Cycle of Infection

Following infection of the host, the virus (G) protein binds to a cellular receptor, which has yet to be specifically identified, and penetrates the cell membrane to release the RNP particles (28). VSV is known to infect a wide range of cell types including many transformed cells, indicating that receptor target(s) for G are commonly expressed molecules (21,34). This property is obviously advantageous when considering VSV as a treatment for malignant disease, because the agent can be potentially used against different tumor types. Phosphatidylserine (PS) on the cell membrane is thought to be involved in binding to G and assisting with VSV endocytosis (26,28). A reduction in pH within the endosome then induces membrane fusion, which liberates the viral cores into the cytoplasm. Some free polymerase protein, which is carried into the cell by VSV, binds to the 3'-end of the genome and starts to sequentially synthesize the individual

Table 2

In Vivo Tumor Models of Oncolytic RNA Viruses other than Rhabdoviridae

Table 2

In Vivo Tumor Models of Oncolytic RNA Viruses other than Rhabdoviridae

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