Stealth Viruses (Part I)

Viruses are submicroscopic infectious agents that replicate inside cells. Viral illnesses are normally controlled by the body's immune system acting primarily through white blood cells called lymphocytes. These cells recognize certain viral proteins that provide the antigens targeted by specific lymphocytes, leading to an anti-viral inflammatory response. Not all viral proteins, however, can function as antigens for effective anti-viral immunity. Indeed, for many viruses, only a very few proteins are involved in lymphocyte recognition of virally infected cells. Loss of these critical antigenic proteins can allow a virus to essentially go unrecognized by the cellular immune system. When such viruses have managed to retain the capacity to damage cells, they can potentially cause a persistent infection resulting in a prolonged illness. The viral nature of such an illness is usually overlooked because of the absence of overt inflammation. Atypically-structured cell-damaging (cytopathic) viruses were initially identified by W. John Martin, M.D., Ph.D., who introduced the term "stealth viruses" to highlight their basic property of evading effective immune recognition.

Detection of Stealth Viruses

Stealth-adapted viruses can be most readily detected using specialized, semi-quantitative, viral culture methods developed and refined by Dr. Martin. Using these procedures, stealth viruses will typically induce a characteristic vacuolating cytopathic effect (CPE) in cultures of human and animal-derived cells. Stealth virus infected cultures can be distinguished from cultures of conventional herpes viruses, adeno-viruses, entero-viruses and retro-viruses, by the appearance and host range of the CPE, and also by using selective immunological and molecular probe based assays, including PCR testing methods.

Cytopathic Effects

A common feature of the CPE-induced by stealth-adapted viruses is marked metabolic disruption. This is expressed as lipid accumulation, cytoplasmic vacuolization, formation of aberrant protein and lipoprotein inclusions, and abnormally shaped nuclei. Comparable foamy vacuolating cellular changes with atypical inclusion-like structures can be seen in detailed examination of brain and other tissues obtained from stealth virus infected patients and from animals inoculated with these viruses. Unlike infections caused by conventional cytopathic viruses, the actual production of readily identifiable viral particles is uncommon. Seemingly, the infected cells are metabolically impaired because various energy and other resources are diverted towards an inefficient and unbalanced synthesis of various virus coded components at the expense of normal cellular functions. Severe defects in energy-generating metabolic pathways are also apparent from the marked mitochondrial changes that are prominent in electron micrographs of virus-infected cells.

Center for Complex Infectious Diseases

Both clinical- and research-based studies on stealth-adapted viruses have been undertaken at the Center for Complex Infectious Diseases in Rosemead, California. CCID is a non-profit organization under the National Heritage Foundation dedicated to understanding the nature, origin, disease associations, modes of transmission, methods of diagnosis and responses to therapy of stealth virus infections, and to the dissemination such information to the medical and lay communities. Information regarding CCID is available from the Internet at Additional information is available from The following sections provide a brief overview of some of the ongoing research activities being conducted at CCID.

DNA Sequencing Studies

A stealth virus isolated from a patient with a chronic fatigue syndrome-like illness was originally noted to have limited DNA sequence homology to human cytomegalovirus (CMV). As additional sequence data became available, it became obvious that this virus was a derivative, not of human CMV, but rather of an African green monkey simian CMV (SCMV). Until the beginning of last year, these monkeys were routinely used to produce live polio virus vaccine. Moreover, although not widely revealed, a joint Food and Drug Administration/Industry study in 1972 indicated that control kidney cell cultures from all 12 African green monkeys tested grew out SCMV, and that most of these isolates were not detectable using standard procedures.

Continued sequencing on the SCMV-derived stealth-adapted virus has shown interesting changes compared to a typical CMV. Of special note is the uneven representation of genes that encode various viral components. As expected, the genes that code the proteins known to provide major target antigens for anti-CMV cytotoxic T-lymphocytes are either absent or mutated. Other genes are overly represented, including genes that code for various chemokines and for chemokine receptors. Interestingly, one of the markedly amplified chemokine receptor coding genes found in the stealth virus genome can also function as a receptor for HIV, suggesting a possible potentiating role of stealth viruses in HIV infected patients.

One set of amplified chemokine-coding genes detected in the stealth-adapted virus is of cellular, rather than viral, origin. Cellular genes can apparently be incorporated into stealth virus genomes, presumably during viral replication. The particular chemokine-coding cellular gene identified within the prototype SCMV-derived stealth virus was probably assimilated as a partially processed RNA molecule since it lacks the normal introns present in cellular DNA. This implies that stealth virus DNA replication is proceeding through RNA intermediates, and that it may, therefore, be dependent upon reverse transcriptase, as could be provided by an assimilated endogenous retroviruses. RNA to DNA replication is much more prone to error than is DNA to DNA replication. This might explain sequence variability between the three copies of the chemokine-coding cell-derived gene that have so far been identified within the stealth virus.

Chemokine receptor genes of both viral and cellular origins have been implicated in the development of several types of malignancies. It is somewhat worrisome, therefore, that the stealth-adapted virus is apparently employing this type of gene for its survival. On the other hand, many therapeutic agents that appear to be of some benefit to stealth virus infected patients are known to inhibit chemokine production and receptor activity.


It has also been determined that stealth viruses have the ability to acquire genetic sequences of bacterial and even fungal origin. Normally, viruses that are infectious for human or animal cells (eukaryotic cells) will not infect bacteria (prokaryotic cells). Stealth viruses appear to have overcome this phylogenetic barrier. The term "viteria" has been coined to define eukaryotic viruses that have acquired bacteria-derived genetic sequences. The sources of the bacterial sequences include microorganisms that are not known to grow intracellularly within eukaryotic cells. This strongly suggests that stealth viruses become viteria by infecting bacteria. Judging from the bacterial sequences so far identified, genes have been captured from a wide variety of both gram positive and gram negative bacteria. The linear arrangements of many of the bacterial-derived sequences are quite different from any of the known major bacteria, suggesting that an active ongoing selection process may be occurring to assist in stealth virus propagation within bacteria. Genetically empowered bacteria, carrying potentially oncogenic stealth-adapted viruses, could become a far more threatening biological weapons program then ever envisioned by military planners.

Bacterial sequences incorporated within stealth-adapted viruses may help explain positive findings in stealth virus infected patients in various tests for known bacteria, including Borrelia burgdoferi (the cause of authentic Lyme disease), mycoplasma (a suggested cause of CFS and Gulf War syndrome); chlamydia (implicated in coronary artery disease and Alzheimer's disease), etc. None of the commonly used assays for these bacteria actually detect cultured organisms, but instead rely upon broadly reactive molecular and/or serological testing that could as easily be explained by the presence of viteria.

Continued in Part II

© Copyright 2001 by W. John Martin, M.D., Ph.D., USA


One Response to “Stealth Viruses (Part I)”

  1. Stealth Viruses (Part II) | Healing Base on December 9th, 2011 14:56

    […] Stealth Viruses (Part II) var addthis_product = 'wpp-262'; var addthis_config = {"data_track_clickback":true,"data_track_addressbar":false};if (typeof(addthis_share) == "undefined"){ addthis_share = [];}Continued from Part I […]

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