Three Big Books

Thursday, May 16, 2019

The USA is to begin testing sick pigs for African Swine Fever Virus

U.S. to begin testing sick and dead pigs for African swine fever

Read the book by the journalist earning about African Swine Fever in the USA for decades. 

African Swine Fever is a big story already because, when and if it spreads to all of Western Europe, all of Asia and the USA (where it may already be in pigs), it will cause the collapse of a major portion of the agricultural export economies of the affected countries. We're talking about many billions of dollars of losses. And the problem is not temporary because those countries will be suspected of harboring the disease in their wild boar and ticks for decades to come. The disease could easily become endemic. 

But the issue is so much more important because of the disturbing body of evidence that shows that African Swine Fever Virus can infect humans (despite what authorities currently insist). Thus far, Europe and America's leading publications and journalists have failed to warn the public of the impending ASFV risk to their health. Here are the biggest African Swine Fever stories they have missed.

1. The African Swine Fever Vaccine for humans.

"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."

2. Evidence of African Swine Fever found in people with fevers.

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.

3. A Russian Scientist warns that African Swine Fever could infect humans.

Russian Scientist: ASF could become a human health risk

"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."

4. 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."

5. How the American science Robert Gallo may have stolen the African Swine Fever research of a Boston University scientist and may have given African swine Fever the fraudulent new name of "HHV-6."

"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

6. The epidemiology that suggests that African Swine Fever in people in Sardinia is misidentified as HHV-8.

The world's highest incidence of Kaposi's sarcoma occurs in Sardinia (Reference) Is it possible that it is due to the fact that African Swine Fever Virus is endemic on the island? (Reference) One study suggests that the incidence of K.S. in northern Sardinia is highest in a countryside area where people have contact with animals. (Reference) Given the high prevalence of HHV-8,--the so-called K.S. herpes virus--in Sardinia (Reference) is it at all possible that HHV-8 may have been misclassified and actually is a human-adapted form of African Swine Fever Virus? (ASFV has been at least visually mistaken for another herpes virus, CMV, in the past.)

A number of experiments could be conducted to explore this hypothesis. In addition to a direct comparison of ASFV and HHV-8, pigs with African Swine Fever Virus could be tested for sequences of HHV-8. People with Kaposi's sarcoma could be tested for sequences of African Swine Fever, including new Asfaviridae sequences recently discovered. (Reference) 

A comparison of the K.S. lesions in humans and ASFV lesions in pigs might be in order.Given that African Swine Fever is currently spreading in Russia and is now threatening Europe and China, (Reference) it would be useful to know whether people who are exposed to pigs with ASFV are at increased risk for HHV-8, Kaposi's sarcoma and the other pathologies associated with HHV-8. A study in sub-Saharan Africa where ASFV is endemic and HHV-8 is also endemic (Reference) might be useful. And areas of Russia where ASFV is spreading could be monitored closely for any signs of an increase of K.S. or HHV-8 infection and HHV-8 related pathologies.HHV-8 is an emerging health problem. HHV-8-associated K.S. is a significant problem in AIDS patients. It may also be the key to Chronic Fatigue Syndrome. HHV-8 has been found in the cerebrospinal fluid of 50% of Chronic Fatigue Syndrome patients. (Reference) HHV-8 has been linked to type 2 diabetes. (Reference) HHV-8 has been detected in B-cells in Castleman's disease and primary effusion lymphoma. (Reference).

If HHV-8 is a form of ASFV, it is possible that pigs might constitute a useful animal model for the study of possible treatments for K.S. and other pathologies associated with HHV-8. And if there is any relationship between ASFV and HHV-8, people may have to be warned to take special precautions around pigs in areas where there are ASFV outbreaks. And countries where undercooked pork is consumed (like Ukraine where salo is a staple) may need to alert the public to cook all pork products thoroughly during ASFV epidemics.

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

8. A sick child tests positive for African Swine Fever virus.

9. Newspaper publisher writes The Chronic Fatigue Syndrome Epidemic Cover-up, a memoir about uncovering the African Swine Fever cover-up in America.

The Chronic Fatigue Syndrome Epidemic Cover-up details the investigative reporting of a New York Native that reveals the Centers for Disease Control and the United States Department of Agriculture lied about the presence of African Swine Fever in pigs and people.

10. Journalist pens The African Swine Fever Novel, an Orwellian novel warning about the consequences of an African Swine Fever Virus epidemic in humans.

The African Swine Fever Novel is available here

11. Prisoners fed meat infected with African Swine Fever

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.

Pigs and African Swine Fever may hold the key to Chronic Fatigue Syndrome.

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.

Spanish researchers seem to show that Chronic Fatigue Syndrome is a form of AIDS

The following post appeared today on Phoenix Rising
I am Manuel Ruiz, medical student in Spain and I am sick with CFS/ME. Together with my girlfriend Rosario, graduated in Medicine from the Complutense University of Madrid, we contacted one of the best research centers in Spain, CIMA, to carry out the project described below.
Currently I have seen quite a few lymphocyte typages that have provided me with CFS/ME patients. They could be grouped into two main groups:
-In the first group they present reduced levels of total t lymphocytes (CD4, CD8, activated t lymphocytes) that indicate the presence of an immunodeficiency of T lymphocytes.
-In the second group the patients have total t lymphocytes (CD4, CD8) and immunoglobulins in normal values. But this does not mean that there cannot be some type of cell immunodeficiency. The analysis of activated CD3+ HLA-DR+ and CD3+ CD4+ HLA-DR+ T lymphocytes is used to see if there is indirectly a decrease in the MHC class II antigenic presentation, since CD4 T lymphocytes are activated through this antigenic presentation made by B lymphocytes (antigen-presenting cells) in the secondary lymphoid organs. Therefore, if there is a decrease in the expression of class II histocompatibility molecules in B lymphocytes, they would not present antigens to CD4 T lymphocytes and these would not be activated. For any T-lymphocyte to be able to perform its functions and become an effector lymphocyte, it is necessary for them to be activated. That is to say, the values of the activated CD4+ HLA-DR+ T lymphocytes indicate indirectly if there is any problem in the class II MHC antigenic presentation made by the B lymphocytes.
There is a congenital immunodeficiency called class II MHC deficiency in antigen-presenting cells, which is associated with a severe decrease in CD4+ (activated) T lymphocytes. This absence of cooperating T lymphocytes (CD4+) causes a deficiency in humoral response (the low number of CD4+ T lymphocytes causes a defect in collaboration between T and B lymphocytes) and cellular response (due to the intrinsic defect in the number of CD4+ T lymphocytes). Patients suffer repeated infections, particularly of the digestive tract. The genetic defect of this severe immunodeficiency is found in several proteins regulating the transcription of HLA class II genes.1
Figure (photo attached): Regulation of class II HLA genes in normal individuals (above) and in patients with class II HLA deficiency (below).1
The following are the ESID (European Society for Immunodeficiencies) diagnostic criteria for this congenital immunodeficiency:2
A. Definitive diagnosis: if both criteria are met:
• Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
• Mutation in one of the genes: CIITA, RFX-B, RFX-5 or RFX-AP.
B. Probable diagnosis: if all four criteria are met:
• Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
• Failure to thrive, opportunistic infections or persistent viral infections.
• Normal number of T and B cells.
• Normal proliferative responses to mitogens.
C. Possible diagnosis: the first of the criteria plus at least one of the following:
• Deficit expression (<5%) of MHC-II molecules in B lymphocytes or monocytes.
• Hypogammaglobulinemia.
• Normal mitogen responses but absent T cell proliferation to antigens.
• Normal number of T and B cells.
• Reduced number of CD4+ cells.
• Failure of mononuclear cells to stimulate a mixed lymphocyte culture.
The four genetic disorders that give rise to this congenital immunodeficiency are clinically indistinguishable. In most cases, there is no Class II expression. However, in others, the intensity of expression of MHC-II molecules may be as high as 5% of normal. Patients with higher expression tend to have a milder course of disease. These patients may survive beyond early childhood.3
We believe that the difference between this congenital immunodeficiency and that found in the second group of CFS/ME is in the number of antigen-presenting cells that have class II MHC deficiency. In the CFS/ME group it would only occur in those cells infected (mostly B lymphocytes) with an intracellular pathogen and in congenital immunodeficiency is in all antigen-presenting cells.
There are several intracellular pathogens that reduce the MHC class II antigenic presentation as an evasion mechanism of the immune system. The best known is the Epstein Barr virus, where it has been demonstrated that the latent protein LMP2A mediated the reduction of CIITA levels by decreasing the expression of PU.1 and E47 in B cells.4 Others such as human cytomegalovirus, human parainfluenza virus type 3, and varicella zoster virus suppress the IFN-γ-induced expression of class II MHC through inhibition of JAK-STAT activation and the transcription route activator, resulting in a reduction of CIITA expression.4 This may confirm the infectious origin of SFC/ME.
Both groups of CFS/ME have a type of immunodeficiency and it appears that those with a total T lymphocyte immunodeficiency (not just activated) are in a more advanced stage of the disease, and those with only decreased activated t lymphocytes are in an early stage. Both justify the recurrent infections that these patients present and the chronic fatigue that they present.
What would be achieved if this hypothesis were met?
-1. A diagnosis of immunodeficiency. We would no longer be invisible to health care.
-2. Access treatments for this type of immunodeficiency.
-3. Begin to develop new specific treatments that eliminate cells with latent intracellular pathogens (such as the Epstein Barr virus).
After everything described, I contacted the research team of Dr. Bruno Paiva ( of CIMA of the University of Navarra.
This is the link of crowdfunding:
I hope you will help us with outreach and fundraising.
I will try to solve all the doubts that I can.
1. Regueiro González J.R., López Larrea C., González Rodriguez S. y Martínez Naves E. Inmunología: Biología y patología del sistema inmunitario. 4ª edición. Editorial Médica Panamerica, 2010.
2. Serrano Martín MªM. , et all. Déficit de expresión de moléculas de clase II del complejo mayor de histocompatibilidad. Anales de pediatría. Marzo 2007. Vol: 66, nº3 pag:227-339. Available in:
3. MHC class II deficiency diagnostic criteria. European Society for Inmunodeficiencies. Available in:
4. Jiun-Han Lin, Ju-Yin Lin, Ya-Ching Chou, Mei-Ru Chen, Te-Huei Yeh, Chung-Wu Lin, Sue-Jane Lin and Ching-Hwa Tsai. Epstein-Barr virus LMP2A suppresses MHC class II expression by regulating the B-cell transcription factors E47 and PU.1. American Society of Hematology. April 2, 2015. Col. 125 no. 14 2228-2238. Available in:

To fully understand the history of the intertwined relationship between Chronic Fatigue Syndrome and AIDS, you need to read this book.

Now an audiobook!

On April 16, 1996, Congressman Jerrold Nadler spoke on the floor of Congress about his request for a General Accounting investigation into how the CDC had handled the Chronic Fatigue Syndrome epidemic. Nadler did that at the urging of Charles Ortleb, the publisher and the New York Native and his reporter Neenyah Ostrom. Ortleb and Ostrom had made the case to Nadler that Chronic Fatigue Syndrome and the virus it had been linked to, HHV-6, were serious public health issues.         
In an interview in New York Native with Neenyah Ostrom,Congressman Nadler said, "Congress can mandate research into CFS as a viral disease. Maybe it will turn out that HHV-6A is the cause of CFS; maybe it will turn out that other viruses are involved. But Congress can mandate research into CFS as a contagious, viral disease. I will certainly try to get Congress to do that as soon as possible."

Unfortunately, back in 1996, Nadler's warning to Congress and the medical establishment fell on deaf ears. But now that the Democrats have regained power in the House of Representatives, the newly prominent Congressman Nadler may finally be able to bring the Chronic Fatigue Syndrome epidemic and HHV-6 to the public's attention.

This book by Charles Ortleb, which details Neenyah Ostrom's diligent reporting on Chronic Fatigue Syndrome, is necessary reading for anyone who wants to know the whole history of an epidemic which has been hidden in plain sight. For a decade, starting in 1988, Ostrom reported on Chronic Fatigue Syndrome and the damage that the virus HHV-6 does to patients. What her reporting uncovered about the true nature of the Chronic Fatigue Syndrome epidemic will shock you. 

In The Chronic Fatigue Syndrome Epidemic Cover-up, Charles Ortleb recounts his newspaper's fascinating struggle to get the medical and political establishment to pay attention to Ostrom's pioneering investigative reporting on Chronic Fatigue Syndrome. 

By the time you finish Ortleb's stunning memoir, you will understand why the CDC has been unwilling to tell the public the truth about Chronic Fatigue Syndrome. The CDC does not want the public to know that Chronic Fatigue Syndrome is a transmissible illness linked to a virus that affects every system in the body. They have covered up the illness for so many decades that the neglected virus is totally out of control. Now it is causing a long list of other illnesses and many cancers. The CDC has put us all in danger.

Ostrom's decade of reporting on HHV-6 was recently vindicated by this statement from scientists at the University of Wurzburg:"While HHV-6 was long believed to have no negative impact on human health, scientists today increasingly suspect the virus of causing various diseases such as multiple sclerosis or chronic fatigue syndrome. Recent studies evensuggest that HHV-6 might play a role in the pathogenesis of several diseases of the central nervous system such as schizophrenia, bipolar disorder, depression or Alzheimer's." 

The big question about Neenyah Ostrom and New York Native is this: How many lives would have been saved if the scientific establishment and the mainstream media had paid more attention to Neenyah Ostrom's reporting on HHV-6 and Chronic Fatigue Syndrome in New York Native?             

One day, if there is any justice in the world, the CDC and the medical establishment will apologize for not paying attention to Neenyah Ostrom's groundbreaking work on Chronic Fatigue Syndrome that Charles Ortleb published in New York Native. That would be a fitting end to one of journalism's greatest David and Goliath stories.    

Anyone who wants to help Congressman Nadler and the other members of Congress who are trying to end the suffering of millions of people with Chronic Fatigue Syndrome, needs to read The Chronic Fatigue Syndrome Epidemic Cover-up.

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.

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Everyone needs to know what the CDC is hiding about CFS and HHV-6. NEW YORK NATIVE contains both volumes of THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP. The print version is $23. Only $7.98 in Kindle.

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