
JOURNAL OF VIROLOGY, 2001, 75 (07) :3474-3479
[7]   Essential role for the dsRNA-dependent protein kinase PKR in innate immunity to viral infection [J].
Balachandran, S ;
Roberts, PC ;
Brown, LE ;
Truong, H ;
Pattnaik, AK ;
Archer, DR ;
Barber, GN .
IMMUNITY, 2000, 13 (01) :129-141
[8]   Vesicular stomatitis virus (VSV) therapy of tumors [J].
Balachandran, S ;
Barber, GN .
IUBMB LIFE, 2000, 50 (02) :135-138
[9]   Phenotypic consequences of rearranging the P, M, and G genes of vesicular stomatitis virus [J].
Ball, LA ;
Pringle, CR ;
Flanagan, B ;
Perepelitsa, VP ;
Wertz, GW .
JOURNAL OF VIROLOGY, 1999, 73 (06) :4705-4712
[10]   Vesicular stomatitis virus expressing a chimeric Sindbis glycoprotein containing an Fc antibody binding domain targets to Her2/neu overexpressing breast cancer cells [J].
Bergman, I ;
Whitaker-Dowling, P ;
Gao, YH ;
Griffin, JA ;
Watkins, SC .
VIROLOGY, 2003, 316 (02) :337-347