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Wednesday, April 29, 2020

Fauci hypes COVID-19 drug with mixed results."Hope, disappointment seen in trials for coronavirus drug Remdesivir appears to work the same in patients whether they receive five or 10 days of treatment. But another study suggested the drug has no benefit. "

"One large COVID-19 study hints at the potential benefit of an experimental drug called remdesivir, even as another study published the same day has disappointing results. But both studies had flaws, making results difficult to interpret in the absence of more research."
Source: NBC

Are these skin lesions a clue that African Swine Fever virus is also involved in COVID-19?

Excitement is building about there being "something in the blood" of Chronic Fatigue Syndrome patients.

COVID-19 vaccine research to be conducted on pigs in Canada.

Are purple lesions in COVID-19 really caused by African Swine Fever?

"Though more research is needed, a growing number of case reports and preliminary studies suggest SARS-CoV-2, the virus that causes COVID-19, can also affect the skin."

African swine fever | Pigs | Animal diseases | Pests, diseases and ...

Do the damaged kidneys in COVID-19 patients resemble the damaged kidneys in pigs with African Swine Fever?

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Is COVID-19 reactivating HHV-6 and causing a Kawasaki type illness in children? Or is it an African Swine Fever coinfection?

Rare inflammatory syndrome seen in US child with Covid-19

HHV-6 and Kawasaki Disease


Eighteen of a total of 22 serum specimens (81.8%) from patients with Kawasaki disease were positive for immunoglobulin G or M antibodies to human herpesvirus 6, whereas 10 of 16 age- and sex-matched healthy controls (62.5%) were seropositive. Additionally, increased geometric mean antibody titers of immunoglobulin G were shown in these patients. These results suggest that the status of human herpesvirus 6 infection may be a reflection of the immunologic alterations that are associated with Kawasaki disease.

An Animal Rights activist discusses the possible relationship between COVID-19 and pigs.

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.”


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, 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 Würzburg, 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


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.

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."

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?

Monday, April 27, 2020

Outbreak of COVID-19-related syndrome in children raises questions about the causation of COVID-19

Britain’s national health authority issued a worrisome alert about children, covid-19 and potential complications
"Some of the children had tested positive for covid-19 while others had not."
Source: Washington Post

Does new COVID-19 outbreak in children resemble African Swine Fever???

Source: Newsweek

"The Paediatric Intensive Care Society shared the alert on Twitter, which reportedly stated that the cases have "common overlapping features of toxic shock syndrome and atypical Kawasaki Disease with blood parameters consistent with severe COVID-19 in children." A life-threatening condition, toxic shock syndrome occurs when bacteria gets inside the body and lets off harmful toxins. Kawasaki Disease, meanwhile, is a condition which generally affects those under the age of five, and is characterized by a rash, swollen glands in the neck, dry cracked lips, red fingers or toes, and red eyes."

Does new COVID-19 syndrome in children raise questions about a second pathogen in the pandemic? Is it African Swine Fever?

A serious coronavirus-related syndrome may be emerging in the UK, according to an “urgent alert” issued to doctors, following a rise in cases in the last two to three weeks, HSJ has learned.
An alert to GPs and seen by HSJ says that in the “last three weeks, there has been an apparent rise in the number of children of all ages presenting with a multisystem inflammatory state requiring intensive care across London and also in other regions of the UK”.
It adds: “There is a growing concern that a [covid-19] related inflammatory syndrome is emerging in children in the UK, or that there may be another, as yet unidentified, infectious pathogen associated with these cases.”

Will Bhupesh Prusty's HHV-6 breakthrough renew interest in the endogenous retrovirus HERV-K18?

HERV-K and HERV-W transcriptional activity in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome


Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFSMS) is an incapacitating chronic disease that dramatically compromise the life quality. The CFS/ME pathogenesis is multifactorial, and it is believed that immunological, metabolic and environmental factors play a role. It is well documented an increased activity of Human endogenous retroviruses (HERVs) from different families in autoimmune and neurological diseases, making these elements good candidates for biomarkers or even triggers for such diseases. Here the expression of Endogenous retroviruses K and W (HERVK and HERVW) was determined in blood from moderately and severely affected ME/CFS patients. HERVK was overexpressed only in moderately affected individuals and HERVW showed no difference. This is the first report about HERVK differential expression in moderate ME/CFS.

HHV-6A infection induces expression of HERV-K18-encoded superantigen

Albert K. Taia, Janos Lukab, Dharam Ablashic, Brigitte T. Huber
published online 08 June 2009.



The human endogenous retrovirus K-18 (HERV-K18) encodes a superantigen that causes deregulation of the immune system. This provirus is transcriptionally silent, but can be induced by Epstein–Barr virus (EBV) infection and IFN-α treatment.


Since the herpesvirus EBV induces HERV-K18 expression in human B cells, it was of interest to determine if other herpesviruses would have similar HERV-K18 transactivation properties. Human herpesvirus (HHV)-6A, a neurotropic virus associated with multiple sclerosis, was a logical candidate for these studies.

Study design

HSB2 cells (HHV-6-negative control), HSB2-ML cells (containing latent HHV-6A genome) and HSB2/HHV-6A cells (HSB-2 cells productively infected with HHV-6A) were compared for their level of HERV-K18 transcription, using quantitative RT-PCR.


Latently infected HSB2-ML cells showed a significant increase in HERV-K18 RNA compared to the control cells. HERV-K18 expression was even greater in HSB2 cells productively infected with HHV-6A for 78h.


These results imply that HHV-6A, either in latent form or during acute infection, directly transactivates HERV-K18. This HERV-K18 induction may be mediated through IFN-α that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.

Judy Mikovits accuses Anthony Fauci of colluding with Robert Gallo and stealing credit from her and Frank Ruscetti for the discovery of HIV

From the Sun:

Covid-19 was originally thought to have come from a so-called “wet market” in the Chinese city.

But there has been mounting speculation linking the disease to the lab, which is one of two in Wuhan, and a possible leak.

Scientists at WIV experimented on bats as part of a project funded by the US National Institutes of Health, which licences it to receive American money, the Mail on Sunday reports.

Research published in April 2018 probed the cross-species transmission of coronaviruses from bats, to other animals, and then to humans.

The study - titled "'fatal swine acute diarrhoea syndrome caused by an HKU2-related coronavirus of bat origin" - was investigating a bat-related coronavirus outbreak on Chinese pig farms.

Bats were captured in a cave and samples were taken from the creatures.

Scientists then grew the virus in a lab before injecting it into three-day-old piglets.

The sick animals were then killed and their intestines were ground up into a slurry and fed to other piglets.



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