[Parts of this article may be too complex for readers to understand. The basic thing you should know is that nearly all ME/CFIDS patients have a virus called HHV-6A and inside that is a retrovirus that one researcher has named the JHK virus. This has been known and kept quiet as we have continued to suffer for many years. Delaying publication serves nobody but the researcher in their quest to wrap up all tests for monetary purposes.-Ed] As a speaker at the New Jersey CFS Association Inc. Eighth Annual CFS Conference, Professor Alan Cocchetto, NCF board member and medical advisor, broke open the truth about ME/CFIDS. It is not a truth that will lead to a sigh of relief, for ME/CFIDS is a severe and debilitating illness that is devastating to those who endure its wrath, but it is a truth that will lead to a better understanding and to treatments that are not just symptomatic. Hopefully, it will lead to all getting well. How did a patient and former engineering professor find out information not readily known by those researching ME/CFIDS? Professor Cocchetto explained, "Most doctors are trained to look at medical journals but patents are a goldmine of information." Anecdotally, human herpes virus 6, variant A (HHV-6A) accounts for about 80% of those with ME/CFIDS, which is known to be both a multicausal and a multisystemic illness. Another 20% have mycoplasma fementans/penentrans or chlamydia pneumonia infections. Those with the latter two causal factors can be helped by antibiotic regimens which are offered by the NCF. According to Dr. Lo of the Armed Forces Pathology Division, if you have a mycoplasma infection too long, you are at increased risk for developing cancer. Therefore, we urge every patient to be tested for this. Mycoplasmas can now be tested for at Dr. Garth Nicolson's new commercial laboratory with your insurance footing the bill. The International Molecular Diagnostics, Inc. uses a DNA analysis technique called Forensic Polymerase Chain Reaction. [Call 714-799-7177. Blood tests are also available for sick pets.] Alas, the remainder of the patients will not be helped by antibiotics or will only be helped to a certain extent since the chlamydia or mycoplasmas are only secondary to the main causative agent....HHV-6A. In the Annals of Internal Medicine's 1992 Lake Tahoe study that took nearly a decade to publish, 70% of Tahoe patients showed active HHV-6A infection, by viral culture assay, and testing was done in Dr. Robert Gallo's laboratory at the National Institutes of Health (NIH). (Ed. Note: Dr. Robert Gallo, as you recall, is the discoverer of AIDS.) MS patients have also shown a 70% HHV-6 infection rate by work done at the National Institute of Neurologic Diseases by Dr. Stephen Jacobson. There are hundreds of papers that show that HHV-6A is the accelerating agent in AIDS. In fact, Professor Cocchetto says that "many researchers have expressed to me that this (ME/CFIDS) resides somewhere between MS, cancer, and AIDS." In the U.S. government patent assigned to Dr. Robert Gallo and the Department of Health and Human Services (# 5,604,093 on 2/97), Dr. Gallo writes that "The presence of HBLV antibodies (Ed. note: HBLV is the former name of HHV-6A) is elevated in the following disease groups: Roseola (Exanthema subitum) Burkitt's lymphoma Hodgkin's disease Mononucleosis-like syndromes Sarcoidosis Sjogren's Syndrome A newly described infectious disease syndrome similar to that seen in Lake Tahoe characterized as an "acute mononucleosis-like syndrome" in adults, commonly known as chronic fatigue syndrome (CFS). ALL (acute lymphocytic leukemia) is diagnosed in children of Japanese, Caribbean, and African origin and HIV-1 antibody positive AIDS, ARC and PGL (persistent generalize lymphadenopathy) patients." Cocchetto explained that characteristics of HHV-6A include that HHV-6A is in the beta herpesvirus family and has a lipid envelope. This fact is "important for intervention," explained Professor Cocchetto, since the lipid envelope, not the virus, is much easier to attack when interceding in the virus. HHV-6A shares 67% homology with cytomegalovirus and the viral strain that ME/CFIDS has is the GS strain, a strain that Dr. Gallo's group discovered from a patient with acute lymphoblastic leukemia. While this does not mean that patients have lymphoblastic leukemia or that they will develop it, it can be hypothesized that this is a smoldering illness that eventually could possibly lead to an aberrant leukemia or lymphoma. HHV-6A can destroy CD4 and CD8 cells as well as Natural Killer (NK) cells. "Patients are losing CD8 counts at the rate of greater than or equal to 20% per year - a phenomenal loss!" exclaimed Professor Cocchetto. HHV-6A also contains Marek's disease (lymphomas seen in chickens) and Adenovirus gene vectors. "What the heck are these are doing in HHV-6A, we can only speculate and as Dr. Ablashi states, HHV-6A can increase EBV replication 5 to 10 fold." Professor Cocchetto went on... "The key is that HHV-6A does something that no other herpes virus does. It has been reported by Dr. Torrisi, from Italy, that it leaves no viral glycoproteins (no marks to show it's been there) on the infected cells!" stated Cocchetto. By comparison, HIV has none of these capabilities. Dr. Paul Levine has written in two different medical publications, that among the Tahoe outbreak patients, there was a reported increase in non-Hodgkin's lymphoma and brain cancer. Most horrific of all, the blood supply is not screened for HHV-6A. Proclaimed Cocchetto, "For the National Institutes of Health or the Center for Disease Control not to take this seriously and go after this with some real financial backing is unconscionable!" (Ed. note: Dr. Ablashi shared his latest article in the Journal of Clinical Virology (in press when this was written) where he and his colleagues conclude that "CFS patients must be acquiring Variant A HHV-6 infection in adulthood." This would indicate that HHV-6A is a primary infection and not a reactivation from childhood - thus not making this a ubiquitous viral infection as many have thought and reported!) Dr. Thomas Bridge, in a patent for the US Government's DHHS (# 5,189,022 on 2/93), found that a "class of peptides which when administered to patients not infected with HIV, but having CFS. reduce fatigue, tension, anger, confusion and improve cognitive and neuromotor performance...In recent work, protein kinase A activity in humans has been shown to be increased by Peptide-T...the principal immunologic test in this study was the PCR signal for HHV-6....It appears that Peptide-T, a protein kinase A enhancer, produces both symptomatic and functional improvement in patients with a diagnosis of Chronic Fatigue Syndrome. It accomplishes this improvement without changing the underlying viral infection." [Ed. note: See related story on Peptide-T and other treatments.] Retroviral Evidence Seen In CFS: Dr. William Carter, of Hemispherx Biopharma (# 5,958,718 on 9/99) when writing about virologic studies, wrote "I have also observed that the majority of these patients are infected with herpes-6...I have also found EB (Epstein-Barr) virus in many of these patients as well as a novel retrovirus similar (though different genetically) to HIV, a retrovirus causing acquired immune deficiency or AIDs. Specimens from several patients I have studied indicate the intriguing possibility of 'pseudotyping' as a means of spreading this disease. By pseudotyping, I refer, for example, to the coat of a herpes type 6 virus surrounding the genetic material for a retrovirus. This would give rise to a novel form of contagion where the infectious agent spreads epidemiologically through the population like a herpes virus but the genetic information being spread is actually that of a retrovirus...leading ultimately to mental deterioration and morbidity." In an earlier patent, Dr. Sidney Grossberg, a world renown virologist from the Medical College of Wisconsin, wrote (# 5,827,750 on 10/98) "The human virus on which the present invention is based has not been classified as to which virus family it belongs, but it most nearly resembles a retrovirus ....The present invention relates to the detection of the presence of an NMA (neuromyasthnia) virus that is associated with CFIDS." He goes on to talk of the "protein spikes in the envelope" which are called peplomers and these spikes are characteristic of a retrovirus. He calls this retrovirus the "JHK virus." He mentions that the retrovirus that is close to the same size is called the "mouse mammary tumor virus." In his only publication on the virus, one that went unannounced by the CFIDS Association despite their funding of him, Grossberg writes ( Res Virol, 1997; 148(3): 191-206 ), "The human B-lymphoblastoid cell line, designated JHK-3, with pre-B-cell characteristics, chronically produces two viruses, Epstein-Barr virus (EBV) and JHK virus, an apparently novel retrovirus...most nearly resembling C-type retroviruses." Professor Cocchetto admitted that the driving force behind uncovering this research was reading Hillary Johnson's Osler's Web: Inside the Labyrinth of Chronic Fatigue Syndrome. In fact, he shared this quote from the book by Dr. Sidney Grossberg, "We may have a genetic recombination of herpes and retrovirus here." [ Ed. note: Perhaps the intriguing full truth given in Ms. Johnson's epic book was the very reason that the CAA gave it such a poor review.] Was this information just coming from the United States? Certainly not! From Denmark, Dr. Mette Summerlund wrote on a "Type C-like human retrovirus linked to Multiple Sclerosis" and used the same language calling it "double infected with EBV and a hitherto uncharacterized human retrovirus..." Dr Michael Holmes, from New Zealand, a name most in the CFS arena recognize, wrote in The Clinical and Scientific Basis for Myalgic Enchelphalomyelitis/Chronic Fatigue Syndrome (1/97) that "structures consistent in size, shape and character with various stages of a Lentivirus (retrovirus) replicative cycle were observed by electron microscopy in cultures from CFS patients..." In 1995, Dr. Jay Levy, a world famous virologist from University of California, wrote on the "Isolation of Infectious Agent for CFS: Innoculation of Animals," from one of his patents, that he used cultures that were "evaluated for reverse transcriptase activity" and "we have found that the CD11b+ cells (suppressor CD8+ cells) decrease during CFS." Going back to 1991, Dr. Elaine DeFreitas, before the CFIDS Association of America cut her funding and her research off, wrote that "These data support an association between an HTLV-II like virus and CFIDS." We can even go back to 1959 when Dr. Bjorn Sigudsson, from the Institute for Experimental Pathology in Iceland, wrote on Icelandic Disease, now known as CFS (ME). "This incredibly intelligent soul," said Professor Cocchetto, conceived the concept that slow viral infections, in particular, the visna (sheep) virus, could take a long time to do its damage before it could be seen. As he lay dying, he dictated to a colleague the similarities between visna (a retrovirus) and multiple sclerosis. ¯