|Feb16-13, 09:26 AM||#1|
Understanding the logistics of oncolytic virotherapy
I have questions about a particular paper: Oncolytic Poxvirus Armed with Fas Ligand Leads to Induction of Cellular Fas Receptor and Selective Viral Replication in FasR Negative Cancer
The authors explain that they're using an oncolytic virus to deliver membrane-bound Fas ligand to cells in a non-specific manner. Their hypothesis is that apoptosis will be induced in normal cells which are FasR+, thereby aborting viral replication, whereas in cancer cells that have knocked out FasR, the virus will replicate fully and lyse the cell.
I'm confused as to how inducing apoptosis in this way will lead to abortive replication in normal cells. If FasL is membrane-bound, won't the virus-infected cell expressing it induce apoptosis in an adjacent, normal cell? That doesn't really seem efficacious.
Am I incorrect in assuming that somewhere along the line, there will be a normal cell that allows for productive replication of the virus?
|Mar3-13, 08:16 PM||#2|
yeah thats the problem if you inject a vial of fluid of virus that might enter the blood stream and go to other places. The idea that favors anti cancer is that cancer cells usually have a higher metabolic requirement which will become the target of most of the virus. You can always modify the virus to bind with unique cancer receptors, but who knows how well that will go on a live person.
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