Although still not widely appreciated among virologists, relatively few components of most viruses are displayed on the surface of virus-infected cells in a manner that allows for effective immunological recognition by T lymphocytes. 3, 4 Changes in a virus can also explain a lack of an accompanying inflammatory reaction. 1, 2 Prenatal virus infections can potentially induce immunological tolerance to virus antigens, as occurs with congenitally acquired hepatitis B virus. One example is infection occurring in an individual without a functioning cellular immune system, as can be seen with JC virus infections in AIDS patients. While inflammation is the expected hallmark of infectious diseases, situations have been described in which the body fails to mount an inflammatory response to an ongoing virus infection. Keywords : Herpes virus, Warts, Zoster, Shingles, Papillomavirus, Post-herpetic neuralgia, Phototherapy, Alternative cellular energy, ACE pathway, ACE pigments, KELEA Abbreviations Stealth adapted viruses, including those which presumptively originated from SCMV contaminated poliovirus vaccines, pose a serious threat to public health and can readily explain the increasing prevalence of neuropsychiatric illnesses, including autism, mental diseases and the chronic fatigue syndrome (CFS). The sequence data also reveal the potential complexity of stealth adapted virus genomes resulting from genetic instability and also from the apparent involvement with replicating cellular and bacterial genes. This process is termed stealth adaptation and comprises the deletion or mutation of the relatively few virus components, which are normally directly targeted on virus infected cells by T lymphocytes. The data provide important insight into a generic mechanism by which viruses avoid effective immunological recognition by the cellular immune system. The available DNA sequence data on an African green monkey simian cytomegalovirus virus (SCMV)-derived stealth adapted virus are summarized.