| Natalie Raso - Weapons of Targeted Destruction: Using Viruses to Kill Cancer | Discussion of KM110r Efficacy |
| Project
Information Abstract Project Summary Background Purpose Scientific Thought Hypotheses Apparatus and Materials Genetically Engineered KM110red Herpesvirus Methodology Procedure for Cell-Line Splitting Procedure for KM110r Infection Procedure for Immunofluorescent Microscopy Imaging Statistical Analyses Proliferation Assay Analyzed Data Major Results Graphed Results Discussion of Statistics Controls and Variables Conclusions Discussion Discussion of KM110r Efficacy Successes and Failures Sources of Error and Data Limitations Future Research Applications Glossary Bibliography Acknowledgements |
It is currently unknown why KM110r
functions as an oncolytic virus, as it can successfully target and destroy
only cancerous cells while remaining non-toxic to normal
cells. One possible reason may have to do
with the truncation of the ICP0 gene. ICP0 might block the interferon
pathway. This would make it antiviral and anti-proliferative, therefore
causing apoptosis and cell arrest. If a normal cell is infected by a
wild-type HSV-1, the interferon in the cell attempts to increase the
resistance of the cells to attacks by viruses. The ICP0 may block the
interferon pathway allowing the virus to infect the normal cell.
If a normal cell is infected by a
virus that is missing ICP0 (such as KM110r), the interferon may
successfully resist viral infection. In this case the normal cell may not
become infected with the virus. In a cancerous cell there is no
interferon to prevent viral infection. Cancer cells are
interferon-defective because they have defects in interferon signalling.
In this situation, either a wild-type or ICP0 deficient virus could
successfully infect the cancerous cell.
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