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Oncolytic Virotherapy

Cancer continues to be a major worldwide challenge although very significant efforts have been made in the last 20 years to cope with this problem.  Advancements in research in biological sciences led to the discovery of present anticancer treatments including chemotherapy and radiotherapy, which are very common. They are widely used regardless of their confined effectiveness and severe side effects that change the patient’s standard of living. At the start of 20th century, there were many opportunities for the development of more active but less toxic anticancer approach. A connection between cancer worsening and viruses has long been reported and different cases of cancer deterioration after vaccination with a weakened virus appeared at the beginning of 20th century. Oncolytic virotherapy is one of the most powerful anticancer tools which is recently developed after the understanding genetic and molecular roots of cancer. Oncolytic virotherapy is the use of viruses to destroy cancer cells. The viruses used in this method are either naturally oncolytic or they are genetically engineered.

Some viruses, known as wild type viruses, such as parvoviruses, myxomavirusess, coxsackievirus and vesicular stomatitis virus excreta have natural ability to attain a strong cytolytic result, limited to cancer cells only. These viruses are under intense research for cancer therapy but their ability to cause lysis in tumors is limited in clinical trials (Everts B, et al., 2005).

Struggles to develop engineered oncolytic viruses have been primarily based on ordinary design. Directed evolution is the main method for developing very selective oncolytic viruses. Viruses are cultured under controlled conditions which increases their diversity. The variety produced by homologous recombination generates a group of viruses that can be passed through several other stages basically aimed to lead them to a preselected finding (e.g. high tumor specificity). The collection of these viruses can be screened out in preclinical trials for a specific virus with necessary therapeutic properties (Kuhan, et al., 2008). Attenuation involves knocking out the viral genes to eliminate viral processes which are expendable in tumors but not in normal cells, thereby engineering the virus to be safer and cancer specific (Chow, et al., 2013).

The primary hurdle to the success of viral infection in tumors is the immune system of the host which is aimed to attack any infectious agent. To overcome this problem, the virus can be covered with organic materials such as polyethylene glycol (Wonga Nan, et al., 2010). Likewise, these agents can be directed to cancerous part by hiding them in macrophages which naturally move to areas of damaged tissue particularly where cancer cells are located (Muthana, et al., 2012).

Oncolytic virotherapy focuses to engineer anticancer agents that can divide only in tumors. A large number of these agents are proceeded in clinical trials for several cancers and are shown to be harmless for normal cells but effective in triggering lysis in tumors. However, more research and study is required to allow these oncolytic agents to work with better efficacy. This may perhaps consist of diminishing immune responses and directing them to cause lysis in cancer cells. If these problems are repressed, oncolytic virotherapy will pass in a new phase of clinical oncology.

 

References

  • Russell, S. J., Peng, K. W., & Bell, J. C. (2012). Oncolytic virotherapy. Nature biotechnology30(7), 658-670.
  • Vile, R., Ando, D., & Kirin, D. (2002). The oncolytic virotherapy treatment platform for cancer: unique biological and biosafety points to consider. Cancer gene therapy9(12), 1062-1067.
  • Seymour, L. W., & Fisher, K. D. (2016). Oncolytic viruses: finally delivering. British journal of cancer.
  • Harrington, K. J. (2013). Oncolytic viruses: methods and protocols. British journal of cancer108(3), 735-735.
  • Liu, T. C., Galanis, E., & Kirin, D. (2007). Clinical trial results with oncolytic virotherapy: a century of promise, a decade of progress. Nature clinical practice Oncology4(2), 101-117.

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Muhammad Hassan Raza