More evidence that African Swine Fever is a human infection and connected to HHV-6?

Virus Identification in Unknown Tropical Febrile Illness Cases Using Deep Sequencing


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3274504/

Was ASFV the real cause of AIDS? The New Scientist, April 28, 1983

The study has found out a high seroprevalence of ASFV antibodies in apparently healthy slaughter pigs and also a high proportion of ASFV antibody seropositive pigs in surveyed districts in Uganda indicating exposure to ASFV. However, there was a lower prevalence of ASFV infection implying that there could be low virulent strains of ASFV circulating in domestic pigs in Uganda which requires further investigation.

http://bmcvetres.biomedcentral.com/articles/10.1186/1746-6148-9-263

Are pigs with African Swine Fever in the Democratic Republic of the Congo making people sick?

"Indeed, pigs in the DRC frequently die from other pathogens; the country often has outbreaks of African swine fever, which has a very high mortality rate."

http://www.sciencemag.org/news/2017/05/could-pigs-be-involved-congos-new-ebola-outbreak




"The African swine fever (ASF) virus, may in the future become dangerous for humans, according to the head of the Russian Epidemiology Service, Chief State Sanitary Doctor Gennady Onishchenko, at the press-conference in St. Petersburg. According to him almost all viruses from time to time go through mutation processes which can give them some additional functions."

 http://www.pigprogress.net/Health-Diseases/Outbreaks/2013/7/ASF-could-become-a-human-health-risk-1308047W/

 

 

Background on African Swine Fever Virus as a human pathogen:

"African Swine fever is an endemic disease in sub-Saharan Africa and many other parts of the developing world. It is caused by the African Swine virus that primarily replicates in macrophages and monocytes leading to the impairment of the structure and function of the immune system of the infected organisms. Until now the African Swine epidemic continues to spread despite all efforts to contain it. Thus, there is an objective need for effective, safe and affordable preventive and therapeutic approaches, in particular for effective vaccines, to control and eventually eradicate this disease. Since the characteristic feature of the African Swine virus is to impair the immune system and to cause immune deficiencies in its hosts the development of vaccines and other therapeutic approaches against the African Swine virus has implications for other immune deficiencies or diseases. Several other viruses are also known to cause immunodeficiency-like syndromes in humans, including cytomegalovirus, Epstein Barr Virus and others. Moreover, a series of cases of so-called "idiopathic" immunodeficiencies have been documented that display CD4+T-lymphocytopenia with opportunistic infections, but show no evidence of HIV infection. Since antibodies for the African Swine virus have been detected in humans, the possibility of human infection with the African Swine virus exists and may thus far have escaped any systematic screening. Thus, any preventive and therapeutic approach to African Swine fever can have far-reaching implications to control immune deficiency conditions in humans."http://www.faqs.org/patents/app/20080207875

Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage.

Loh J, Zhao G, Presti RM, Holtz LR, Finkbeiner SR, Droit L, Villasana Z, Todd C, Pipas JM, Calgua B, Girones R, Wang D, Virgin HW.

Departments of Pathology & Immunology and Molecular Microbiology, Department of Medicine and Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Microbiology, Faculty of Biology, University of Barcelona, Barcelona, Spain.

"The family Asfarviridae contains only a single virus species, African swine fever virus (ASFV). ASFV is a viral agent with significant economic impact due to its devastating effects on populations of domesticated pigs during outbreaks, but has not been reported to infect humans. We report here the discovery of novel viral sequences in human serum and sewage which are clearly related to the Asfarvirus family, but highly divergent from ASFV. Detection of these sequences suggests that greater genetic diversity may exist among Asfarviruses than previously thought, and raises the possibility that human infection by Asfarviruses may occur."

http://www.ncbi.nlm.nih.gov/pubmed/19812170?dopt=Abstract

African Swine Fever Virus (Asfarviridae) sequences found in people with febrile illnesses

Abstract

Virus Identification in Unknown Tropical Febrile Illness Cases Using Deep Sequencing

Dengue virus is an emerging infectious agent that infects an estimated 50–100 million people annually worldwide, yet current diagnostic practices cannot detect an etiologic pathogen in ∼40% of dengue-like illnesses. Metagenomic approaches to pathogen detection, such as viral microarrays and deep sequencing, are promising tools to address emerging and non-diagnosable disease challenges. In this study, we used the Virochip microarray and deep sequencing to characterize the spectrum of viruses present in human sera from 123 Nicaraguan patients presenting with dengue-like symptoms but testing negative for dengue virus. We utilized a barcoding strategy to simultaneously deep sequence multiple serum specimens, generating on average over 1 million reads per sample. We then implemented a stepwise bioinformatic filtering pipeline to remove the majority of human and low-quality sequences to improve the speed and accuracy of subsequent unbiased database searches. By deep sequencing, we were able to detect virus sequence in 37% (45/123) of previously negative cases. These included 13 cases with Human Herpesvirus 6 sequences. Other samples contained sequences with similarity to sequences from viruses in the Herpesviridae, Flaviviridae, Circoviridae, Anelloviridae, Asfarviridae, and Parvoviridae families. In some cases, the putative viral sequences were virtually identical to known viruses, and in others they diverged, suggesting that they may derive from novel viruses. These results demonstrate the utility of unbiased metagenomic approaches in the detection of known and divergent viruses in the study of tropical febrile illness.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3274504/

Detection of African swine fever virus-like sequences in ponds in the Mississippi Delta through metagenomic sequencing

" . .. further study is needed to characterize their potential risks to both public health and agricultural development."

http://link.springer.com/article/10.1007%2Fs11262-013-0878-2

ASF virus, adapted to grow in VERO cells, produces a strong cytopathic effect in human macrophages leading to cell destruction.

http://vir.sgmjournals.org/content/34/3/455.short

Did HHV-6 Come from Pigs?

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HHV-6 and African Swine Fever Virus: Are they related?

Do they cause the same spectrum of immunological illnesses in pigs and people?

While the African Swine virus has been primarily detected in pigs and certain other animals, antibodies against the African Swine virus have also been found in humans. The fact that there was no description of any finding of the African Swine virus in humans may thus be attributable to oversight or a lack of understanding for the significance of African Swine fever virus for the pathogenicity of immune deficiencies in humans.

http://www.faqs.org/patents/app/20080207875#ixzz1YVVxZ1Ka

"All the evidence now available indicates that of the two viruses, HIV and HHV-6A, the most destructive by far is HHV-6A which has all the characteristics of African Swine Fever Virus."

--Mark Konlee

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"The 19R Protein of HHV-6 has significant amino acid sequence homology . . . to a protein encoded by African Swine Fever Virus."

--Glenda L. Lawrence, John Nicholas and Bart G. Barrell
Journal of General virology (1995), 76, 147-152

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"African Swine fever is an endemic disease in sub-Saharan Africa and many other parts of the developing world. It is caused by the African Swine virus that primarily replicates in macrophages and monocytes leading to the impairment of the structure and function of the immune system of the infected organisms. Until now the African Swine epidemic continues to spread despite all efforts to contain it. Thus, there is an objective need for effective, safe and affordable preventive and therapeutic approaches, in particular for effective vaccines, to control and eventually eradicate this disease. Since the characteristic feature of the African Swine virus is to impair the immune system and to cause immune deficiencies in its hosts the development of vaccines and other therapeutic approaches against the African Swine virus has implications for other immune deficiencies or diseases. Several other viruses are also known to cause immunodeficiency-like syndromes in humans, including cytomegalovirus, Epstein Barr Virus and others. Moreover, a series of cases of so-called "idiopathic" immunodeficiencies have been documented that display CD4+T-lymphocytopenia with opportunistic infections, but show no evidence of HIV infection. Since antibodies for the African Swine virus have been detected in humans, the possibility of human infection with the African Swine virus exists and may thus far have escaped any systematic screening. Thus, any preventive and therapeutic approach to African Swine fever can have far-reaching implications to control immune deficiency conditions in humans."
http://www.faqs.org/patents/app/20080207875

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Vaccination with viral protein-mimicking peptides postpones mortality in domestic pigs infected by African swine fever virus.

Ivanov V, Efremov EE, Novikov BV, Balyshev VM, Tsibanov SZh, Kalinovsky T, Kolbasov DV, Niedzwiecki A, Rath M.
Dr Rath Research Institute BV, 1260 Memorex Drive, Santa Clara, CA 95050, USA.

Abstract

Periodic outbreaks of African swine fever virus (ASFV) infection around the world threaten local populations of domestic pigs with lethal disease and provide grounds for pandemic spread. Effective vaccination may bring this threat under control. We investigated the effectiveness of select peptides mimicking viral proteins in establishing a protective immune response. Forty-six synthetic peptides based on the analysis of the complete nucleotide sequence of ASFV were tested for immunogenicity in mice. The 17 best immune response-inducing peptide candidates were selected for further investigation. Twenty-four domestic pigs, 3-4 months old and weighing 20-25 kg, were divided into six groups (n=4) and immunized by subcutaneous injection using a standard three-round injection protocol with one of four peptide combinations prepared from the 17 peptides (Groups 1-4) or with carrier only (Group 5). Group 6, the control, was not vaccinated. Animal body temperature and behavior were monitored during and post immunization for health assessment. Two weeks after the last round of immunizations, the pigs were infected with live ASFV (Espania 70) at 6.0 Ig GAE50/cm3, and the survival rate was monitored. Blood samples were collected for analysis the day before infection and on days 3, 7 and 10 post-infection, or from deceased animals. The serum titers of specific immunoglobulins against synthetic peptides and whole inactivated ASFV were determined by enzyme immunoassay before and after infection. The presence of viral DNA in blood serum samples was determined by polymerase chain reaction. Viral infection activity in blood sera was determined by heme absorption in cultured porcine bone marrow and porcine leukocyte cells. Repeating the injection of synthetic peptides in both the mice and pigs produced an immune response specific to individual peptides, which differed widely in the intensity scale. Specific anti-whole virus immunoglobulin binding activity in the swine serum samples from all groups was below the detection limit. Viral DNA was positively identified in all the samples infected with viral preparations. Viral infection activity was present in all the infected animals and steadily increased with time. On day 3 after infection, the viral titer was significantly lower in Groups 1 and 3 than in the unvaccinated controls. In deceased animals, the viral titer was significantly lower in Groups 1 and 3 than in the controls. All infected animals died within 17 days of infection. The average survival rate was significantly higher in Groups 1 and 3 (12.0 and 14.3 days, respectively) than in the controls (9.8 days). Vaccination with specific synthetic peptides significantly delayed mortality in domestic pigs infected with ASFV. These results justify further investigation aimed at developing an effective vaccine against ASFV infection.
Mol Med Report. 2011 May;4(3):395-401. doi: 10.3892/mmr.2011.454. Epub 2011 Mar 14.

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Are HHV-6, HHV-6 and HHV-8 Really Porcine Lymphotropic Herpes Viruses?

Are pigs and pork infected with HHV-6, HHV-6 and HHV-8? Is the pig version of these viruses causing the PRRS epidemic of immune deficiency in pigs all over the world? Would pigs make the best model for HHV-6, HHV-7 and HHV-8 treatment experiments?

http://vir.sgmjournals.org/cgi/reprint/80/4/971.pdf
Robert Gallo's Laboratory's Research on the relationship between HHV-6 (originally called HBLV) and African Swine Fever Virus.

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HHV-6 and John Beldekas's research on African Swine Fever virus

"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."
Mark Konlee in Positive Health News, January 14, 1996
Spin Magazine on John Beldekas

Florida Pig Farm Poses Riddle

"AIDS victims and pigs stricken with chronic African swine fever have common characteristics, Beldekas said, including fever, abnormally large lymph nodes, skin lesions, immune-related pneumonia, and a reduction of white blood cells. Both diseases can be spread through exposure to infected blood, blood products and semen, Beldekas said, but the animal virus can also be transmitted by infected ticks. Accordingly, they say, the animal virus may somehow be a factor in the transmission of AIDS, which could have spread from infected pigs to humans through tick bites, and then from human to human through sexual contact or direct infection of blood."
--By JON NORDHEIMER, SPECIAL TO THE NEW YORK TIMES

AIDS TESTS PLANNED FOR PIGS

"The Florida Health Department announced today that it would conduct additional tests on swine herds in Belle Glade, Fla., to determine whether the animals might have been infected with the virus believed to cause AIDS. The announcement came in response to a finding last month by a biochemist that blood from some of the pigs may have contained antibodies to the virus for acquired immune deficiency syndrome." --Keith Schneider, the New York Times Published: June 4, 1986

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Human herpesvirus-6 as a possible cause of encephalitis and hemorrhagic cystitis after allogeneic hematopoietic stem cell transplantation

Y-J Kim, D-W Kim, D-G Lee, S-T Park, Y-H Park, C-K Min, S Lee, J-H Choi, J-W Lee, W-S Min, W-S Shin and C-C Kim
Leukemia, May 2002, Volume 16, Number 5, Pages 958-959

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Is this another clue that HHV-6 is a form of African Swine Fever Virus? Here's evidence that the pig virus can actually infect humans:

Detection of Novel Sequences Related to African Swine Fever Virus in Human Serum and Sewage.

Loh J, Zhao G, Presti RM, Holtz LR, Finkbeiner SR, Droit L, Villasana Z, Todd C, Pipas JM, Calgua B, Girones R, Wang D, Virgin HW.
Departments of Pathology & Immunology and Molecular Microbiology, Department of Medicine and Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania; Department of Microbiology, Faculty of Biology, University of Barcelona, Barcelona, Spain.

"The family Asfarviridae contains only a single virus species, African swine fever virus (ASFV). ASFV is a viral agent with significant economic impact due to its devastating effects on populations of domesticated pigs during outbreaks, but has not been reported to infect humans. We report here the discovery of novel viral sequences in human serum and sewage which are clearly related to the Asfarvirus family, but highly divergent from ASFV. Detection of these sequences suggests that greater genetic diversity may exist among Asfarviruses than previously thought, and raises the possibility that human infection by Asfarviruses may occur."

J Virol. 2009 Oct 7.

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Robert Gallo's Laboratory's Research on the relationship between HHV-6 (originally called HBLV) and African Swine Fever Virus.

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Implication of the host nucleus during African swine fever virus (ASFV) infection

Ballester M, Rodríguez-Cariño C, Pérez M, Gallardo C, Rodríguez JM, Salas ML, Rodriguez F. Implication of the host nucleus during African swine fever virus (ASFV) infection. CReSA. Spain. http://www.cresa.es
Researchers of the CReSA have demonstrated the relevance of the host nucleus during ASFV infection. These discoveries might have important implications when searching for antiviral strategies against ASF that is currently causing real economical problems in many sub-Saharan countries and knocking at the door of the EU.
In the present study, new evidences supporting the implication of the host nucleus during ASFV infection are provided. Thus, during the initial phase of ASFV replication, an early phosphorylation and disassembling of lamin A/C (a multifunctional protein localized both in the nuclear periphery and nucleoplasm of eukaryotic cells and involved in nuclear stability, chromatin structure and gene expression) was detectable, coinciding with the sites where the newly synthesized ASFV DNA was found. This early phosphorylation and disassembling of lamin A/C might facilitate the interaction of ASFV DNA with nuclear proteins required for proper viral DNA conformation and/or initiation of the replication process, as it has been previously reported for other nuclear viruses such as herpesviruses.
At late times post-infection, the nascent ASFV DNA, the lamin A/C and nucleoporin p62 (another nuclear marker) were also found within the cytoplasm of the infected cells (Figure 1), pointing towards some kind of budding-like mechanism of the ASFV DNA from the nucleus to the cytoplasm of the infected cell.
On the other hand, intra-nuclear lamina, the SC-35marker (specifically labelling the splicing speckles) and the RNA pol II redistributed in enlarged foci within the nucleoplasm of the ASFV infected cells from very early after the infection; a picture previously described for no-infected cells in the presence of transcription inhibitors. Western blot analysis with antibodies that recognize different forms of the RNA pol II allowed to confirm that early after ASFV infection the RNA pol II was hypophosphorylated to be finally degraded at late times post-infection. All together these results indicate a possible mechanism to block the cellular transcription early during viral infection, contributing to the cellular shut-off described during the ASFV infection.
Our results clearly demonstrate that nuclear interactions during infection with ASFV are more important than previously believed.
http://www.pig333.com/swineabstracts/implication-of-the-host-nucleus-during-african-swine-fever-virus-asfv4668/

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A Virus That Causes An "Acquired Immune Deficiency Syndrome" in Pigs May Be The Real Cause Of CFS And AIDS

It may seem silly to look at a pig illness to identify the cause of CFS, but it really isn't. Pigs and humans pass viruses back and forth all the time; in fact, flu viruses change from year to year because they pass from people to pigs and back again and in so doing, mutate, or change, considerably.
There is an illness of pigs, African Swine Fever, that an expert in the field has called "an acquired immune deficiency syndrome of pigs," because it produces symptoms that are so similar to those of AIDS. African Swine Fever is caused by a virus, African Swine Fever Virus (ASFV).
Like AIDS, there is no treatment for African Swine Fever, and no vaccine to prevent ASFV infection. When African Swine Fever is suspected in a herd of pigs, the entire herd is slaughtered to prevent the spread of the very contagious, deadly virus. Because of the vast economic implications such slaughters of pig herds would have on U.S. agriculture, it is against the law to study ASFV on mainland U.S.A. The only place where the virus can be studied, by law, is the Plum Island Animal Disease Center on Plum Island, off the shore of Long Island, New York.
Similarities between the symptoms of ASF and AIDS -- as well as the fact that Haiti, one of the areas in which AIDS appeared earliest, had recently had an ASFV epidemic -- caught the attention of a young scientist in 1983. Dr. Jane Teas, who was working as a researcher at Harvard, began collaborating with Boston University scientist Dr. John Beldekas to try to figure out if ASFV could be causing AIDS.
In 1986, Drs. Teas and Beldekas published a report in the British medical journal The Lancet showing that they had found evidence of ASFV infection in AIDS patients. But after that, the trail was stopped cold, when a group of scientists gathered by the U.S. Department of Agriculture at Cold Spring Harbor Laboratory (on Long Island) issued a memorandum that no further research should be performed to test the ASFV hypothesis. Usually, when a line of research proves not to be fruitful, scientists naturally stop pursuing it; it was, however, unprecedented for a group of scientists gathered by the government to declare that a line of research should no longer be pursued. That is, however, exactly what the scientists gathered by the USDA at the Cold Spring Harbor Laboratory did.
Shortly thereafter, however, two research groups to whom Dr. Teas and Dr. Beldekas had provided information and scientific materials announced almost simultaneous discoveries of a "new" human virus, found in AIDS patients: HHV-6.
HHV-6 and ASFV are very similar viruses; they are the same size, and they infect and kill the same kinds of cells. They both cause bleeding problems (they are "hemorrhagic" viruses), and both attack the immune system, allowing secondary (or "opportunistic") infections to become fatal. They both cause neurological disease. Both viruses mutate (change) easily.
Furthermore, both HHV-6 and ASFV are characterized by having many strains, or types, of virus. ASFV, it has been known for decades, can cause a whole range of illness, from extremely acute (in which 100 percent of infected animals die within days) to chronic (in which animals develop immune system and neurological symptoms, but generally survive).
HHV-6, also, has many strains that can cause different levels of disease, from an illness with mild fever and rash, to a fatal, hemorrhagic disease in which the patient rapidly bleeds to death. HHV-6 can cause a collapse of the immune system, and is associated with many kinds of neurological phenomena, including the development of brain lesions. Like ASFV, HHV-6 is found in people with acute illness -- that is, AIDS -- and chronic illness, CFS.
Where did this new human virus come from?
Is it a zoonosis, an animal virus that has mutated and become capable of infecting humans?
When Dr. Teas and Dr. Beldekas were trying to determine if ASFV could be involved in causing AIDS, a major objection to the theory was that pigs in the U.S. were not sick. If a pig virus were causing AIDS, some experts argued, then shouldn't the pigs be sick?
There is, in fact, a world-wide epidemic among domesticated pigs that bears a great resemblance to African Swine Fever; it has been called "Mystery Swine Disease." Although a "new" virus (called "Lelystadt virus" for the city in which it was isolated) is thought to be causing "Mystery Swine Disease," the new virus has not yet been compared to all the strains of the old virus, ASFV.
Lelystad virus also has not been compared to the new human virus, HHV-6.
One reason that there has been very little progress in fighting both AIDS and CFS may be because HHV-6 is actually the virus that is causing most, if not all, of the damage to the immune system in both syndromes.
If HHV-6 is causing the immune system damage in AIDS and CFS and if HHV-6 is really a strain of ASFV, there is the very real possibility that some scientists have deliberately misled the public.
--Neenyah Ostrom, America's Biggest Cover-Up: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic And Its Link to AIDS

Transmission cycle of African Swine Fever Virus

From an FAO Field Manual on Recognizing African Swine Fever

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The following are the characteristics of the African Swine Virus: 1. it targets the immune system of the host 2. it has the following morphological features, in particular it structurally and functionally impairs the lymph nodes and other integral parts of the immune system; 3. its hematological changes includes a significant decrease of CD4 and T-cell counts; 4. both viruses share similar clinical findings, namely lymph node swelling, increased susceptibility to infections, and others; 5. it has both an acute and chronic form of infectious states; 6. it is known to display a high frequency of alteration of their genetic sequence in order to escape the host defense system; 7. it is endemic in sub-Saharan Africa and few other regions.

http://www.faqs.org/patents/app/20080207875#ixzz1YVX7KRSg

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We are in the middle of the tragic HHV-6 epidemic. The big question about HHV-6 is this: What can't it do? What system in the body does it not infect and harm? In addition to AIDS it may be the key factor (or cause) in a number of current "mysterious" epidemics like chronic fatigue syndrome, autism and Morgellons by inducing expression of HERV-K18-encoded superantigen. Where did it come from? Who really discovered it? Robert Gallo or Jane Teas and John Beldekas? Technically speaking, is it really a herpes virus? Or is it actually a member of the asfaviridae family? Does it belong in a class by itself? Is it really a slow-acting zoonotic hemorrhagic virus? Is it also infecting animals? Are sick animals the original and current source of it? Which ones? What is the relationship of HHV-6, HHV-7 and HHV-8 to Porcine Lymphotropic Herpes Virus? Are pigs suffering from Porcine Reproductive and Respiratory Disease (PRRS) infected with some form of HHV-6, HHV-7 and HHV-8? Having established itself in complex diseases of the immune system in the late 20th Century, is HHV-6 becoming the biggest unrecognized human (and porcine) medical crisis of the 21st Century? Are we living in "The Age of HHV-6 Denialism" and when will it end? On this site you'll find lots of HHV-6 links and a great deal of food for thought.

We especially want to welcome scientists from Russia, China, Germany and other countries who are researching the relationship between African Swine Fever Virus and HHV-6, HHV-7 and HHV-8. Your work may help end this international tragedy.

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Important and provocative books about HHV-6 and the epidemics it may be causing available from Amazon in print editions or on Kindle:

The Virus Within by Nicholas Regush (Print Edition)
What Really Killed Gilda Radner? Frontline Reports on the Chronic Fatigue Syndrome Epidemic by Neenyah Ostrom (Print Edition)
50 Things You Should Know About the Chronic Fatigue Syndrome Epidemic by Neenyah Ostrom (Print Edition)
America's Biggest Cover-Up: 50 More Things Everyone Should Know About the Chronic Fatigue Syndrome Epidemic And Its Link to AIDS by Neenyah Ostrom (Print Edition)
The Closing Argument by Charles Ortleb (Available on Kindle and in a Print Edition. Free for Kindle owners with Amazon Prime.)