Human oncogenic viruses: nature and discovery

Abstract

Seven kinds of virus collectively comprise an important cause of cancer, particularly in less developed countries and for people with damaged immune systems. Discovered over the past 54 years, most of these viruses are common infections of humankind for which malignancy is a rare consequence. Various cofactors affect the complex interaction between virus and host and the likelihood of cancer emerging. Although individual human tumour viruses exert their malignant effects in different ways, there are common features that illuminate mechanisms of oncogenesis more generally, whether or not there is a viral aetiology. This article is part of the themed issue ‘Human oncogenic viruses’.

Prevention of liver cancer with new curative hepatitis C antivirals: Real‐world challenges

“…Although less than 15% of all human cancers are produced by viruses, the epidemiology and treatment paradigms of these neoplasms are unique . There are 6 oncogenic viruses that cause tumors in humans, including hepatitis B virus and hepatitis C virus (HCV; Table ).…”

“…Interestingly, although a large number of people in the world harbor at least 1 of these oncoviruses, only a small proportion of carriers go on to develop cancer. Human immunodeficiency virus (HIV) contributes indirectly to viral cancers by causing immune dysfunction, and this is why the AIDS virus is considered within the category of cancer viruses by the International Agency for Cancer Research …”

Short‐ and long‐term evolution in our arms race with cancer: Why the war on cancer is winnable

“…First, proliferation of infected cells may directly augment the replication of viral genome (Ewald & Swain Ewald, , ). Second, in cases where host immune responses to virus‐infected cells involves the initiation of cell‐cycle arrest and programmed cell death, viruses may enhance their survival by opposing cell‐cycle arrest, with uncontrolled cell proliferation as a consequence (Chang, Moore, & Weiss, ). Evolution in these viral populations will, in both the short and long terms, oppose both direct antiviral treatments (e.g., in response to screen‐and‐treat programs against hepatitis B and C virus infections; Plummer et al., ) and anticancer treatments.…”

“…Established infections of oncogenic viruses should evolve to oppose our cancer therapies, but it is unclear how readily viruses could manipulate the cancer phenotype of their host's cells to evade our treatments; empirical work on this question is needed. Furthermore, the finding that many tumor cells host only latent or “pseudolatent” viruses that are not actively replicating (Chang et al., ) suggests that viral evolution may not strongly oppose anticancer treatments. Once the cancer progresses to threaten host survival, the evolutionary interests of the cancer cells and the oncogenic virus are no longer well aligned (Chang et al., ; Ewald & Swain Ewald, ) and the reproductive value of viruses remaining in the host will be low; thus, oncogenic viruses may not strongly oppose treatments of metastatic cancer, especially if they arrest cancer development rather than creating an outright cure.…”

DNA methyltransferases in virus‐associated cancers

“…Caner is a main public health issue, and only in the United States, 1 735 350 new cancer cases is projected to occur in 2018 . Many factors can be involved in causing oncogenesis, but among them, the role of tumor viruses is remarkable . It is believed that approximately 12% of human cancers are casually associated with viruses including human papillomavirus, Epstein‐Barr virus, Kaposi's sarcoma‐associated herpesvirus, hepatitis B virus, hepatitis C virus, human T‐lymphotropic virus 1, and Merkel cell polyomavirus, the most recent member of human oncogenic virus .…”