Towards a multi-level and a multi-disciplinary approach to DNA oncovirus virulence

Abstract

One out of 10 cancers is estimated to arise from infections by a handful of oncogenic viruses. These infectious cancers constitute an opportunity for primary prevention through immunization against the viral infection, for early screening through molecular detection of the infectious agent, and potentially for specific treatments, by targeting the virus as a marker of cancer cells. Accomplishing these objectives will require a detailed understanding of the natural history of infections, the mechanisms by which the viruses contribute to disease, the mutual adaptation of viruses and hosts, and the possible viral evolution in the absence and in the presence of the public health interventions conceived to target them. This issue showcases the current developments in experimental tissue-like and animal systems, mathematical models and evolutionary approaches to understand DNA oncoviruses. Our global aim is to provide proximate explanations to the present-day interface and interactions between virus and host, as well as ultimate explanations about the adaptive value of these interactions and about the evolutionary pathways that have led to the current malignant phenotype of oncoviral infections. This article is part of the theme issue ‘Silent cancer agents: multi-disciplinary modelling of human DNA oncoviruses’.

The Cancer Principle-II: Cancer as the Origin of All Life on Earth

“…proliferation, invasiveness and virulence all along, to finally be able to activate the human oncogene by producing mutations so that it can completely incapacitate and overpower the highest evolved species by attaching its double stranded DNA to that of the humans [18,19] . In this perspective it is not surprising that virulence in some form or the other has always been on the rise through the entire course of evolution to achieve a sort of invincibility even in their continuous battle against human intelligence, finally landing in the genetic mode of transmission [20] .…”

Oncogenic and Stemness Signatures of the High-Risk HCMV Strains in Breast Cancer Progression

“…Between 15% and 20% of all human cancers possess a direct infectious origin [ 19 ]. To start with, human papillomavirus (HPV) strains were classified into high- and low-risk strains after being isolated from different lesions.…”

Downregulation of miR-143/145 Cluster in Breast Carcinoma Specimens: Putative Role of DNA Oncoviruses

“…Approximately 12% of all human malignancies have a viral origin. Among them, DNA oncoviruses, including human papillomavirus (HPV) and Epstein-Barr virus (EBV), account for a notable proportion and impose a high disease burden that is becoming greater in the world (6,7). Human papillomavirus, a member of the Papillomaviridae family, is a major etiological cause of cervical cancer.…”