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Review
. 2017 Jan 19;13(1):e1006078.
doi: 10.1371/journal.ppat.1006078. eCollection 2017 Jan.

Common Commensal Cancer Viruses

Patrick S Moore  1 , Yuan Chang  1
Affiliations
Review

Common Commensal Cancer Viruses

Patrick S Moore et al. PLoS Pathog. .
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Classical epidemiology is poorly equipped to determine multifactorial causality for common commensal tumor viruses, such as EBV.
Multifactorial causal reasoning is shown for a simple electrical circuit (inset) with two switches, Switch 1 and Switch 2, either of which can “cause” the light bulb to turn on. An analogous pathway is shown for the genesis of Burkitt lymphoma, in which EBV is responsible for a portion of tumors, but also only in the biological context of other factors, such as cMYC translocations. Since EBV is nearly ubiquitous, teasing out its contribution to a rare cancer like Burkitt lymphoma is supremely difficult using standard epidemiologic methods, but is readily evident using molecular biologic information that has been available for decades. EBV is clonal in these tumors based on terminal repeat copies and Epstein–Barr encoding region (EBER) in situ hybridization typically reveals the presence of EBV genome in all tumor cells but not surrounding nontumor cells. These facts are biologically implausible for a non-causal passenger infection [6].
See this image and copyright information in PMC

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