Role of Super Immune Activation Secondary to Infection in the Context of Cancer
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Abstract
By 2008, it was estimated that there were about 12.7 million new cases of cancer worldwide, resulting in 7.6 million deaths. We are aware of the heterogeneity that exists and that it is impossible to link its development in any organ to a single pathophysiological mechanism. The greatest risk factor for developing cancer is aging, as age is directly proportional to accumulated aberrations and exposure to carcinogens. Most cancers occur in people who have no overt immunodeficiency. It is evident, then, that tumor cells must develop mechanisms to escape or evade the immune system in immunocompetent hosts. The main mechanisms of innate immunity against viruses are inhibition of infection by type I interferons and NK cell-mediated death of infected cells. The hypothesis is that perhaps the ability of epigenetic modification, which varies from virus to virus, is not exclusively reduced to the ability to activate genes that lead to cancer; but also randomly empower the organism to activate tumor suppressor genes.
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