In Part 1 we saw that cancer is a multistep process involving complex genetic abnormalities that deregulate signalling pathways, and it involves the cooperation of multiple deregulating genetic pathways.1 Given the widespread involvement of HERVs and related products in human genetic chemistry it is likely that they will be involved in carcinogenesis. We might anticipate that such viral involvement will arise from the known oncogenic potential of viruses, particularly retroviruses. We also need to consider that HERVs, unlike exogenous retroviruses, have been subject to selection working at holobiontic level within the human genome over long time periods. From this we might anticipate additional potential for carcinogenesis deriving from the cooption, or dysregulation, of established symbiotic roles of whole viruses, viral genes and viral regulatory sequences involved in normal genetic pathways.
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