The cellular immune system normally responds to relatively few of the different structural components that comprise the complete virus. Mutation or deletion of the genes coding for these few antigenic components is an immune evasion mechanism termed “stealth adaptation.” I initially used this term to describe a virus derived from an African green monkey simian cytomegalovirus (SCMV). This article provides an extended discussion of the Public Health relevance of previously reported findings relating to this virus. Of particular significance, the virus did not evoke inflammation in the chronic fatigue syndrome (CFS) patient from whom the virus was repeatedly cultured, nor in virus inoculated animals. The viral genome consists of multiple fragments of double stranded DNA with lengths of approximately twenty thousand nucleotides (20 kb). This is in marked contrast to the > 225 kb size of the normal SCMV genome. Purified virus DNA was cloned, and sequence data were subsequently obtained. Most of the cloned sequences match to regions corresponding in their entirety to only approximately half of the originating SCMV genome. These matching sequences are very unevenly distributed along the SCMV genome. Moreover, there are significant genetic sequence differences between clones matching to identical regions of the SCMV genome. In addition to the SCMV matching sequences, there are sequences that match to regions of the human genome. There are also sequences that match closely to genes of bacterial origin. The major sources of the bacterial sequences in the initially cultured stealth adapted virus are from Mycoplasma fermentans and Ochrobactrum quorumnocens bacteria. These findings have extended the generic concept of stealth adaptation to include not only the loss or mutation of portions of the originating virus genome, which would have otherwise resulted in cellular immune recognition, but also the potential incorporation/acquisition of additional “renegade” genetic sequences from cellular genes and from other microbial genomes. The apparent acquisition of cellular genetic sequences by stealth adapted viruses may potentially lead to the infectious transmission of genetically determined illnesses. The inclusion of bacterial sequences is also concerning since it indicates possible bacteria mediated transmission of infectious stealth adapted viruses. Furthermore, the transmissible bacterial sequences can potentially result in the mistaken diagnosis of a stealth adapted virus infection for a bacterial disease. Examples are likely to include chronic Lyme disease and PANDAS, a severe childhood psychiatric illness. Public Health officials should respond urgently to the existence of stealth adapted viruses.