Presented at

International Conference on Emerging Infectious Diseases

Centers for Disease Control

March 26, 2002

 

W. J. Martin MD PhD

Center for Complex Infectious Diseases

 

Stealth Adapted Viruses

 

Abstract

Stealth-adaptation is a mechanism that allows cytopathic viruses to evade immune elimination through the deletion of genes coding the major antigens targeted by the cellular immune system. A prototype stealth-adapted virus, repeatedly cultured from a patient with chronic fatigue syndrome (CFS) was cloned and partially sequenced. It has a fragmented, genetically unstable, genome. It has retained numerous viral sequences that can be aligned to various regions of the genome of human cytomegalovirus (HCMV).

 

Where the comparison can be made, the sequences match much more closely to those of African green monkey simian cytomegalovirus (SCMV) indicating an unequivocal origin from SCMV. Kidney cells from cytomegalovirus seropositive African green monkeys were, until recently, routinely used to produce live poliovirus vaccine. The SCMV-derived stealth-adapted virus has five adjacent, but divergent, open reading frames that potentially code for molecules related to the US28 CC chemokine receptor protein of HCMV.

 

In addition, the virus has acquired cellular sequences from infected cells, including a set of three divergent genes that potentially code for proteins related to the putative oncogenic CXC chemokine known as melanoma growth stimulatory activity (MGSA/Gro-alpha). The genes in the prototype SCMV-derived stealth-adapted virus, supports current experimental therapeutic approaches based on chemokine suppression. Interestingly, the MGSA-related genes generally lack introns and were, therefore, presumably assimilated into viral DNA from cellular RNA through reverse transcription. The virus has also acquired genetic sequences from various bacteria. This finding has led to the secondary designation of this type of novel microorganism as viteria.

 

Molecularly heterogeneous viruses, inducing similar cytopathic effects in culture (and when examined, non-inflammatory vacuolating cellular damage in brain and tissue biopsies), have been cultured from numerous patients with severe neurological, psychiatric, immunological and neoplastic diseases. In controlled, blinded, studies, cytopathic effects were recorded in 9% of healthy individuals donating blood for transfusion; in contrast to the positive results recorded in virtually all blood samples from patients with various illnesses. The differing clinical manifestations in infected patients may reflect the assimilation of different cellular and other sequences in various stealth-adapted viruses.  Stealth–adapted viruses (and viteria) pose a major threat to Public Health.

 

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Background Information

 

A.   There is an increasing incidence of diseases with accompanying signs and symptoms of brain damage. These include neurological and psychiatric illnesses, childhood behavioral disorders, and such common conditions as chronic fatigue, Gulf War Syndrome, so-called "chronic Lyme disease", and many cancers. Altogether, these diseases have an enormous social impact.

 

B.   An infectious cause of many of these chronic illnesses has not been considered primarily because there is no inflammation in the involved tissues.

 

C.   Brain biopsies do, however, show cells with damaged mitochondria, lipid vacuoles, and irregular inclusions. Examples are shown in the figures 1-5.

 

D.   Viral cultures from patients with neuropsychiatric and other illnesses, regularly develop clusters of foamy vacuolated cells. These cellular changes are consistent with infection by actively cytopathic viruses. Figures 6-7.

 

E.   The cultures are also remarkable in the production of large quantities of lipids, including cholesterol esters, and pigmented, protease-resistant, aggregates and ribbon-shaped materials, some of which incorporate metals. Figures 8-15.

 

F.   Viral cultures can induce severe, non-inflammatory, widespread illness when inoculated into cats. The cytopathic effect (CPE) seen in tissues of infected animals is comparable to that seen in the tissue cultures.

 

G.   While the viruses causing CPE in viral cultures differ in different patients, one viral isolate was unequivocally derived from an African green monkey simian cytomegalovirus (SCMV). The issue of probable SCMV contamination of live polio virus vaccines produced in kidney cells of African green monkeys was identified by Industry and FDA in 1972. Unfortunately, this potential problem with live polio virus vaccines was not publicly disclosed, nor scientifically addressed.

 

H.   Continued sequencing of DNA isolated from this cultured virus shows intriguing genetic modifications. Apparent loss of critical viral genes can explain how the virus evades the cellular immune system. Sequencing also reveals the surprising presence of an assortment of bacterial genes, including genes very closely related to those of Brucella, Mycoplasma, Streptococcus, and other bacterial species. This finding shows the capacity of such viruses to pass, and possibly, to have been passed, through bacteria. Stealth viruses can also potentially incorporate cancer causing cellular genes, as shown by the presence of a cancer-related chemokine gene in the SCMV-derived stealth-adapted virus.

 

     

Methods and Brief Summary of Sequencing Study

 

DNA isolated from the stealth virus culture was cloned and sequenced.  Nucleotide sequences were analyzed using Blast Programs at NCBI. 

 

While the complete genome of human (HCMV) is known, only partial sequence data are available for African green monkey (SCMV), Baboon (BaCMV) and rhesus monkey (RhCMV) cytomegaloviruses.

 

Most of the clones aligned to CMV sequences. Near identity of some clones to SCMV. 

 

Several clones contained atypical sequences of bacterial origin.

 

Other clones partially matched to human proteins, including to a cancer associated chemokine, and to various highly reiterated genes present in the human genome. 

 

The sequence data clearly establish the existence of atypically structured viruses.

 

 

Conclusions

 

Atypically structured, non-inflammation inducing cytopathic viruses definitely exist.

 

Some of these viruses were derived from simian CMV and have presumably entered the human population from SCMV contaminated batches of live polio vaccines. 

 

Non-inflammatory cytopathic viruses are grouped under the term "stealth." They can  be regularly cultured from patients with complex multi-system illnesses, including  various cancers. Positive stealth virus cultures were found in approximately 10% of University students donating blood for transfusion. Community outbreaks do occur.

 

Stealth-adaptation is considered to be a generic process that can involve many types of cytopathic viruses. It presumably occurs through the loss of genes coding for major antigens normally targeted by the cellular immune system. 

 

Tissue culture provides the best method to screen for stealth-adapted viruses.  Viral cultures can also provide useful insights into pathology, including formation of lipids, and of protease-resistant protein complexes. 

 

The production of lipids and pigmented materials is viewed as a reparative  process helping to maintain cell viability. There is a marked reduction in the intensity of the CPE if the culture medium is not frequently replaced. 

 

Bacteria and cell-derived genes are present in the SCMV-derived stealth virus culture. This important finding indicates the potential intermixing of cellular, viral and bacterial genes in the creation of new highly pathogenic organisms. Viteria is used to define viruses with bacterial sequences.  Atypical bacteria can commonly be cultured from stealth virus infected patients.

 

Stealth viruses are found in cancer patients, many of who have symptoms of an underlying neuropsychiatric illness. The prospect of bacteria transmitting cancer causing viruses is a very serious and urgent public health concern. 

 

Bacterial genes can help explain partial and inconsistent serological and/or PCR diagnostic findings for mycoplasma, (in CFS, Gulf War Syndrome): Borrelia (in "chronic Lyme disease"), streptococcus (in PANDAS), etc. 

 

Apparent expansion of chemokines and chemokines-receptor genes provide an adjunctive approach to anti-stealth virus therapy. Many therapeutic agents are available that can lead to cytokine/chemokine suppression.

 

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Additional information including; 15 Micrographs, Sequencing data and references are available at these links:

 

http://www.ccid.org/stealth/presentations/part2.htm

 

http://www.ccid.org/stealth/presentations/part3.htm

 

http://www.ccid.org/stealth/presentations/part4.htm

 

http://www.ccid.org/stealth/presentations/part5.htm

 

http://www.ccid.org/stealth/presentations/part6.htm

 

Further information is available on the internet at    www.ccid.org.         

 

PUBLICATIONS

1. Martin WJ, Zeng LC, Ahmed K, Roy M. Cytomegalovirus-related sequences in an atypical cytopathic virus repeatedly isolated from a patient with the chronic fatigue syndrome. Am. J. Path. 145: 441-452, 1994.

2. Martin WJ. Stealth virus isolated from an autistic child. J. Aut. Dev. Dis. 25:223-224,1995

3. Martin WJ, Ahmed KN, Zeng LC, Olsen J-C, Seward JG, Seehrai JS. African green monkey origin of the atypical cytopathic 'stealth virus' isolated from a patient with chronic fatigue syndrome. Clin. Diag. Virol. 4: 93-103, 1995.

4. Martin WJ, Glass RT. Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology 63: 115-118, 1995.

5. Gollard RP, Mayr A, Rice DA, Martin WJ. Herpesvirus-related sequences in salivary gland tumors. J. Exp. Clin. Can. Res. 15: 1-4, 1996.

6. Martin WJ. Genetic instability and fragmentation of a stealth viral genome. Pathobiology 64:9-17, 1996.

7. Martin WJ. Severe stealth virus encephalopathy following chronic fatigue syndrome-like illness: Clinical and histopathological features. Pathobiology 64:1-8, 1996.

8. Martin WJ. Stealth viral encephalopathy: Report of a fatal case complicated by cerebral vasculitis. Pathobiology 64:59-63, 1996.

9. Martin WJ. Simian cytomegalovirus-related stealth virus isolated from the cerebrospinal fluid of a patient with bipolar psychosis and acute encephalopathy. Pathobiology 64:64-66, 1996.

10. Martin WJ, Anderson D: Stealth virus epidemic in the Mohave Valley. Initial report of viral isolation. Pathobiology 65:51-56, 1997.

11. Martin WJ. Cellular sequences in stealth viruses. Patobiology 66:53-58, 1998.

12. Martin WJ. Bacteria related sequences in a simian cytomegalovirus-derived stealth virus culture. Exp Mol Path. 66: 8-14, 1999.

13. Martin WJ. Stealth adaptation of an African green monkey simian cytomegalovirus. Exp Mol Path. 66:3-7, 1999.

14. Martin WJ. Melanoma Growth stimulatory activity (MGSA/GRO-alpha) chemokine genes incorporated into an African green monkey simian cytomegalovirus (SCMV)-derived stealth virus. Exp Mol Path. 66: 15-18,1999.

15. Martin WJ, Anderson D. Stealth Virus Epidemic in the Mohave Valley: Severe vacuolating encephalopathy in a child presenting with a behavioral disorder. Exp Mol Path. 66:19-30 1999.

16. Martin WJ. Chemokine receptor-related sequences in an African green monkey simian cytomegalovirus (SCMV)-derived stealth virus. Exp Mol Path. 69: 10-16, 2000.

17. Martin WJ. Stealth viruses. Explore 10: Number 4, 17-21, 2001.

18. Martin WJ. Chronic fatigue syndrome among clinicians: A potential role of occupational exposure to stealth viruses. Explore 10: Number 5, 7-10, 2001

19. Martin WJ. Chemokines and stealth viruses. A blueprint for therapy in infected humans and animals. Explore 11, Number 1, 7-11, 2002.