Abstract
Stealth adapted viruses differ from the viruses from which they are derived in not being effectively recognized by the cellular immune system. This is because of the deletion or mutation of the genes coding for the relatively few virus components, which are generally targeted by cytotoxic T lymphocytes.
Stealth adapted viruses do not, therefore, normally evoke inflammation, the hallmark of most infectious illnesses. A stealth adapted virus was repeatedly cultured from the blood of a patient with the chronic fatigue syndrome (CFS).
Polymerase chain reaction (PCR) performed on the culture identified the virus as being derived from an African green monkey simian cytomegalovirus (SCMV). The PCR also amplified a genetic sequence closely related to a normal cellular gene. Further analysis of the viral DNA indicated that it was fragmented and genetically unstable. Moreover, additional genetic sequences have been incorporated into the replicating virus genome. Several of the additional sequences are originally of cellular origin with subsequent genetic modifications. Other incorporated sequences are of bacteria origin.
PCR performed on cultures from some other CFS patients, led only to the amplification of modified cellular sequences, including a sequence apparently derived from the rhesus monkey genome. It is proposed that as part of the stealth adaptation process, sequences of the original infecting virus can be largely displaced by cellular and/or bacteria sequences, which have essentially switched their affiliation to that of the stealth adapted virus. For this reason, they are referred to as renegade sequences.
The term “renegade viruses.” is also proposed to describe those viruses in which the originating conventional virus sequences have yet to be detected. The findings are relevant to efforts to seek a virus cause of many common illnesses, including CFS, and to the possible misattribution of certain illnesses to bacterial infections.
