The HHV-6 Foundation threatens lawsuit over Quebec City HHV-6 AIDS & MECFS protest
The HHV-6 Foundation is covered with the dark cloud of Robert Gallo's fraudulent AIDS research. With the help of scientists like Dharam Ablashi, he ran one of the most corrupt scientific organizations in history. (See Science Fictions.) The HHV-6 Foundation is a Gallo, Fauci, and Ablashi enabler. The HHV-6 Foundation is helping to cover up a massive AIDS and Chronic Fatigue Syndrome fraud. The scientists at the Quebec City HHV-6 Conference need to wake up and take a stand against the massive fraud that is now intertwined with HHV-6 research.
The HHV-6 Foundation should be sounding the alarm to Congress. They have turned HHV-6 into a nothingburger rather than the AIDS-related public health crisis it is. The organization has one of Gallo's corrupt sidekicks at the scientific helm. Ablashi is part of the problem, not the solution. Recently, the HHV-6 Foundation admitted that HHV-6 is similar to a pig virus. Now the question is, Did Ablashi and Gallo steal credit from John Beldekas for its discovery? Are HHV-6 scientists engage on a wild goose chase because Ablashi and Gallo stole the research of the late John Beldekas? Would they be more concerned about HHV-6 if they knew the truth about its origins in pigs? Would they now be using pigs as animal models for HHV-6 diseases like Chronic Fatigue Syndrome, MS, autism and AIDS?
https://mailchi.mp/hhv-6foundation.org/hhv-6-research-newsletter?e=077d285f75
The Quebec City Declaration of the
Be in Quebec City on June 23-26 to demand the participants help expose and end the HHV-6 cover-up! HHV-6 is a lethal infection triggering many diseases. Thanks to the work of Bhupesh Prusty, we are now at a turning point in the HHV-6 and Chronic Fatigue Syndrome cover-up. You can make a difference. Show your support. Spread the word and come to Quebec City to demand serious action on the HHV-6 pandemic.
http://conference.hhv-6foundation.org/
At the protest in Quebec City, urge all the HHV-6 researchers to support the CFS/AIDS New Deal.
The CFS/AIDS New Deal
Mark Konlee on HHV-6 and African Swine Fever
https://keephopealive.org/report10.html
To the Editor: Last September, while conducting a preliminary sociomedical study on acquired immune deficiency syndrome in Rwanda, in the eastern part of central Africa, I was surprised to learn that 50 percent of the pig population had died in an African swine fever epidemic that had begun in December 1983. The epidemic spread northward from Burundi to south-central Rwanda near Butare. This is the same area where Dr. Philippe van de Perre of St. Pierre's Hospital in Brussels and his associates found that 27 of 33 female prostitutes had AIDS or AIDS-related complex, what must certainly be the highest proportion of persons with such symptoms in any at-risk sample yet studied. Eighteen percent of samples of adult blood donors and hospital employees in Kigali, the capital city, were seropositive to human immunodeficiency virus antibody last year. This year, the percentage has increased to 24. Human immunodeficiency virus, in Rwanda at least, appears to be the necessary but not sufficient condition to produce AIDS. Perhaps the African swine fever epidemic and the high rate of illness among prostitutes near Butare is just a coincidence. But, with the recent African swine fever scare caused by the discovery of sickly pigs near Belle Glades, Fla., and with the report by Dr. John Beldekas of Boston University and his associates of some evidence of infection by the African swine fever virus in nearly half of a sample of 21 AIDS patients in the United States, epidemiologists and veterinarians might do well to explore the possibility that this virus is a co-factor in AIDS transmission in central Africa and perhaps other regions of the world. DOUGLAS A. FELDMAN New Haven, July 23, 1986 The writer, a medical anthropologist, is a research fellow at Yale University's Human Relations Area Files Inc.
Books every honest and courageous scientist at the Quebec City HHV-6 Conference needs to read and discuss with other HHV-6 researchers.
The HHV-6 Foundation should be sounding the alarm to Congress. They have turned HHV-6 into a nothingburger rather than the AIDS-related public health crisis it is. The organization has one of Gallo's corrupt sidekicks at the scientific helm. Ablashi is part of the problem, not the solution. Recently, the HHV-6 Foundation admitted that HHV-6 is similar to a pig virus. Now the question is, Did Ablashi and Gallo steal credit from John Beldekas for its discovery? Are HHV-6 scientists engage on a wild goose chase because Ablashi and Gallo stole the research of the late John Beldekas? Would they be more concerned about HHV-6 if they knew the truth about its origins in pigs? Would they now be using pigs as animal models for HHV-6 diseases like Chronic Fatigue Syndrome, MS, autism and AIDS?
Should this Ablashi paper on HHV-6 and African Swine Fever be retracted?
HBLV[HHV-6] is not ASFV.
http://www.researchgate.net/publication/19958785_HBLV_is_not_ASFV
https://mailchi.mp/hhv-6foundation.org/hhv-6-research-newsletter?e=077d285f75
The Quebec City Declaration of the
HHV-6 Rights of Man
1. The right not to be lied to about the role of HHV-6 in Alzheimer's Disease.
2. The right not to be lied to about the role of HHV-6 in AIDS.
3. The right not to be lied to about the role of HHV-6 in Chronic Fatigue Syndrome.
4. The right not to be lied to about the role of HHV-6 in Autism.
5.The right not to be lied to about the role of HHV-6 in Multiple Sclerosis.
6. The right not to be lied to about the role of HHV-6 in Brain Cancer.
7. The right not to be lied to about the role of HHV-6 in Heart Disease.
8. The right not to be lied to about the role of HHV-6 in Encephalitis.
9. The right not to be lied to about the role of HHV-6 in Cognitive Dysfunction.
10. The right not to be lied to about the role of HHV-6 in Drug Hypersensitivity Syndrome.
11. The right not to be lied to about the role of HHV-6 in Bone Marrow Suppression.
12. The right not to be lied to about the role of HHV-6 in Lymphadenopathy.
13. The right not to be lied to about the role of HHV-6 in Colitis.
14. The right not to be lied to about the role of HHV-6 in Endocrine Disorders.
15. The right not to be lied to about the role of HHV-6 in Liver Disease.
16. The right not to be lied to about the role of HHV-6 in Hodgkin's Lymphoma.
17. The right not to be lied to about the role of HHV-6 in Glioma.
18. The right not to be lied to about the role of HHV-6 in Cervical Cancer.
19. The right not to be lied to about the role of HHV-6 in Hypogammaglobulinemia.
20. The right not to be lied to about the role of HHV-6 in Optic Neuritis.
21. The right not to be lied to about the role of HHV-6 in Microangiopathy.
22. The right not to be lied to about the role of HHV-6 in Mononucleosis.
23. The right not to be lied to about the role of HHV-6 in Uveitis.
24. The right not to be lied to about the role of HHV-6 in Stevens-Johnson Syndrome.
25. The right not to be lied to about the role of HHV-6 in Rhomboencephalitis.
26. The right not to be lied to about the role of HHV-6 in Limbic Encephalitis.
27. The right not to be lied to about the role of HHV-6 in Encephalomyelitis
28. The right not to be lied to about the role of HHV-6 in Pneumonitis.
29. The right not to be lied to about the role of HHV-6 in GVHD.
30. The right not to be lied to about the role of HHV-6 in Ideopathic Pneumonia.
31. The right not to be lied to about the role of HHV-6 in Pediatric Adrenocortical Tumors
32. The right not to be lied to about the role of HHV-6 in the reactivation of endogenous retroviruses.
33. The right not to be lied to about the impact of HHV-6 on T-Cells.
34. The right not to be lied to about the impact of HHV-6 on B-Cells
35. The right not to be lied to about the impact of HHV-6 on Epithelial Cells.
36. The right not to be lied to about the the impact of HHV-6 on Natural Killer Cells.
37. The right not to be lied to about the the impact of HHV-6 on Dendritic Cells.
38. The right not to be lied to about the the impact of HHV-6 infection of the brain.
39. The right not to be lied to about the the impact of HHV-6 infection of the liver.
40. The right not to be lied to about the ability of HHV-6 to affect cytokine production.
41. The right not to be lied to about the ability of HHV-6 to affect Aortic and Heart Microvascular Endothelial cells.
42.
The right not to be lied to about the role of an HHV-6 cover-up in a
massive HIV Fraud Ponzi Scheme that in a number of ways resembles the
Tuskegee Syphilis Experiment and Nazi medicine.
Be in Quebec City on June 23-26 to demand the participants help expose and end the HHV-6 cover-up! HHV-6 is a lethal infection triggering many diseases. Thanks to the work of Bhupesh Prusty, we are now at a turning point in the HHV-6 and Chronic Fatigue Syndrome cover-up. You can make a difference. Show your support. Spread the word and come to Quebec City to demand serious action on the HHV-6 pandemic.
http://conference.hhv-6foundation.org/
At the protest in Quebec City, urge all the HHV-6 researchers to support the CFS/AIDS New Deal.
The CFS/AIDS New Deal
The CFS/AIDS New Deal calls for equal funding for Chronic Fatigue Syndrome and AIDS research, treatment, and prevention, and that they be researched side-by-side to determine if they are actually one epidemic. The CFS/AIDS New Deal also calls for a special institute to study the role of HHV-6 in the CFS/AIDS epidemic now that Bhupesh Prusty has made it clear that it is the key to Chronic Fatigue Syndrome.
Please call your member of Congress and urge them to support the CFS/AIDS New Deal.
Mark Konlee on HHV-6 and African Swine Fever
https://keephopealive.org/report10.html
The African Swine Fever Virus
Connection to AIDS
The first letter linking AIDS to African Swine Fever Virus (ASFV) was published in The Lancet, Apr. 23, 1983, by Jane Teas of the Harvard School of Public Health, Boston MA. Jane Teas and her colleague, John Beldekas, of the Boston University School of Medicine, found that the symptoms of ASFV in swine (pigs) was almost identical to symptomology found in AIDS patients. Common symptoms of both diseases are: fevers, swollen lymph nodes, pneumonia, skin lesions (like KS) and wasting syndrome. In pigs, ASFV is usually fatal, often within two weeks of the onset of symptoms, although there are some swine that survive ASFV infection. Letters linking AIDS to ASFV also appeared in The Lancet (June 11, 1983) by St. John RK and a letter by Jane Teas in Ann NY Acad. Sci, 1984;437:270-2. Another on “African Swine Fever and AIDS” in The Lancet, on Mar 8, 1986 by Beldekas and Teas.
AFRICAN SWINE FEVER VIRUS FOUND IN NINE AIDS PATIENTS
From 1983 to 1986, Jane Teas (Dept. of Pathology, Human Ecology Assn., Boston), John Beldekas (Boston University Medical School) and James R Hebert (Dept. of Epidemiology, Am Health Fdn, NY) searched for evidence of the ASF virus in AIDS patients. An article on their findings was published in The Lancet on March 8, 1986. What they found was the presence of ASFV in the blood of 9 of 21 AIDS patients using haemadsorption tests and found ASFV in 10 AIDS patients using immunofluorescence tests. Sixteen controls were used in the tests and one tested positive for ASFV. Beldekas also noted “giant cell formations, a characteristic of ASFV in swine cell cultures.” Beldekas indicated that possibly a new variant strain of ASFV was an infectious agent in AIDS and would cross react with Lisbon 60 strain which is known to cross react with all other strains of ASFV. African Swine Fever Virus is not supposed to infect people. What was ASFV doing in the blood of 9 AIDS patients and why was it not found in all 21?
What may have been happening in the 12 AIDS patients who did not test positive for ASFV in the blood was that the virus may have been replicating in the cells. This will never be known since DNA amplification by PCR was not used in the test. The same problem occurs when testing for HHV-6A. In HHV-6A, it sometimes requires PCR tests to find the virus. A person infected with HHV-6A or ASFV who does not test positive for the presence of antibodies may show the presence of the virus by DNA amplification through PCR. Dr. Patricia Salvato MD (Houston, TX) found 98% of her patients with full blown AIDS to have HHV-6A by PCR amplification. This does not mean the other 2% were not also infected with the HHV-6A as the blood sample may not have had the presence of the virus that was elsewhere in the patient (i.e. lymph system). Antibody tests are less reliable than PCR. It is well known that some persons test negative for HIV antibody who are actually infected with HIV.
BELDEKAS MEETS GALLO AT NCI AND PRESENTS HIS FINDINGS.
In August, 1986, John Beldekas was invited to go to the NCI and present his findings on the link between ASFV and AIDS, which he did. Beldekas gave samples of all his lab work to Gallo. Later, the government asked Beldekas to turn over all his reagents and lab work to the government, which he did. Beldekas had found ASFV presence in nine of 21 AIDS patients using two standard procedures. At the meeting, Gallo was reported saying: “we know it is not ASFV.” How could Gallo know this as he hadn’t done any of his own tests to look for ASFV?
Two months later, Gallo published an article in Science (Oct 31, 1986) that he discovered a new possible co-factor in AIDS, a virus he called Human B Cell Lymphotropic Virus which he named HBLV. Like ASFV, HBLV infected B cells and also lived in macrophages. Did Gallo steal Beldekas’s ASF virus he found in AIDS patients and rename it HBLV? Later on, when Gallo found that HBLV could also infect other immune cells, he changed the name of HBLV to HHV-6. Eventually, Gallo identified his HBLV as the variant A strain of HHV-6 and called it a human herpesvirus.
WHAT THE MERCK VETERINARY MANUAL SAYS ABOUT AFRICAN SWINE FEVER VIRUS
“THE MERCK VETERINARY MANUAL” is the definitive publication used by veterinarians for information on animal diseases. It can be found in most public libraries. Here it part of what it says about African Swine Fever virus in hogs.
“The first sign is fever...There is early leukopenia (low white blood cells). The animals usually stop eating and become listless, uncoordinated and cyanotic....Vomiting, diarrhea and eye discharges are sometimes observed. Gross lesions...include hemorrhages of lymph nodes...and congestive splenomegaly...Hairless portions exhibit edematous areas of cyanosis (swollen purple lesions)...Pleural, pericardial and peritoneal fluids are excessive...severe edema of the lungs and walls of the gall bladder....virus usually replicates in macrophages in tonsils and regional lymph nodes.”
COMMON SYMPTOMS FOUND IN ASF AND AIDS
What Merck’s is saying is plain English is that ASFV symptoms include fevers, low white blood cells, fluids in the lungs (pneumonia?), swollen lymph nodes, diarrhea, swollen veins that are purple (Kaposi’s sarcoma?), congested spleens and a kind of dementia (listless and uncoordinated). These symptoms are also found in AIDS in varying degrees. John Beldekas writing in The Lancet, March 8, 1986 stated: “Both AIDS and chronic ASFV are characterized by fever, hyperplastic lymph nodes, skin lesions, hypergammaglobulinaemia, immune-mediated pneumonia, thrombocytopenia, encephalopathy, high titre non-neutralizing antibody production, and lymphocyte depression.” Beldekas identified nine symptoms common to both viral infections.
ASFV, AND POSSIBLY HHV-6A, IS INACTIVATED AT 56 DEGREES C.
Merck’s Manual also says the ASF virus is killed at 56 degrees Centigrade. An article appearing in The Lancet, Jan 26, 1985, by Montagnier, Spire, Dormat and Cherman was titled “Inactivation of Lymphadenopathy-associated virus by heat” said that “Lymphadenopathy associated virus (in AIDS) is inactivated by heating at 56 degrees C for 30 minutes. Since other researchers found that the HIV virus is inactivated at 60 degrees C and not 56, and it is known that HHV-6A is active in the lymph nodes (Gallo, Carrigan, Knox), the virus inactivated by Montagnier must not have been HIV, but rather HHV-6A.
THE DENDRITIC CELLS INFECTED IN ASF AND IN AIDS.
An article by DA Gregg et al appearing in J. Vet Diagn Invest., Jan. 1995, makes the observation that in African Swine Fever (ASF), the interdigitating dendritic cells (IDCs) are infected and that they lose their ability “to initiate an immune response.” He closed by noting: “Infection of IDCs (dendritic cells) has also been demonstrated in human immunodeficiency virus, and these infections have some aspects in common.”
INCREASES IN CD8 CELLS FOUND IN AIDS and in African Swine Fever
An article by A Canals et al, published in Vet Microbiol, Nov., 1992, found that in peripheral blood mononuclear cells (PBMC) from pigs infected with ASFV, there was “progressive increase of the CD8 subset when the cells were stimulated with infective (ASF) virus.” In AIDS patients, one of the first things noticed in blood tests was the CD4/CD8 inversions. In healthy humans, HIV-, CD4s are always higher than CD8s. In AIDS, CD8s increase and are almost always higher than the CD4s.
In Chronic Fatigue Syndrome (CFS), Dr. Patricia Salvato found 78% of her CFS infected with HHV-6. Dr. Nancy Klimas found a 19% elevation in CD8 counts in her CFS patients (1). In CFS and AIDS, African Swine Fever virus (sic:HHV-6A) increases CD8 counts, the same as it does in swine.
1. “Immunologic Abnormalities in Chronic Fatigue Syndrome, “ by Nancy Klimas; J. of Clinical Microbiology, June, 1990.
ASFV and HHV-6A ARE THE SAME SIZE - 200 nm Both have lipid membranes.
S. Zaki Salahuddin, Robert Gallo et al state that HBLV (HHV-6A) has “a lipid membrane and a diameter of the enveloped particle of about 200 nm.” (1). The African Swine Fever Virus (ASFV) has been identified as having a “lipid membrane” and a “diameter of 200 nm” by J.L Carrasosa et al (2) and S.S. Breese (3).
1.Science Reports, Vol. 234, Oct 31, 1986, 597.
2.Virology, 132, 160-172
3.Virology, 28, 420-428.
HAITI - THE FOCAL POINT OF BOTH AIDS AND ASFV
An article by MJ Torres-Anjel published in Ann NY Acad Sci, Jun 16, 1992, says that “The AIDS viral ecology coincided with African Swine Fever (ASF) in the Americas. Haiti became the focal point for both infections.” He noted that in the wars for independence in Africa (Angola etc), there were massive movements of soldiers from the American continent to Africa and back.
AN AIDS PATIENTS REPORTS A FLARE-UP IN HIS KS LESIONS AFTER EATING PORK
In Dec., 1995, I had a discussion with a PWA from Rio Rancho, NM, who has Kaposi Sarcoma. At the time, he told me that on three occasions when he ate pork, he had a flare-up and growth in his KS lesions. He did not get this effect from beef, turkey or chicken. He said: “when I eat pork, the KS goes wild.” He was not aware that research by Gallo and others have found the presence of HHV-6A in KS lesions. Since the ASF virus is known to systemicly infect pigs, it would not be surprising that eating pork would provide chow for ASFV(HHV-6A) in humans and adds more evidence that ASFV and HHV-6A are one and the same virus. This virus likes pork.
ASFV and HHV-6A ARE BOTH DNA LYMPHOTROPIC VIRUSES.
Gallo, Carrigan, Knox and other researchers have identified HHV-6A as a DNA lymphotropic virus that can infect T cells, B cells and monocytes and is systemicly infective and is found in most organs of persons with full blown AIDS. The Merck Veterinary Manual says this about ASFV: “This DNA virus replicates primarily in cells of the monocyte-macrophage system and is found in nearly all fluids and tissues of acutely infected pigs.” The fact that both viruses are DNA types and have tropism for infecting immune cells and can cause systemic infections adds further proof that both viruses are one and the same.
OTHER FACTORS HHV-6A AND ASFV HAVE IN COMMON
Both ASFV and HHV-6A are hemorrhagic (cause bleeding) (1) and the immune reaction to ASFV in pigs shows an absence of effective neutralizing antibodies. (2). Since Dr. Salvato found 98% of her patients with full blown AIDS had replication of HHV-6A in the cells, as determined by PCR. This is comparable evidence of an absence of effective neutralizing antibodies. Both ASFV and HHV-6 are Icosahedral viruses (3, 4) and both are envelope viruses (5, 6). Also, both viruses, ASFV and HHV-6A, mature in the cytoplasm (4, 5). The replication of ASFV and HHV-6 (A) is inhibited by Phosphonoacetic acid. (6, 7). The replication of both viruses is also inhibited by Phosphoformic acid (Foscarnet) (6, 8).
1. Neenyah Ostrom, The New York Native, Oct 10, 1994.
2. Merck’s Veterinary Manual.
3. R. Gallo et al, Science Reports, Oct 31, 1986 (601)
4. Carlos Martins and M. Lawman in a Letter to The Lancet, June 28, 1986 (1504).
5. P Biberfeld et al, J. Natl Cancer Inst, 1987, Nov; 79(5):933-41.
6. DV Ablashi et al, In Vivo, May-Jun, 1991; 5 (3):193-9
7. M.A. Moreno et al, J. gen. Virol, 93, 252-258.
8. John Beldekas et al, The Lancet, March 8, 1986, 565.
S.F. JOSEPHS ET AL LETTER TO AIDS RES. HUMAN RETROVIRUSES
In his letter to AIDS Res Hum Retroviruses of Oct. 4, 1988, Josephs, of the National Institute of Health (NIH) and an associate of R. Gallo, said that HBLV is not African Swine Fever Virus and said that HBLV (HHV-6A) matures in the nucleus of the cell whereas ASFV matures in the cytoplasm. He is correct in saying that ASFV matures in the cytoplasm (1). However, P Biberfeld found “unenveloped nucleocapsids” of HBLV (HHV-6A) “in the cytoplasm.”(2). Josephs offered no clinical evidence in his letter that HBLV (HHV-6A) matured in the nucleus of cells (3).
1. Carlos Martins and M. Lawman in a Letter to The Lancet, June 28, 1986 (1504).
2. P Biberfeld et al, J. Natl Cancer Inst, 1987, Nov; 79(5):933-41.
3. S.F. Josephs et al in a Letter to AIDS Res Hum Retroviruses, Oct 4, 1988(5):317-8.
ASFV AND HHV-6A HAVE 20 FACTORS IN COMMON. AN IN-VIVO TEST IS NEEDED: INFECT SWINE WITH HHV-6A TO DETERMINE IF IT CAUSES AFRICAN SWINE FEVER
So far, in this article, I have listed a total of 20 factors that ASFV and HHV-6A have in common. Ten are common areas of symptomology and 10 are particular characteristics of the virus. What is just as significant is the absence of clinical evidence that shows a difference between the two viruses. The only real test to settle the issue is for researchers to attempt to infect a pig with blood from an AIDS patients with Lymphadenopathy and see if it brings on African Swine Fever. If the real virus that causes AIDS came from pigs, then infecting them with the AIDS virus (HHV-6A) should cause them to develop ASFV. If it does, it will be case closed. Are there any researchers reading this article that are willing to do an in-vivo test on live swine? America's Biggest Cover-up
A book came out late in Nov., 1993, titled America's Biggest Cover-up, by Neenyah Ostrom. It alleges that HHV-6 (A) may be the primary causative factor in both AIDS and Chronic Fatigue Syndrome. There are two strains of HHV-6, variants A and B. HHV-6 (Variant B) is a common herpes virus and is not a life threatening infection. Ostrom, a prolific researcher and writer, has written articles for The New York Native on HHV-6 and other AIDS related topics for several years (1). Ostrom says the variant A strain of HHV-6 is the culprit in both CFS and in AIDS. Ostrom has interviewed most of the major researchers in the field, as well as countless patients and government officials. She has found many similarities between Chronic Fatigue Syndrome and AIDS and believes that they are part of the same epidemic. She argues that until their connection is admitted by top government researchers, there is little hope that real progress will be made in stopping these two expressions of the same syndrome. Ostrom also says in her book that HHV-6A is really the African Swine Fever virus (ASF). Ostrom reports that CFS patients have lost much of their B cell and natural killer (NK) cell protection and both groups are susceptible to night sweats and many forms of cancer, lymphomas and TB. The book is available at your local bookstore.
1. New York Native, PO Box 1475, NY, NY 10008
Gallo and Carrigan on HHV-6
Dr. Robert Gallo has recently written an article on "Disseminated Human Herpes Virus 6 Infection in AIDS" and stated "this concept, which has gained additional ground, is primarily based on the frequent isolation of HHV-6 from AIDS patients and its ability to infect and kill CD4 T cells, and on the demonstration of several unique interactions between HHV-6 and HIV." It is also significant that Gallo has stated that HHV-6, like HIV, can infect B cells. Both Gallo and Carrigan believe that AIDS is caused by the actions of two viruses instead of one.
A growing body of scientific research by Robert Gallo, Donald Carrigan and others indicate that HHV-6(A) can infect and disrupt the function of B cells and at least one weaker subset of NK cells. According to Carrigan, HHV-6A stops B cells from maturing into plasma cells. Plasma cells produce antibodies.
Gallo found a subset of NK cells that was immune from attack by HHV-6A. This subset of NK cells was capable of destroying other immune cells infected with HHV-6A. If this subset of NK cells (CD56+?), can be sufficiently stimulated into activity, they should be able to substantially reduce the viral load of both HHV-6A (ASFV) and HIV.
1. HOW YOUR IMMUNE SYSTEM WORKS, by Jeff Baggish MD (Ziff Davis Press, Emeryville, CA))
ASFV(HHV-6A) activates HIV infection of CD8 cells, Monocytes and B cells
In Dec., 1995, I ran a computer search for HHV-6 on AIDSLINE at the National Library of Medicine and retrieved several articles. One abstract by P Lusso et al (Int. AIDS Conf, Jun 1991) showed why HIV is more dangerous in the presence of ASFV. ASFV causes many more immune cells, besides the CD4 cell, to present the CD4 receptor on their membrane which makes the other immune cells also subject to infection by HIV. Like HIV, ASFV also uses the same CD4 receptor to invade immune cells. The immune cells with the CD4 receptor may be invaded by both HIV and ASFV (HHV-6A) at the same time.
Of HIV in the presence of HHV-6A, Lusso wrote: “Since CD4 is the receptor for HIV-1, HHV-6 may thus broaden the cellular host-range of HIV-1, favoring its spread in co-infected patients.” What Lusso is saying that HIV in the presence of HHV-6 is invasive of many more immune cells than without HHV-6.
Several authors, including Gallo, have published scientific reports that did not specify if the HHV-6 virus they were referring to was strain variant A or B. This has caused some confusion in the scientific community. However, several scientific journals where articles were published have identified HHV-6(A) as being either of the following isolates: U1102 or GS. GS stands for the initials of a PWA from whom the virus was isolated. One Abstract cited U1102 as a HHV-6, variant A, isolate from a Ugandan AIDS patient. References to U1102 as being HHV-6A have been published in the following medical journals:
1. J. Virol. 1995, Aug; by Araujo JC et al
2. Virology, 1995, May; by UA Gompels et al
3. J. Virol Methods., 1995, Feb.; by L Foa-Tomasi et al
4. J. Immunology, 1994, Jun.; by M Furukawa et al
5. Virology, 1994, May; by F Kashanchi et al
6. Oncogene, 1994, Apr; by J. Thompson et al
7.J. Virol. 1993, Aug; by B Pfeffer at al
8. J. Med. Virol, 1992, Aug; by B Chandran et al
9. Int. AIDS Conf, 1994. by K Yamanishi et al.
SCIENTIST REPORTS THAT HIV IN THE PRESENCE OF HHV-6A REPLICATES 10 to 15 TIMES FASTER.
An article appearing in Virology, May 15, 1994, by F. Kashanchi says that “(HHV-6) strain A transformed rodent cells and transactivated the HIV-1 LTR 10 to 15 fold in both monkeys fibroblasts and human T-lymphocytes.” The abstract concluded by saying that “the data presented suggest that HHV-6 could have a co-factor role in the progression of AIDS.” The mechanism of how HHV-6A increases HIV replication is already known from other research by Gallo. HHV-6A causes many more immune cells to present the CD4 receptor, which is what both HIV and HHV-6A use to infect immune cells.
According to Donald Carrigan, HHV-6A makes HIV up to 100 times more virulent and invasive of immune cells and does widespread damage to the lymphoid tissue where antigen presenting cells are produced. “Without the dendritic antigen presenting cells,” said Carrigan, “the CD4s don’t know what to do.” Carrigan cites HHV-6A as the primary cause of swollen lymph nodes in AIDS patients. Carrigan said he spoke recently with a person HIV+ for 11 years who never had any symptoms and has a totally normal T cell count and blood profile. This person has never used any drugs or alternative treatments of any kind. He said: “HIV without HHV-6A may be a benign virus.” He indicated he was interested is testing blood samples from long term HIV+ non-progressors to see if they are missing the suspected co-factor - HHV-6A.
HHV-6A RETINITIS
An article was published in Invest. Ophthalmol. Vis. Science, 36:2040, 1995 by Qavi, Hamida, Green, Lewis, Hollinger, Pearson and Ablashi on “ HIV-1 and HHV-6 Antigens and Transcripts in Retinas of Patients with AIDS in the absence of Cytomegalovirus.” The article was reviewed by Neenyah Ostrom in the New York Native in Oct., 1995. Ostrom writes: “ Powerful evidence has just been published suggesting that Human Herpes Virus 6 (HHV-6) may be a frequent cause of vision loss suffered by more than half of all AIDS patients. Although most eye disease has been attributed to Cytomegalovirus (CMV) infection, it now appears that, along with the identification of HHV-6 as the most common infection found in AIDS patients, HHV-6 may in addition be causing a significant percentage of the AIDS Retinitis formerly blamed on CMV.”
(HHV-6A) IS SUBSTANTIALLY DIFFERENT FROM HHV-6B, A COMMON HERPES VIRUS
It should be noted that HHV-6A shares more in common with CMV than with variant B, which is a common herpes virus. (1) The genome of HHV-6A has only 21% similarity with the Variant B common herpes virus, but has 67% similarity with the CMV virus (3). Acyclovir, which is used to treat the common herpes virus (HHV-6B), is not effective against variant A. (2). Other research has shown that antibodies to HHV-6(B) are not effective against variant A (ASFV).(4).
1. J. Virol, 1991, Oct. by SF Josephs et al .
2. In Vivo, May-Jun, 1991, by DV Ablashi et al.
3. Virology, 1995, May, by UA Gompels et al.
4. J. Virol Methods, 1995, Feb, by L Foa-Tomasi et al
Neenyah Ostrom, writing in The New York Native, June 15, 1992 stated: [ASFV also strongly resembles CMV, according to retired USDA Plum Island Animal Disease Laboratory ASFV researcher William Hiss. In a 1971 textbook, African Swine Fever Virus, Hess pointed out that “...Herpes simplex virus and ...human Cytomegalovirus have morphological appearances similar to ASF virus when seen in thin sections.” In other words, when tissue infected with ASFV are examined under the microscope, the ASFV “looks like human herpes virus.”]
Gallo has named the co-factor in AIDS patients as Human HerpesVirus 6 or HHV-6. However, I think Gallo knows more than he is willing to discuss publicly. The US Government does not want the rest of the world blaming us for contributing to the start of the AIDS epidemic. You can be certain that “for national security reasons” the CIA will always deny that its biowarfare department cultured a strain of the ASF virus to make it more damaging and destructive to Cuba’s pork industry. However, the CIA could not possibly have known in advance the world-wide implications of AIDS that would result when they released this virus in Cuba and it began to infect humans.
AIDS WITHOUT HIV. CARRIGAN REPORTS ONE CONFIRMED DEATH FROM HHV-6A WITHOUT HIV.
Carrigan cited one case of a 2 yr. old child who died from HHV-6A from infections due to severe immune dysfunction. Carrigan said that “under certain conditions, HHV-6A may cause AIDS without HIV.” The child did not have HIV but was diagnosed as having died from AIDS. The article will be published in the Journal of AIDS in March, 1996. Carrigan said that “both HIV and HHV-6A are being sexually transmitted together.” Carrigan also said that in infants, those who receive both HIV and HHV-6A from the mother progress to full blown AIDS quickly while the children who are HIV+ without HHV-6A are living as long term non-progressors.
KILLER T CELLS AND FUNCTIONAL NK CELLS CAN KILL CELLS INFECTED WITH HIV and/or HHV-6A
In my discussion with Donald Carrigan (12/18/95), he said that cytotoxic Killer T cells (A type of CD8 cell) can kill cells infected with HHV-6A if there are a sufficient number of CD4 cells and Antigen Presenting Cells available. The Antigen Presenting Dendritic cells, also known as CD35, are produced in the lymph nodes. However, if the CD4s and Antigen Presenting cells are insufficient, as may happen when CD4 counts are very low or serious damage has been done to the lymph nodes, then the Killer T cells do not know what to do and would not be effective in lowering the HIV and HHV-6A viral load. This brings us to the immune cells of last resort - the Natural Killer (NK) cells. They are the most active immune cells that do not require help from any other immune cell to carry out their function of destroying cells infected with viruses. Carrigan agreed with me that if the subsets of NK cells that are resistant to HIV and HHV-6A infection could be sufficiently activated, they could bring both HIV and HHV-6A under control by destroying cells infected with either or both of these viruses. Some subsets of NK cells and CD8’s can be infected with HHV-6A. However other subsets are resistant to these viruses.
Note: In lab tests, NK cells are listed as the following subsets: CD56+; CD16+ and CD3-. Total absolute NK cell counts for all subsets range from 40 to 380 cells per cubic millimeter (UL) of blood. The mean average is 210 cells/UL. 210 or higher is the total number of NK cells for which we should strive to restore normal NK function. If normal NK activity can be combined with CD8s of 800 or higher, an AIDS patient will have a functional immune system, with few opportunistic infections, even if the CD4 count in the blood is zero. Zero CD4 blood counts does not mean all CD4 cells are gone as many are in the lymph nodes, where the battle is ongoing.
http://www.keephopealive.org/report10.html
A letter to the New York Times about African Swine Fever
To the Editor: Last September, while conducting a preliminary sociomedical study on acquired immune deficiency syndrome in Rwanda, in the eastern part of central Africa, I was surprised to learn that 50 percent of the pig population had died in an African swine fever epidemic that had begun in December 1983. The epidemic spread northward from Burundi to south-central Rwanda near Butare. This is the same area where Dr. Philippe van de Perre of St. Pierre's Hospital in Brussels and his associates found that 27 of 33 female prostitutes had AIDS or AIDS-related complex, what must certainly be the highest proportion of persons with such symptoms in any at-risk sample yet studied. Eighteen percent of samples of adult blood donors and hospital employees in Kigali, the capital city, were seropositive to human immunodeficiency virus antibody last year. This year, the percentage has increased to 24. Human immunodeficiency virus, in Rwanda at least, appears to be the necessary but not sufficient condition to produce AIDS. Perhaps the African swine fever epidemic and the high rate of illness among prostitutes near Butare is just a coincidence. But, with the recent African swine fever scare caused by the discovery of sickly pigs near Belle Glades, Fla., and with the report by Dr. John Beldekas of Boston University and his associates of some evidence of infection by the African swine fever virus in nearly half of a sample of 21 AIDS patients in the United States, epidemiologists and veterinarians might do well to explore the possibility that this virus is a co-factor in AIDS transmission in central Africa and perhaps other regions of the world. DOUGLAS A. FELDMAN New Haven, July 23, 1986 The writer, a medical anthropologist, is a research fellow at Yale University's Human Relations Area Files Inc.
The African Swine Fever Virus Rights of Man
1. The right not to be lied to about whether African Swine Fever Virus is infecting human beings.
2. The right not to be lied to about how many different strains of African Swine Fever are capable of infecting humans.
3.
The right to know if African Swine Fever is being disguised in pigs by
giving it euphemisms of other diseases like PRRS and PEDV.
4. The right not to be lied to about the role of ASFV in AIDS.
5. The right not to be lied to about the role of ASFV in Chronic Fatigue Syndrome.
6. The right not to be lied to about the role of ASFV in Autism.
7.The right not to be lied to about the role of ASFV in Multiple Sclerosis.
8. The right not to be lied to about the role of ASFV in Brain Cancer.
9. The right not to be lied to about the role of ASFV in Heart Disease.
10. The right not to be lied to about the role of ASFV in Encephalitis.
11. The right not to be lied to about the role of ASFV in Cognitive Dysfunction.
12. The right not to be lied to about the role of ASFV in Drug Hypersensitivity Syndrome.
13. The right not to be lied to about the role of ASFV in Bone Marrow Suppression.
14. The right not to be lied to about the role of ASFV in Lymphadenopathy.
15. The right not to be lied to about the role of ASFV in Colitis.
16. The right not to be lied to about the role of ASFV in Endocrine Disorders.
17. The right not to be lied to about the role of ASFV in Liver Disease.
18. The right not to be lied to about the role of ASFV in Hodgkin's Lymphoma.
19. The right not to be lied to about the role of ASFV in Glioma.
20. The right not to be lied to about the role of ASFV in Cervical Cancer.
21. The right not to be lied to about the role of ASFV in Hypogammaglobulinemia.
22. The right not to be lied to about the role of ASFV in Optic Neuritis.
23. The right not to be lied to about the role of ASFV in Microangiopathy.
24. The right not to be lied to about the role of ASFV in Mononucleosis.
25. The right not to be lied to about the role of ASFV in Uveitis.
26. The right not to be lied to about the role of ASFV in Stevens-Johnson Syndrome.
27. The right not to be lied to about the role of ASFV in Rhomboencephalitis.
28. The right not to be lied to about the role of ASFV in Limbic Encephalitis.
29. The right not to be lied to about the role of ASFV in Encephalomyelitis
30. The right not to be lied to about the role of ASFV in Pneumonitis.
31. The right not to be lied to about the role of ASFV in GVHD.
32. The right not to be lied to about the role of ASFV in Ideopathic Pneumonia.
33. The right not to be lied to about the role of ASFV in Pediatric Adrenocortical Tumors
34. The right not to be lied to about the role of ASFV in the reactivation of endogenous retroviruses.
35. The right not to be lied to about the impact of ASFV on T-Cells.
36. The right not to be lied to about the impact of ASFV on B-Cells
37. The right not to be lied to about the impact of ASFV on Epithelial Cells.
38. The right not to be lied to about the the impact of ASFV on Natural Killer Cells.
39. The right not to be lied to about the the impact of HHV-6 on Dendritic Cells.
40. The right not to be lied to about the the impact of ASFV infection of the brain.
41. The right not to be lied to about the the impact of ASFV infection of the liver.
42. The right not to lied to about the ability of ASFV to affect cytokine production.
43. The right not to be lied to about the ability of ASFV to affect Aortic and Heart Microvascular Endothelial cells.
44. The right not be lied to about the relationship of ASFV to HHV-6, HHV-7 and HHV-8.
44. The right not be lied to about the relationship of ASFV to HHV-6, HHV-7 and HHV-8.
