Three Big Books

Thursday, May 30, 2019

No Collusion, No Obstruction in Chronic Fatigue Syndrome Research!

Please support HHV-6 University by purchasing one or our books about the cover-up of the relationship between HHV-6 and Chronic Fatigue Syndrome, AIDS, and many other immunological illnesses. Click book to read a free excerpt.

Wednesday, May 29, 2019

Is this the most tragic Chronic Fatigue Syndrome and HHV-6 story?

From The Virus Within by Nicholas Regush.

In the fall of 1996, Tina, in her forties, spiraled ever deeper into depression, suffering from repeated attacks of migraine headaches. Desperate, she offered herself the only prescription that seemed fitting: suicide by drug overdose.
When news of her suicide attempt spread throughout the area, people were shocked. What could drive Tina to such straits? Yet the real tragedy was still on the horizon.
Several months before, Tina had experienced a flurry of flu-like symptoms: difficulty in breathing, nausea, diarrhea, fever, and aches all over her body. The symptoms were noted in her medical record, but she made nothing of them. After all, such symptoms are common and transient, usually abating without medical intervention.
In fact, many early symptoms of disease are subtle and do not attract attention until the disease is well established. This is probably why it took so long for Tina's son Len to receive appropriate medical consideration.
In September 1997, soon after the young boy returned to school after summer vacation, his teacher, Gail, detected a change in his personality from the previous year. Len seemed sad and withdrawn more often than usual, and what had been occasional flashes of anger occurred with increasing frequency. Gail also noticed that his writing skills were in decline. She reasoned that such changes were to be expected in a boy whose mother had attempted suicide.
By early 1998, Len's behavior had deteriorated. In school he was so aggressive with classmates and defiant with his teacher that he was twice suspended. Other times he was so fatigued during afternoon classes that he would fall asleep. On most days he was either too tired or distracted to complete his homework. He was also undergoing physical changes. There were days when he complained of muscle and joint pain and of having weak legs. Once he soiled his clothes and on another occasion could not control his bladder.
Observing Len's erratic and baffling behavior, school officials concluded that he was likely "acting out" in response to a troubled home life. They also decided his schoolwork difficulties were the result of an attention-deficit disorder and that what he needed was old-fashioned school discipline. That approach did not bring any benefit. In April, Len became so aggressive that he threatened his brother, Fred, with a knife. He had also started to have double vision, particularly when he was tired or stressed. Tina, who by this time had awakened to her son's plight, agreed with school officials that Len needed medical testing.
The first warning sign came from a CT (computerized axial tomography) brain scan that revealed some shadowy areas that appeared to be abnormal. Len was then referred by the hospital to a neurologist, who began a more detailed medical investigation. The neurological exam, which included tests for muscle tone and strength, revealed nothing of concern except for swelling in both eyes of his optic disc, the small blind spot on the surface of the retina. The swelling usually occurs when increased pressure is applied from the brain to the optic disc; nerves that surround the optic nerves from the disc are connected to nerve-covering sheaths of the brain.
Hoping for a clearer look at Len's brain, his doctor requested an MRI (magnetic resonance imaging) scan that can produce more detailed images than the CT. The MRI revealed, in the words of the doctor, "fairly extensive white matter disease present with a frontal lobe predominance." Though the "white matter"—the inner areas of the brain rich in nerve fibers—appeared to be diseased, only when sample tissue was removed from Len's frontal lobe a few weeks later did it become evident that the white matter nerve cells had holes and looked like Swiss cheese.
While the tests continued, the only therapy offered was steroids to ease the swelling in the eyes and opiates to tame the headaches he was having. Len's mysterious condition continued to deteriorate rapidly. Soon he could no longer walk without help. He felt wiped out much of the day and had severe headaches. He developed speech impediments and an abnormal sensitivity to light. His teacher, Gail, who visited Len at home, found making emotional contact with him increasingly difficult. Tina feared the worst.
Over the next three months, doctors at several medical centers were asked to consult on the case. Their reviews of biopsy materials led to conflicting opinions. One doctor suggested Len was suffering from a tumor while others thought that some of his nerve fibers were being damaged because they were losing their protective myelin sheaths.
But not one of the doctors initially involved in the case thought of searching for a virus that could be hiding well camouflaged in the pieces of tissue extracted from Len's frontal lobe.

Porton Down might have an African Swine Fever scandal on their hands.

Is Robert Downing helping to cover-up the role of African Swine Fever in Kaposi's sarcoma?

Please support HHV-6 University by purchasing one or our books about the cover-up of the relationship between HHV-6 and Chronic Fatigue Syndrome, AIDS, and many other immunological illnesses.

Do pigs harbor Chronic Fatigue Syndrome and AIDS viruses? Is African Swine Fever a zoonosis?

Pirbright and ViroVet join forces to develop African swine fever antivirals

Was the late John Beldekas right. Is the HHV-6 family of viruses (HHV-6/7/8) really a family of pig viruses capable of causing multisystemic damage to pigs, people, and other species? 

John Beldekas

(Photo by Jane Teas)

"In August, 1986, John Beldekas was invited to go to the NCI and present his findings on the link between ASFV [African Swine Fever virus] 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."
--Mark Konlee

Mark Konlee on African Swine Fever

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.


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.


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.


“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.”


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.


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.


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.”


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.


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.


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.


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.


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.


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.


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


This report by S.S. Froland (1) of the Dept. of Immunology, Oslo, Norway, was about a family of three - father, mother and daughter who all died from immune dysfunction in 1976 from classic AIDS symptoms which included Lymphadenopathy, lymphocyte depletion, CMV, weight loss, pneumonia, dementia and other neurological manifestations and candidiasis.

The father, who was a sailor, had made ports of call in Africa in the early 1960’s. The symptoms of Lymphadenopathy and upper respiratory infections first appeared in 1966. His medical records showed that, during this period when he visited African ports, he had contracted sexually transmitted diseases twice. (1) An autopsy showed the presence of multinucleated giant cells in the lymph nodes.

Unlike other reported AIDS cases before 1979, frozen blood serum from all three patients had been kept since 1971. When the blood serum was analyzed, all three patients tested positive for HIV-1 antibody by immunoassays with confirmation by Western Blot. The sera tested negative for HIV-2 (1). This is the first confirmed case of AIDS with an origin linked to Africa that occurred in the 1960’s.

Did the virus that infected the Norwegian family originate from African pigs that was transmitted to people? Viruses from swine have done this before. In 1919, there was a world wide epidemic known as “The Swine Flu.” Over one million people died from pneumonia related to this flu. Humans have an affinity to pick up viruses that start in swine and vice versa. One PWA told me that the Italian community was not affected by the swine flu of 1919 and credits this to the amount of garlic consumed daily by Italians. The AIDS virus or viruses (possible HIV also?) that started in African swine in the 1960’s could not have been virulent (easily transmitted) between people or the epidemic would have started sooner than it did.

1. S.S. Froland et al, The Lancet, June 11, 1988 (1344-45)


It is no secret that the U.S. as well as foreign governments have been involved in research on germ and biological warfare agents for many years. Part of biowarfare research is to culture viruses so they become more deadly and contagious. It has been reported that Eduardo Perez, a Cuban national, who was on trial in a New York Federal District Court testified on Sept. 10, 1984, that in 1980, as part of a CIA biological warfare scheme against the Castro Cuban economy, “a ship traveled from Florida to Cuba with germs”.

Drew Fetherston and John Cummings, wrote a story linking ASF to anti-Castro operatives, that was published in Newsday, Jan. 9, 1977. Fetherson and Cummings interviewed Cuban exiles and intelligence sources for several months. Their primary U.S. intelligence source said he had been given a container with ASFV1 at Fort Gulick, in the Panama Canal Zone. (1) From Panama, the container with ASFV was taken to a place in Cuba, near Guantanamo around March, 1971. The outbreak of ASF in Cuban pigs became known to have occurred two months later, in May, 1971, causing the Castro regime to order the destruction of 500,000 pigs. Pork is the second largest industry in Cuba after sugar cane. Syndicated columnist Jack Anderson wrote several articles on sources he contacted that indicated that the CIA had engaged in biowarfare against Castro’s swine industry and that Castro’s allegations that the CIA had planted the ASFV virus in Cuba were correct.

Once released in Cuba, ASFV (HHV-6A) may have been brought back to the United States by Cuban refugees and the ASF virus could have been enjoined with the already benign HIV virus making a lethal combination that started the AIDS epidemic. For the record, the CIA has denied having developed and released the ASF virus in Cuba. However, the secretive nature of their sometimes clandestine activities often requires the release of disinformation as well as withholding information for “national security reasons.” Translation: it is OK for them to lie to the public to avoid embarrassment.


My own version of a possible scenario as to what happened is that the ASF virus was taken from Africa to US labs as part of their biowarfare research program. The CIA may have taken the most virulent strains of ASFV, which existed in Uganda. The Ugandan strain is known to destroy cells and is more aggressive than the Portuguese strain(1). The ASF virus may have been cultured to make it more virulent and contagious. to more effectively destroy Castro’s second biggest industry - pigs. The CIA released the enhanced ASF virus in Cuba in an attempt to create economic hardship and destabilize the communist government. However, the enhanced ASF virus had an unexpected side effect. It could more easily jump species and infect humans as well as pigs.

When you consider the Norwegian family that died of AIDS in 1976 with symptomology starting in 1966, it indicates that AIDS had its origin in Africa in the 1960’s, and may have been transmitted from swine to people, who could have contracted the disease by eating undercooked pork or handling raw pork with infected blood. However, this earlier AIDS virus was not easily transmittable or the AIDS epidemic would have started in the 1960’s. When we learn more about the genome (genetic structure) of HHV-6A, we should be able to determine which African strain of the ASF virus the CIA used for biowarfare against Cuba.

At the time of the ASF outbreak in the pig population in Cuba, Cuban civilians eating pork infected with the ASF virus were reported getting sick(1). What was the ASF viral status of the tens of thousands of Cubans evicted by Castro during the “Mariel Boatlift”, which occurred after the second ASF outbreak in 1980? News reports at the time indicated many were gay, ill or prisoners. Was this Castro’s return gift? Did Cuban refugees bring the ASF virus to southern Florida where some gay Cuban refugees intermingled with the gay population? There is much evidence to support this as many gays took in the Cuban male exiles as roommates. Was HIV, as a benign virus, already present in some members of the gay community? Did the co-infection of ASF (HHV-6A) and HIV start the AIDS epidemic? The preponderance of evidence suggest that this is the scenario that unfolded.

Some Gays in New York City invited Cuban refugees to move in with them. Late in 1980, the first cases of GRID (Gay Related Immune Deficiency) appeared in New York City. At about the same time, Haiti had an outbreak of both African Swine Fever and AIDS (2). The Hepatitis B vaccination trials were in progress in the gay community. When an infected donor’s blood was used in the development of the Hepatitis B vaccine, this quickly spread the disease through major gay centers in the United States. Also, at the same time, blood products from infected donors may have ended up in small pox vaccinations given by the World Health Organization (WHO) to millions of persons in Africa. This could explain the simultaneous outbreak of AIDS on both continents. As the two viruses spread through exchange of body fluids, they spread the AIDS epidemic. However, the persons receiving only the ASFV (HHV-6A) virus, and not HIV, developed Chronic Fatigue Syndrome with Lymphadenopathy, low grade fevers and fatigue while the persons receiving only HIV without HHV-6A became long term HIV+ non-progressors with no symptoms at all. In AIDS, both viruses work synergisticly to infect immune cells, most organs and cause neurological damage. The most damaging of the two viruses is ASFV which makes it the primary cause of AIDS with HIV as a co-factor. If you can get rid of ASFV, you no longer have AIDS or chronic immune dysfunction.

This disease model explains why AZT and all the drug combinations of the past decade have been ineffective in treating AIDS. The drug combination have been directed at HIV and not at the primary cause of AIDS that Gallo calls HHV-6A and which is a variant strain of African Swine Fever.

1. AIDS INC., by Jon Rappoport, Human Energy Press, San Bruno, CA.

2. Ann NY Acad Sci, Jun 16, 1992, by MJ Torres-Anjel.

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.


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.


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.”


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.


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.


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.


An article by A Canals (1) discusses an in-vivo test where ASFV was inactivated by UV light. Although, he did not say what wavelength was used. (UVA, with a longer wavelength, inactivates viruses and other pathogens. Some research in cell cultures suggest that UVB may activate HIV replication.) Canals found that active ASFV caused an increase in CD8+ subsets when added to cell cultures of blood cells whereas ASFV inactivated by UV light caused an increase in both CD4+ and CD8+ subsets.

This article raises the possibility that blood taken from a patient infected with HHV-6A and exposed to UV light (UVA1, 340 to 400 nm)) and then later reinfused into the patient might stimulate neutralizing antibodies and increases in CD4 and CD8 subsets, which would be a positive gain in immunity for the patient. Would tanning in a salon with UVA also have some benefits in increasing CD4 and CD8 subsets? Would it kill some HIV and HHV-6A in the capillaries and cells near the surface of the skin?. Tanning salons usually have both types of beds available - UVB or UVA. In cell cultures, UVA did not activate HIV, but UVB and UVC did cause increases in viral replication (2). However, no studies have attempted to repeat these results with UVB in-vivo ( in persons) measuring viral load by PCR. However, one study with six patients using UVB was done in Canada.

J.B. Hudson found only one person out of six, who had 42 UVB light treatments, change his P24 antigen status from negative to positive. All other immune markers (CD4, CD8 and beta-2 microglobulin levels) stayed stable in all six patients. None of the six patients on UVB light treatments had any opportunistic infections while receiving the UV treatment (5).

In one experiment, G. Miolo et al found that “total inactivation of the HIV-1 (200SFU) was obtained in the presence of 1 microgram ml-1 of TMP and 20 kJ m-2 of UVA light.” (3) Tmp is “8-trimethylpsoralen.” In another experiment on cell cultures, MM Saucier found that “heat inactivation, or UV-light treatment of viruses before assays almost completely ablates its ability to induce proliferation.” (4). There is a complete lack of clinical evidence indicating increases in HIV or HHV-6A viral load, as measured by PCR, (or increases in beta-2 microglobulin levels), in AIDS patients using tanning beds or being exposed to natural sunlight. All the reports that suggest that PWAs should not tan or expose their skin to the sun is coming from lab cultures that do reflect the actual conditions that occur in people receiving UV light. The lab cultures are using a bovine serum that does not exist in people. If the researchers cannot duplicate in-vivo (with people) the same viral replication with UVB or UVC light that they are seeing in the lab, then it means the labs tests have some inherent flaws in design.

1. A. Canals et al, Vet Microbiol., 1992, Nov: 33 (1-4): 117-27.

2. L.E. Benade et al, Transfusion. Aug, 1994; 34 (8):680-4

3. G. Miolo, J Photochem Photobiol b., 1994 Dec: 26(3):241-7

4. M.M. Saucier, Symp Nonhum Primate Models AIDS, 1993, Sept 19-23, Abstract No 93. Atlanta, GA.

5. J.B. Hudson et al, Div. of Microbiology, Univ. of British Columbia, Vancouver, Canada.
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.

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