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Review
. 2014 Oct 23;6(10):4047-79.
doi: 10.3390/v6104047.

Human viruses and cancer

Abigail Morales-Sánchez  1 , Ezequiel M Fuentes-Pananá  2
Affiliations
Review

Human viruses and cancer

Abigail Morales-Sánchez et al. Viruses. .

Abstract

The first human tumor virus was discovered in the middle of the last century by Anthony Epstein, Bert Achong and Yvonne Barr in African pediatric patients with Burkitt's lymphoma. To date, seven viruses -EBV, KSHV, high-risk HPV, MCPV, HBV, HCV and HTLV1- have been consistently linked to different types of human cancer, and infections are estimated to account for up to 20% of all cancer cases worldwide. Viral oncogenic mechanisms generally include: generation of genomic instability, increase in the rate of cell proliferation, resistance to apoptosis, alterations in DNA repair mechanisms and cell polarity changes, which often coexist with evasion mechanisms of the antiviral immune response. Viral agents also indirectly contribute to the development of cancer mainly through immunosuppression or chronic inflammation, but also through chronic antigenic stimulation. There is also evidence that viruses can modulate the malignant properties of an established tumor. In the present work, causation criteria for viruses and cancer will be described, as well as the viral agents that comply with these criteria in human tumors, their epidemiological and biological characteristics, the molecular mechanisms by which they induce cellular transformation and their associated cancers.

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Figures

Figure 1
Figure 1
Direct mechanisms of viral carcinogenesis. After infecting target cells, tumor viruses are persistently maintained as genetic elements; viral genomes can form episomes (upper panel example, herpesviruses) or integrate into the host genomic DNA (lower panel example, retroviruses and HBV).
Figure 2
Figure 2
Indirect mechanisms of viral carcinogenesis. (A) Chronic inflammation. Infected cells produce chemokines attracting immune cells, which establish a chronic inflammatory microenvironment that persistently damage the local tissue. Cancer evolves within this cycle of infection, induced inflammation and tissue damage. (B) Immunosuppression. The prototype agent for immunosuppression is HIV. In immunocompetent individuals EBV infection is efficiently controlled by cytotoxic CD8 T cells; as HIV infection progresses and immune responses collapse, individuals become at increased risk of developing EBV associated lymphomas.
Figure 3
Figure 3
Other indirect mechanisms: Oncomodulation (A) and chronic antigen-driven lymphoproliferation (B). (A) In oncomodulation HCMV does not participate in the initial transformation of the glia; perhaps the virus has an increased tropism for tumor cells once the glioma has formed. Here, the virus only infects a fraction of the tumor cells activating signaling pathways that favor tumor growth; (B) B cells with antigen receptors specific for HCV antigens chronically respond to infected hepatocytes and free virus. This chronic stimulation increases the risk of unregulated lymphoproliferation and lymphoma.
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