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Tuesday, April 28, 2020

Rudy Giuliani raises questions about Fauci's Involvement with Wuhan lab that did bat/pig coronavirus experiments: "Back in 2014, the Obama administration prohibited the U.S. from giving any money to any laboratory, including in the U.S., that was fooling around with these viruses. Prohibited! Despite that, Dr. Fauci gave $3.7 million to the Wuhan laboratory — and then even after the State Department issued reports about how unsafe that laboratory was, and how suspicious they were in the way they were developing a virus that could be transmitted to humans," he claimed. He added, "We never pulled that money. So, something here is going on, John. I don’t want to make any accusations. But there was more knowledge about what was going on in China with our scientific people than they disclosed to us when this first came out. Just think of it: If this laboratory turns out to be the place where the virus came from, we paid for it. We paid for the damn virus that’s killing us.”

Source:
https://www.washingtonexaminer.com/news/paid-for-the-damn-virus-thats-killing-us-giuliani-rips-fauci-over-grants-to-wuhan-laboratory


A powerful statement about Bhupesh Prusty's research on HHV-6 in Chronic Fatigue Syndrome from the University of California, San Diego


For ME/CFS patients, viral immunities come at a devastating, lifelong cost

New research shows a connection between a common human herpes virus-6 exposure that leaves a DNA copy of the virus behind and many of the symptoms of a disabling disease called myalgic encephalomyelitis/chronic fatigue syndrome

Mylagic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling and complex illness. Affected persons often cannot pursue ordinary activities -- physical or mental -- because of an incapacitating loss of energy and other symptoms, and may find themselves confined to bed or house-bound for years.
Anyone can develop ME/CFS, though it most commonly afflicts people between the ages of 40 and 60; women more often than men. In nearly every case, ME/CFS begins after a sequence of severe environmental exposures, injuries or infections. Until relatively recently, the utter mystery and complexity of ME/CFS persuaded some that it was not a "real" condition. In 2015, the National Academy of Medicine declared ME/CFS to be a serious, chronic, complex and systemic disease.
In a new study, to be published in the May 1, 2020 print edition of https://www.immunohorizons.org/content/4/4/201ImmunoHorizons, a team of researchers at University of California San Diego School of Medicine and three German universities describe an underlying biological basis for ME/CFS, one that illustrates how efforts by the body to boost immune system protections can come at physiological cost elsewhere.
"These findings are important because they show for the first time that there is an antiviral activity in the serum of patients with ME/CFS that is tightly associated with an activity that fragments the mitochondrial network and decreases cellular energy (ATP) production," said Robert Naviaux, MD, PhD, professor of medicine, pediatrics and pathology at UC San Diego School of Medicine.
Naviaux is co-senior author of the study with Bhupesh K. Prusty, PhD, a scientist in the Department of Microbiology and Institute for Virology and Immunobiology at Julius Maximilians University in W├╝rzburg, Germany.
"This provides an explanation for the common observation that ME/CFS patients often report a sharp decrease in the number of colds and other viral infections they experience after they developed the disease. Our work also helps us understand the long-known, but poorly understood link of ME/CFS to past infections with Human Herpes Virus-6 (HHV-6) or HHV-7," said Naviaux.
More than 90 percent of people are exposed to HHV-6 by three years of age. The virus DNA can insert itself into a chromosome and remain latent in just a few cells for years, silently being copied each time the cell divides. For most people, this causes no problem.
"However, we found that exposure to new metabolic or environmental chemical stresses caused cells with an integrated copy of HHV-6 to secrete an activity that warned neighboring cells of the threat," said Naviaux. "The secreted activity not only protected neighboring and distant cells from new RNA and DNA virus infections, but also fragmented the mitochondrial network and lowered their intracellular ATP reserve capacity. Cells without an integrated copy of HHV-6 did not secrete the antiviral activity.
"Our results show that cellular bioenergetic fatigue and cellular defense are two sides to the same coin in ME/CFS. When energy is used for cellular defense, it is not available for normal cell functions like growth, repair, neuroendocrine and autonomic nervous system functions."
The findings further illuminate a concept called cell danger response theory, which Naviaux and colleagues have been investigating for years. CDR theory posits that chronic disease is the consequence of the natural healing cycle becoming blocked by disruptions at the metabolic and cellular levels. In this case, persons with ME/CFS obtained protections against certain kinds of infections, but at a cost of fragmenting mitochondrial function. Persistence of fragmented mitochondria and the associated abnormalities in cell signaling block normal healing and recovery, and can lead to a lifetime of illness.
Mitochondria are organelles in cells that break down nutrients to create a fuel called adenosine triphosphate (ATP), the primary energy carrier in all living organisms. ATP provides the energy used to drive many cellular processes, including muscle contractions, nerve impulses and chemical synthesis.
"This paper will be a paradigm shift in our understanding of potential infectious causes behind ME/CFS. Human herpesvirus 6 and HHV-7 have long been thought to play a role in this disease, but there was hardly any causative mechanism known before," said senior co-author Prusty.
"For the first time, we show that even a few HHV-6 infected or reactivated cells can drive a powerful metabolic and mitochondrial remodeling response that can push even the non-virus containing cells towards a hypometabolic (abnormally low metabolic) state. Hypometabolic cells are resistant to other viral infections and to many environmental stresses, but this comes at the cost of severe symptoms and suffering for patients with ME/CFS."
###
Co-authors include: Philipp Schreiner, Stephanie Lamer and Andreas Schlosser, Julius-Maximilians University, Germany; Thomas Harrer, University of Erlangen-Nuremberg; and Carmen Scheibenbogen, Charite-Universitatsmedizin Berlin.

Is it time to call Chronic Fatigue Syndrome HHV-6/CFS?





Human Herpesvirus-6 Reactivation, Mitochondrial Fragmentation, and the Coordination of Antiviral and Metabolic Phenotypes in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome




Philipp Schreiner, Thomas Harrer, Carmen Scheibenbogen, Stephanie Lamer, Andreas Schlosser, Robert K. Naviaux and Bhupesh K. Prusty



Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifactorial disorder with many possible triggers. Human herpesvirus (HHV)–6 and HHV-7 are two infectious triggers for which evidence has been growing. To understand possible causative role of HHV-6 in ME/CFS, metabolic and antiviral phenotypes of U2-OS cells were studied with and without chromosomally integrated HHV-6 and with or without virus reactivation using the histone deacetylase inhibitor trichostatin-A. Proteomic analysis was conducted by pulsed stable isotope labeling by amino acids in cell culture analysis. Antiviral properties that were induced by HHV-6 transactivation were studied in virus-naive A549 cells challenged by infection with influenza-A (H1N1) or HSV-1. Mitochondria were fragmented and 1-carbon metabolism, dUTPase, and thymidylate synthase were strongly induced by HHV-6 reactivation, whereas superoxide dismutase 2 and proteins required for mitochondrial oxidation of fatty acid, amino acid, and glucose metabolism, including pyruvate dehydrogenase, were strongly inhibited. Adoptive transfer of U2-OS cell supernatants after reactivation of HHV-6A led to an antiviral state in A549 cells that prevented superinfection with influenza-A and HSV-1. Adoptive transfer of serum from 10 patients with ME/CFS produced a similar fragmentation of mitochondria and the associated antiviral state in the A549 cell assay. In conclusion, HHV-6 reactivation in ME/CFS patients activates a multisystem, proinflammatory, cell danger response that protects against certain RNA and DNA virus infections but comes at the cost of mitochondrial fragmentation and severely compromised energy metabolism.

https://www.immunohorizons.org/content/4/4/201

From 1988-1997, a newspaper called New York Native warned the world about HHV-6. The AIDS activists and HIV establishment tried to silence them, but they continued to publish uncompromising information about HHV-6 and Chronic Fatigue Syndrome that the CDC, Fauci, and NIH didn't want the public to know about. Now read the whole story about New York Native and the cover-up of HHV-6 epidemic that includes AIDS, Chronic Fatigue Syndrome, Multiple Sclerosis, autism, and many other immunological illnesses.

African swine fever (ASF) is an asymptomatic infection of warthogs and bushpigs, which has become an emergent disease of domestic pigs, characterized by hemorrhage, lymphopenia, and disseminated intravascular coagulation.

Pigs all over China have a disease that causes Disseminated Intravascular Coagulation. Are they the source of Disseminated Intravascular Coagulation in COVID-19 patients?
We still don't know if the COVID-19 virus in circulating in pigs in Wuhan and Hubei. If pigs are the source of COVID-19, it raises the possibility that all the catastrophic blood problems are caused by a cofactor of African Swine Fever virus. Are people getting both COVID-19 and African Swine Fever related Disseminated Intravascular Coagulation as a result of a coinfection that began in China's pigs?

Is Disseminated Intravascular Coagulation in COVID-19 patients caused by a cofactor like African Swine Fever virus?

"Since the end of last century, however, it has been emphasized that DIC equals a sign that “Death Is Coming”. DIC is now recognized an independent disease entity characterized by the intravascular activation of coagulation with loss of localization arising from different causes, including trauma and sepsis."
https://www.biomedcentral.com/collections/DIC


We still don't know if the COVID-19 virus in circulating in pigs in Wuhan and Hubei. If pigs are the source of COVID-19, it raises the possibility that all the catastrophic blood problems are caused by a cofactor of African Swine Fever virus. Are people getting both COVID-19 and African Swine Fever related Disseminated Intravascular Coagulation as a result of a coinfection that began in China's pigs?

Three Big Books

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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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