Oncomedicine 2019; 4:35-42. doi:10.7150/oncm.34897 This volume


“Duel” and “Duet”: The Paradox of Carcinogenic Viruses and Targeted Virotherapeutics

Anup P. Challa1, Chikezie O. Madu2, Yi Lu3,✉

1. Department of Chemical and Biomolecular Engineering, Vanderbilt University, Nashville, Tennessee 37235, USA. anup.p.challa@vanderbilt.edu
2. Departments of Biological Sciences, University of Memphis, Memphis, TN 38152. USA. maduco@scsk12.org
3. Departments of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA. ylu@uthsc.edu

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Challa AP, Madu CO, Lu Y. “Duel” and “Duet”: The Paradox of Carcinogenic Viruses and Targeted Virotherapeutics. Oncomedicine 2019; 4:35-42. doi:10.7150/oncm.34897. Available from /v04p0035.htm

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Graphic abstract

In recent years, researchers have identified seven major viruses implicated in oncogenesis, spanning across four Baltimore virological classifications. Thus, viruses are known contributors to 19 human cancers, as well as 10 chronic comorbidities known to reduce quality of life among affected patient populations. This etiology, though minor among other sources of carcinogenesis, remains an interesting area of research for oncologists and molecular biologists in its potential for understanding the complex role of exogenous oncogenes in the growth of malignant tumors.

Conversely, biomolecular researchers have seen newfound success in viral engineering: through designing natural virions to transfect tumor cells, investigators can effectively harness viral vectors for the treatment of numerous malignancies. Recent studies propose this mechanism through lytic replication within cancerous cells, allowing for destruction of neoplasms through cell death. Furthermore, adaptive and innate immune responses are stimulated in this oncolytic virotherapy, destroying virions and tumor vasculature. With responses such as these, viruses are used to battle a variety of cancers, maintaining specificity against the infection of noncancerous cells. Recent advancements also include the application of type II CRISPR-Cas9 systems in re-activation of host cell cycle controls.

Thus, the relationships between viruses and neoplasia are complex. This paper seeks to explore the implications of “duel” viruses in oncogenesis, as well as “duet” virus approaches to the treatment of disparate malignancies.

Keywords: oncogenesis, duel, duet, viruses