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Friday, November 28, 2014

Chronic Fatigue Syndrome and the Brain

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Giving Back Tuesday

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HHV-6 + vaccines = Autism, CFS, AIDS, MS??????

Chronic fatigue syndrome and fibromyalgia following immunization with the hepatitis B vaccine: another angle of the 'autoimmune (auto-inflammatory) syndrome induced by adjuvants' (ASIA).



The objectives of this study were to gather information regarding demographic and clinical characteristics of patients diagnosed with either fibromyalgia (FM) or chronic fatigue (CFS) following hepatitis B vaccination (HBVv) and furthermore to apply the recently suggested criteria of autoimmune (auto-inflammatory) syndromes induced by adjuvants (ASIA), in the aim of identifying common characteristics that may suggest an association between fibromyalgia, chronic fatigue and HBV vaccination. Medical records of 19 patients with CFS and/or fibromyalgia following HBVv immunization were analyzed. All of which were immunized during 1990-2008 in different centers in the USA. All medical records were evaluated for demographics, medical history, the number of vaccine doses, as well as immediate and long term post-immunization adverse events and clinical manifestations. In addition, available blood tests, imaging results, treatments and outcomes were analyzed. ASIA criteria were applied to all patients. The mean age of patients was 28.6 ± 11 years, of which 68.4 % were females. 21.05 % had either personal or familial background of autoimmune disease. The mean latency period from the last dose of HBVv to onset of symptoms was 38.6 ± 79.4 days, ranging from days to a year. Eight (42.1 %) patients continued with the immunization program despite experiencing adverse events. Manifestations that were commonly reported included neurological manifestations (84.2 %), musculoskeletal (78.9 %), psychiatric (63.1 %), fatigue (63.1 %), gastrointestinal complains (58 %) and mucocutaneous manifestations (36.8 %). Autoantibodies were detected in 71 % of patients tested. All patients fulfilled the ASIA criteria. This study suggests that in some cases CFS and FM can be temporally related to immunization, as part of ASIA syndrome. The appearance of adverse event during immunization, the presence of autoimmune susceptibility and higher titers of autoantibodies all can be suggested as risk factors. ASIA criteria were fulfilled in all patients eluding the plausible link between ASIA and CFS/FM.

Wednesday, November 26, 2014

HHV-6 University Cartoons

HHV-6 University Cartoons

CFS and HHV-6 Books on Kindle Unlimited

These two unique books about CFS and HHV-6 are available on Kindle Unlimited.

The Chronic Fatigue Syndrome Follies: Cartoons about an epidemic of lies. [Kindle Edition]

A collection of cartoons about the cover-up of the Chronic Fatigue Syndrome epidemic. Anyone who knows the whole sorry story about the Chronic Fatigue Syndrome epidemic will tell you that it is one of the great tragedies in world history. A syndrome with so many similarities to AIDS that it has been called "AIDS Minor," CFS has been swept under the rug for three decades while millions of people have seen every aspect of their lives ruined. Patients have trouble deciding whether the government scientists in charge of researching it are liars or just plain stupid and incompetent. In other word,s CFS is the perfect subject for the pen of a caustic satirist. Cartoonist Julian Lake has used his sharp wit to capture the absurdities of a vast epidemic that has been hidden in plain sight by medical authorities who have put the whole world at risk. But sufferers of CFS are no different from the victims of any other political injustice. They may have have been lied to and may have had to live with compromised immune systems, but they haven't lost their sense of humor. There are times in the darkest chapters of history when one just has to laugh. This collection of often hilarious, uncompromising cartoons will garner smiles of recognition from anyone who has any familiarity with the crazy, ugly story of Chronic Fatigue Syndrome and the outrageous attempts to cover it up. The cartoons in this collection are like drones that never miss their targets.

The Closing Argument

"Ortleb's courageous and tireless investigative journalism (starting with his work as publisher @ NY Native Newspaper back in the 1980s') is second-to-none. While I generally prefer reading non-fiction over fiction, this novel leaves you jaw-dropped. It is clear that Ortleb is scientifically, well-researched in the field of CFS/AIDS, and understands the pandemic from its inception. Once again, Ortleb pushes the envelope with The Closing Argument --- moving humanity forward"

Brigitte Huber on HERV-18 as CFS Risk Factor (and encoder of superantigen)

"HERV-K18 causes massive T-Cell activation" 

"Superantigen wreaks havoc in the immune system?"

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

Description of Brigitte Huber's 2010 CFS Research Project:


DESCRIPTION (provided by applicant): The etiology of Chronic Fatigue Syndrome (CFS) is far from understood and is likely due to multiple genetic components. Infection with EBV and treatment with IFN-a have been implicated in the pathogenesis. Our laboratory has shown that EBV-infection, and exogenous IFN-a?, activate transcription of the env gene of a Human Endogenous Retrovirus, HERV-K18. This provirus is normally silent, but when induced it encodes a superantigen (SAg), which is a class of proteins that is capable of deregulating the immune system. Three alleles of HERV-K18 env have been documented, K18.1, K18.2, K18.3, whose gene products have SAg activity, but are predicted to differ biochemically and functionally. Our working hypothesis is that HERV-K18 is a risk factor for CFS. In a pilot study, the allele and genotype distributions of the HERV-K18 env gene were compared between various groups of CFS patients and healthy controls. Although only a limited number of samples were available in the various cohorts, the odds ratios that were obtained were statistically significant. The most intriguing interpretation of these data are that they provide genetic evidence for the unique etiology of at least one group of CFS patients. Thus, it may be possible to delineate different subtypes of CFS, depending on the clinical history of the patients. It is now proposed to substantiate these pilot results, using a much larger cohort of 400 CFS patients associated with EBV that has been assembled by the co-investigator, Dr. Renee Taylor. Dr. Ben Katz, board certified in both Pediatrics and Pediatric Infectious Diseases, will clinically evaluate the patient cohort, and Dr. Inga Peter, a genetic epidemiologist and biostatistician, will oversee the statistical analyses. In addition, the expression pattern of the HERV-K18 SAg during active disease versus intermission will be measured. Furthermore, T cell stimulatory activity of this SAg, expressed on peripheral blood lymphocytes of patients during the course of the disease, will be tested ex vivo, using a T cell hybridoma reporter assay that has been developed in our lab. Since SAg-activated T cells produce massive quantities of chemokines, lymphokines and neurokines, the expression of the HERV-K18 SAg could influence not only the immune system, but other organs as well. A positive association between CFS and either HERV-K18 alleles or expression patterns would open new avenues for the development of clinical treatments of this chronic disease. CFS is a disease that affects a significant number of people worldwide, yet the underlying mechanism(s) of pathogenesis remains unclear. The herpesvirus EBV and IFN-a have been suggested to be associated with CFS, although these concepts are far from accepted. We propose a novel genetic aspect in the EBV/ CFS association, namely the presence of certain HERV-K18 alleles that differ in their superantigen activity

HHV-6 and Dendritic Cells

 Dendritic cells.jpgDendritic cell revealed.jpg

 Dendritic cells (DCs) are antigen-presenting cells, (also known as accessory cells) of the mammalian immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.


Human herpesvirus 6 impairs differentiation of monocytes to dendritic cells

"OBJECTIVE:Monocyte-derived dendritic cells (DCs) play important roles in the immune response against infections and malignancies. Human herpesvirus 6 (HHV-6) infects monocytes and is reactivated in immunodeficient patients. To clarify the mechanisms of HHV-6-induced immunodeficiency, we investigated the effect of HHV-6 infection on differentiation of monocytes to DCs."

Phenotypic and functional alterations of dendritic cells induced by human herpesvirus 6 infection.

"The present data also suggest that the dysfunction of HHV-6-infected DCs is attributable mainly to impairment of the antigen capture and intracellular antigen-processing pathways."




Tuesday, November 25, 2014

Coming Soon: Cartoons about Chronic Fatigue Syndrome and Its Discontents


 Cartoons about an epidemic of lies. Available November 30!

A collection of cartoons about the cover-up of the Chronic Fatigue Syndrome epidemic. Anyone who knows the whole sorry story about the Chronic Fatigue Syndrome epidemic will tell you that it is one of the great tragedies in world history. A syndrome with so many similarities to AIDS that it has been called "AIDS Minor," CFS has been swept under the rug for three decades while millions of people have seen every aspect of their lives ruined. Patients have trouble deciding whether the government scientists in charge of researching it are liars or just plain stupid and incompetent. In other word,s CFS is the perfect subject for the pen of a caustic satirist. Cartoonist Julian Lake has used his sharp to capture the absurdities of a vast epidemic that has been hidden in plain sight by medical authorities who have put the whole world at risk. But sufferers of CFS are no different from the victims of any other political injustice. They may have have been lied to and may have had to live with compromised immune systems, but they haven't lost their sense of humor. There are times in the darkest chapters of history when one just has to laugh. This collection of often hilarious, uncompromising cartoons will garner smiles of recognition from anyone who has any familiarity with the crazy, ugly story of Chronic Fatigue Syndrome and the outrageous attempts to cover it up. The cartoons in this collection are like drones that never miss their targets.

30 Years later

Times finally acknowledges changes in the brains of CFS patients.

cartoon, brain, hhv-6, egg

Monday, November 24, 2014

HHV-6 Transmission

cartoon, hhv-6 , transmission, congress, fauci, public health,hiv, cfs, chronic fatigue syndrome
"Both intrauterine and sexual transmission of human herpesvirus (HHV)-6 and HHV-7 have been suggested."

"Transmission of this virus is believed to occur as a result of exposure to saliva." 

"Human herpesvirus 6 (HHV-6) is transmitted from parent to child in an integrated form and characterization of cases with chromosomally integrated HHV-6 DNA."

"HHV-6 has a very high prevalence (close to 100% of the world’s population has been exposed). It is transmitted mainly by saliva. Transmission occurs usually within the first two years of life; primary infection is often associated with a febrile condition and sometimes with the onset of roseola (exanthem subitum). Two variants of the virus are known, HHV-6A and HHV-6B. HHV-6 is mainly lymphotropic, infecting a broad range of immune cells including T cells, monocytes, NK cells; however the virus can also infect many other tissues such as brain or liver."

"Virus replicated in the salivary glands and secreted in saliva is the epidemiologically proven source of transmission. Other routes of transmission have been suggested but remain to be proven." 

"Infection with human herpes virus 6 (HHV-6) occurs in infancy or early childhood. Primary HHV-6 infection accounts for 10-20% of all febrile illnesses in infants and children less than 3 years of age seen in pediatric emergency departments. Serious complications have been described such as meningitis, encephalitis, hepatitis (including neonatal hepatitis), disseminated infection and hemophagocytic syndrome. At least one case of verified transmission from mother to foetus has been described. HHV-6 is closely related to CMV, which is transmitted from mother to infant in 0.5-2.0 of all pregnancies, most often as a result of reactivation of the virus."

 "Respiratory transmission among persons with close contact with one another is the major route of primary infection."

Unique route for human herpesvirus transmission: HHV-6 and chromosomal integration

Saturday, November 22, 2014

HHV-6 and Morgellons

HHV-6 and Glioblastoma

 "Glioblastoma has been associated with the viruses HHV-6, and cytomegalovirus."

Posts on HHV-6 and Autism

Posts on HHV-6 and Chronic Fatigue Syndrome

Posts on HHV-6 and AIDS

Posts on Konnie Knox and HHV-6

Posts on HHV-6 and cancer

Sometimes you just have to laugh.

research, researcher, NIH, CDC, cartoon, cartoons

If you like this cartoon you'll love this hilarious little book.

The Chronic Fatigue Syndrome Follies [Paperback]

Thursday, November 20, 2014

Will Lipkin notice the KS virus (HHV-8) in the Gut microbiome of CFS patients?

HHV-8 and Chronic Fatigue Syndrome

Prevalence in the cerebrospinal fluid of the following infectious agents in a cohort of 12 CFS subjects: human herpes virus-6 and 8; chlamydia species; mycoplasma species; EBV; CMV; and Coxsackievirus.

Levine, S. Journal of Chronic Fatigue Syndrome, 2001, 9, 1/2, 41-51.
Abstract: Over the last decade a wide variety of infectious agents have been associated with the CFS as potential etiologies for this disorder. Many of these agents are neurotrophic and have been linked previously to other diseases involving the central nervous system (CNS). Human herpes virus-6 (HHV-6), especially the B variant, has been found in autopsy specimens of patients who suffered from MS. Because patients with CFS manifest a wide range of symptoms involving the CNS as shown by abnormalities on brain MRIs, SPECT scans of the brain and results of tilt table testing we sought to determine the prevalence of HHV-6, HHV-8, Epstein-Barr Virus (EBV), cytomegalovirus (CMV), mycoplasma species, chlamydia species, and Coxsackie virus in the spinal fluid of a group of 12 patients with CFS (CDC criteria '94).
We found evidence of HHV-6, HHV-8, chlamydia species, CMV and Coxsackie virus in 6/12 samples. Plasma tests were negative. It was surprising to obtain such a relatively high yield of infectious agents in cell free specimens of spinal fluid that had not been centrifuged. Future research in spinal fluid analysis, in addition to testing tissue samples by polymerase chain reaction (PCR) and other direct viral isolation techniques will be important in characterizing subpopulations of CFS patients, especially those with involvement of the CNS.
The low rate of isolation of HHV-6 may be related to the lack of gross neurological findings in the patients at the time of testing.

Kaposi's sarcoma-associated herpesvirus (HHV-8)

CFS and Paralysis

Is it really zapping HHV-6?

New oral medication, PRID-201, shows promise in treating fibromyalgia

 "Many herpes viruses are known to significantly upregulate COX enzymes in the body, which in turn are important for efficient viral replication," Pridgen said. "In theory, physical or emotional stress in patients can reactivate the virus and result in perpetuation of the symptoms of fibromyalgia. Effectively suppressing latent viruses may significantly improve the pain and related symptoms of FM."

cfs, cartoon, hhv-6, chronic fatigue syndrome, PRID-201


Wednesday, November 19, 2014

Changes in cerebrospinal fluid biomarkers in human herpesvirus-6-associated acute encephalopathy/febrile seizures.


To determine the involvement of oxidative stress in the pathogenesis of acute encephalopathy associated with human herpesvirus-6 (HHV-6) infection, we measured the levels of oxidative stress markers 8-hydroxy-2'-deoxyguanosine (8-OHdG) and hexanoyl-lysine adduct (HEL), tau protein, and cytokines in cerebrospinal fluid (CSF) obtained from patients with HHV-6-associated acute encephalopathy (HHV-6 encephalopathy) (n = 16) and complex febrile seizures associated with HHV-6 (HHV-6 complex FS) (n = 10). We also examined changes in CSF-8OHdG and CSF-HEL levels in patients with HHV-6 encephalopathy before and after treatment with edaravone, a free radical scavenger. CSF-8-OHdG levels in HHV-6 encephalopathy and HHV-6 complex FS were significantly higher than in control subjects. In contrast, CSF-HEL levels showed no significant difference between groups. The levels of total tau protein in HHV-6 encephalopathy were significantly higher than in control subjects. In six patients with HHV-6 infection (5 encephalopathy and 1 febrile seizure), the CSF-8-OHdG levels of five patients decreased after edaravone treatment. Our results suggest that oxidative DNA damage is involved in acute encephalopathy associated with HHV-6 infection.

Neuroprotective effects of edaravone: a novel free radical scavenger in cerebrovascular injury.

Recanalization and neuroprotection have been mainly targeted for the specific treatment of acute ischemic stroke. Free radicals play a crucial role in brain ischemic injury by exacerbating membrane damage through peroxidation of unsaturated fatty acids of cell membrane, leading to neuronal death and brain edema. Free radicals have been implicated in stroke pathophysiology as pivotal contributors to cell injury. Edaravone (3-methyl-1-phenyl-2-pyrazolin-5-one) is a novel potent free radical scavenger that has been clinically used to reduce the neuronal damage following ischemic stroke. Edaravone exerts neuroprotective effects by inhibiting endothelial injury and by ameliorating neuronal damage in brain ischemia. Edaravone provides the desirable features of NOS: it increases eNOS (beneficial NOS for rescuing ischemic stroke) and decreases nNOS and iNOS (detrimental NOS). Post- reperfusion brain edema and hemorrhagic events induced by thrombolytic therapy may be reduced by edaravone pretreatment. Increased productions of superoxide and NO in the brain after reperfusion and a concomitant surge in oxygen free radicals with increased NO during recirculation lead to formation of peroxynitrite, a superpotent radical. Edaravone, which inhibits oxidation and enhances NO production derived from increased eNOS expression, may improve and conserve cerebral blood flow without peroxynitrite generation during reperfusion. Clinical experience with edaravone suggests that this drug has a wide therapeutic time window. The combination therapy (a thrombolytic plus edaravone) is likely to target brain edema, reduce stroke death and improve the recovery from neurological deficits in stoke patients.

Wikipedia on Edaravone
Edaravone (Radicut) is a neuroprotective agent used for the purpose of aiding neurological recovery following acute brain ischemia and subsequent cerebral infarction.[1] It acts as a potent antioxidant and strongly scavenges free radicals, protecting against oxidative stress and neuronal apoptosis.[2][3][4] It has been marketed solely in Japan by Mitsubishi Pharma since 2001.[1] and marketed in India by Edinburgh Pharmaceuticals by the brand name Arone
Edaravone has been shown to attenuate methamphetamine- and 6-OHDA-induced dopaminergic neurotoxicity in the striatum and substantia nigra, and does not affect methamphetamine-induced dopamine release or hyperthermia.[5][6] It has also been demonstrated to protect against MPTP-mediated dopaminergic neurotoxicity to the substantia nigra, though notably not to the striatum.[7][8][9]

The Totally Genius Microbiome Project

cartoon, cartoons, microbiome, lipkin, retrovrus,

Glenn Beck is being mocked the way CFS patients are every day of their lives.

Chronic Fatigue Syndrome and Autism

cartoon, cartoons, autism, chronic fatigue syndrome

t-shirt, cartoon, hhv-6, cover-up

HHV-6 transmission:

cartoon, cartoons, yuppie flu, chronic fatigue syndrome, transmission

The Chronic Fatigue Syndrome Follies [Paperback]

HHV-6 Treatment News: Endo Approved for Generic Valcyte

Use of valganciclovir in patients with elevated antibody titers against Human Herpesvirus-6 (HHV-6) and Epstein-Barr Virus (EBV) who were experiencing central nervous system dysfunction including long-standing fatigue.


Response to valganciclovir in chronic fatigue syndrome patients with human herpesvirus 6 and Epstein-Barr virus IgG antibody titers.

 Valganciclovir treatment, independent of the baseline antibody titers, was associated with self-rated improvement in physical and cognitive functioning for CFS patients who had positive HHV-6 and/or EBV serologies. Longer valganciclovir treatment correlated with an improved response.


Thursday, November 13, 2014

Wednesday, November 12, 2014

Is Glenn Beck's Mysterious Autoimmune Disease Caused by HHV-6?

 The Scientific World Journal
Volume 2013 (2013), Article ID 867389, 7 pages

Review Article
Possible Role of Human Herpesvirus 6 as a Trigger of Autoimmune Disease

In the recent years, several reports have provided important information linking HHV-6A/B to autoimmune diseases (AD) including multiple sclerosis [1–7], autoimmune connective tissue diseases [8–11], and Hashimoto’s thyroiditis [12]. In addition, it has been suggested that HHV-6A/B infection might be related to the onset of autoimmune disorders, including Sjogren’s syndrome [13], purpura fulminans, severe autoimmune acquired protein S deficiency [14], severe and acute autoimmune hepatitis [15, 16], and autoimmune hemolytic anemia/neutropenia [17]

Contaminomics: Why Some Microbiome Studies May Be Wrong

 "Contamination can also waste valuable time and money and, when it applies to medical research, create false hope for patients. The most egregious recent example involved a virus called XMRV, which was touted as a possible cause of chronic fatigue syndrome (CFS), after a 2009 paper identified it in samples from CFS patients. After a long saga involving much follow-up work, allegations of misconduct, the retraction of the original paper, and much angst for patients, it is now clear that XMRV was a contaminant."

The Atlantic on CFS

Porcine Lymphotropic Herpesviruses

cartoon, pig, pigs, porcine, hhv-6, hhv-7, african swine fever

Chromosomally integrated human herpesvirus 6 in heart failure: prevalence and treatment

European Journal of Heart Failure,  Clinical Article

Kühl U, et al. – Human herpesvirus 6 (HHV–6) A and B are two betaherpesviruses that are associated with many conditions including roseola, drug–induced hypersensitivity syndrome, limbic encephalitis, and myocarditis. The data suggest that virus replication in cardiac tissue of ciHHV–6 heart failure patients suggests that ciHHV–6 reactivation causes persistence of unexplained heart failure symptoms. The authors demonstrated that antiviral treatment, effective in decreasing viral transcripts and clinical complaints of cardiomyopathies, is a new therapeutic option for ciHHV–6–associated diseases. 

cartoon, hhv-6, egg, heart, cardiac, cardiovascular

Monday, November 10, 2014

Porcine lymphotropic herpesviruses 1 and 2

PLHV-1 and -2 are highly homologous to each other but not to PLHV-3. The two viruses are widespread in domestic pigs and are closely related to several ruminant gammaherpesviruses, most of which are etiologically implicated in the occurrence of malignant catarrhal fever (MCF), a lymphoproliferative inflammatory disease with an often fatal outcome. PLHV-1 and -2 are also related to Epstein-Barr Virus, Human Herpesvirus-8 and other gammaherpesviruses.

Porcine CMV is a betaherpesvirus, and suggested that it is most closely related to HHV-6 and HHV-7.

 Analysis of Porcine Cytomegalovirus DNA Polymerase by Consensus Primer PCR

Sequencing data on the PCR product confirmed that Porcine CMV is a betaherpesvirus, and suggested that it is most closely related to HHV-6 and HHV-7.

Infection of porcine cells with human herpesviruses.


Porcine organs are valuable candidate materials for xenotransplantation to humans. Long-term maintenance of well functioning transplants is a prerequisite for success. Transplanted organs may be damaged by immune reactions or by infectious agents in hosts. Human herpesviruses (HHVs) establish life-long latency in humans after a primary infection. They can be reactivated with various stimuli, including immunosuppression. This study was performed to verify the infectivity of some HHVs toward porcine cells. PK-15 cells infected with HHV-1 and HHV-2 showed cytopathology from 1 day after infection. Immunofluorescent (IF) staining of HHV-1- and HHV-2-infected PK-15 cells with respective antibodies demonstrated the expression of the respective viral antigens. Permissiveness of PK-15 to HHV-1 and -2 was confirmed by an infection test on Vero cells. Islet cells infected with HHV-5 showed no gross morphologic changes during the experimental course. A limited portion of islet cells reacted only to anti-IE1 and anti-IE2, but not to anti-UL44 or anti-gB antibody by IF staining, whereas a small portion of endothelial cells reacted to anti-IEs and anti-UL44, but not to anti-gB antibody. HHV-1 and -2 can permissively infect porcine cells, but HHV-5 infects a small proportion of cells with limited viral protein expression. HHV-4 could not transform peripheral blood mononuclear cells from miniature pigs. Collectively, because some HHVs can infect and damage porcine cells or impair their functions, HHVs should be cautiously monitored and controlled in humans when porcine cells or organs are transplanted to human beings.

Latent Human Herpes Virus-6: functionally dormant but not extinct - a hidden 'transposon' awaiting the ideal trigger?
Human herpesvirus-6 (HHV-6) achieves latency by integrating into human genome. Can activation
of integrated HHV-6 shorten telomeres and cause unstable telomeric ends that contribute to
disease? Can activated, partial or full-length viral genome reintegrate into human chromosome
or is it lost completely? Can latent or activated HHV-6 influence the host cell through partial
transcription or translation? Preliminary data shows that chromosomally integrated HHV-6 is not
always silent.
Common drugs and environmental exposure can activate it. Whole or parts of viral
genome can shuffle in and out of host chromosomes resulting in genomic instability. Further,
the "semi-latent" virus is functionally active enough to influence cells without forming infectious
viral particles. Over 95% of human population carry latent HHV-6/-7 that can get activated
while exposed to specific, timely, relevant triggers. Hence, it might constitute a prime factor in
effectuating several human diseases, with thus far unidentified and unexplored origins.

Evidence linking HHV-6 with multiple sclerosis: an update

Publication date: December 2014 Source:Current Opinion in Virology, Volume 9 Author(s): Emily C Leibovitch , Steven Jacobson Following reports of elevated antiviral antibodies in MS patient sera and viral DNA detection in MS plaques nearly two decades ago, the neurovirology community has actively explored how herpesviruses such as HHV-6 might be involved in MS disease pathogenesis. Though findings across the field are non-uniform, an emerging consensus of viral correlates with disease course and evidence of HHV-6-specific immune responses in the CNS provide compelling evidence for a role, direct or indirect, of this virus in MS. Ultimately, the only way to demonstrate the involvement, or lack thereof, of HHV-6 or other herpesviruses in this disease is through a controlled clinical trial ...

Human Herpes Virus 6 Infection in 54 Patients after Allogeneic Hematopoietic Stem Cell Transplantation: Clinical Manifestations and Outcome

CONCLUSIONS: This retrospective study confirms a correlation of HHV-6 with high morbidity and mortality rates after alloSCT, thus suggesting a regular HHV-6 monitoring in alloSCT recipients. The regular monitoring of HHV-6 DNA, using a real-time PCR assay, may be useful for identifying active HHV-6 infection and for the introduction of a pre-emptive treatment, possibly reducing the incidence of the most severe clinical complications. Despite HHV-6 detection typically occurred early after alloSCT, a better immune reconstitution has the potential to improve clinical outcome.

Technics Used For The Demonstration of HHV-6 or HHV-7 Antigens in Tissues

"Block non-specific reactivity with pig serum,
1:20 dilution in TBS buffer 10 min
and remove buffer by blotting"

Detection of two novel porcine herpesviruses with high similarity to gammaherpesviruses.

This Little Piggy has HHV-6

t-shirt, cartoon, hhv-6, pigs, pig, porcine

Is HHV-6 a Human and Porcine Virus?


Evidence for the existence of porcine gammaherpesviruses was obtained by PCR and sequence analysis. Initially, samples of peripheral blood mononuclear cells (PBMC), spleens, lungs, kidneys and livers of pigs from Germany and Spain were tested with a PCR assay which targets conserved regions of the herpesvirus DNA polymerase gene with degenerate and deoxyinosine-substituted primers. Amplicons of identical sequence were obtained from one spleen and two PBMC samples. This sequence showed a high percentage of identity with the DNA polymerase genes of herpesviruses of the oncogenic subfamily Gammaherpesvirinae. Alignment of amino acid sequences showed the highest identity values with bovine gammaherpesviruses, namely alcelaphine herpesvirus type 1 (68%), ovine herpesvirus type 2 (68%) and bovine lymphotropic herpesvirus (67%). Comparison with pseudorabies virus and porcine cytomegalovirus, which are the only porcine herpesvirus species presently known, showed values of only 41%. PCR analysis of PBMC (n = 39) and spleen (n = 19) samples from German pigs, using primers specific for the novel sequence, revealed a prevalence of 87 and 95%, respectively. In this analysis, three out of eight spleen samples from Spanish pigs were also positive. Subsequent sequencing of the amplicons revealed the presence of two closely related gammaherpesvirus sequences, differing from each other by 8% at the amino acid level. The putative novel porcine herpesviruses, from which these sequences originated, were tentatively designated porcine lymphotropic herpesvirus type 1 and type 2 (PLHV-1 and PLHV-2). When using pig organs for xenotransplantation, the presence of these viruses has to be considered.

Presence of Antibody to Human Herpesvirus 6 in Monkeys

Sunday, November 09, 2014

Why HHV-6 is often confused with CMV.

"Some regions of HHV-6 are known to share sequence homology with other viruses, such as CMV and HHV-7, which may obscure the specificity of the results."

Pets and HHV-6: Epidemiological evidence that HHV-6 causes CFS in humans and animals?

" Dr. Thomas Glass, a pathologist and dental surgeon at the Oklahoma Health Sciences Center who helped identify victims of the Oklahoma City federal building bombing, has performed studies that appear to show that chronic fatigue syndrome and, therefore, its putative viral cause can be transmitted between humans and their pets."

Two of the viral isolates were tested by Dr. Tom Glass for the ability to induce disease in cats. The results were quite striking and added considerable weight to the concept of a stealth viral encephalopathy. This work was published in "Pathobiology"

Study 1:The conclusion of this study was that CFIDS patients not only have pets, but that there is a significant animal interaction and that a large number of these animals have atypical or unusual diseases which at least mimic CFIDS.

Study 2:The conclusions of the second study were that animals of CFIDS patient. demonstrated a wide range of disease and dysfunctional signs, similar to their CFIDS owners

Date:   3/7/2005 8:21:33 PM   ( 9 y ) ... viewed 2739 times
The Human/Animal Interaction of Chronic Fatigue and Immune Dysfunction Syndrome: A Look At 127 Patients and Their 463 Animals
By R. Tom Glass, D.D.S., Ph.D. Professor Emeritus of Oral and Maxilofacial Pathology and Pathology University of Oklahoma, Health Sciences Center Tulsa, OK 74114
Throughout the recognized existence of Chronic Fatigue and Immune Dysfunction Syndrome, anecdotal reports have linked domestic animals with CFIDS, but no formal scientiflc studies were reported (1,2). Cats and dogs were implicated by their owners most frequently. The usual association with the presence of the animal in the household of a CFIDS patient, followed by the development of strange diseases or dysfunctions in the animal, many of which mimic CFIDS. The severity of the diseases often necessitated euthanasia. In a fewer number of cases, the onset of CFIDS in the patient was associated with an exposure to a domestic animal which was later found to show signs of CFIDS.

Observations from my animal biopsy service demonstrate two interesting findings in animals of CFIDS patients (unpublished findings). Gingival biopsies from cats demonstrated an unusual epithelial viral vesicle associated with an equally unusual submucosal inflammatory response. Several melanomas were found in dogs of CFIDS patients which had the unique feature of a striking progression of the tumor in the absence of an inflammatory response.

Both dogs and cats are known to be susceptible to a wide range of viruses. With the exception of rabies, no zoonotic (animal to human or human to animal) viral infection transmission has been demonstrated between typical domestic animals and humans (3).

These observations and recognitions prompted the following questions:

1. Do CFIDS patients have domestic animals (pets)?
2. What is the interaction between CFIDS patients and their pets?
3. Do the domestic animals have any clinical signs of CFIDS?
4. What type of signs or manifestations of CFIDS do animals of CFIDS patients demonstrate?
5. What is the relationship between the interaction of CFIDS patients and their animals and the onset and course of CFIDS?

and resulted in a series of studies to answer the questions.

The first study was a retrospective study of Center for Disease Control and Prevention (CDC) criteria-met CFIDS patient: using a standardized questionnaire which included patient comments. The study subjects came from a university medical center and CFIDS support groups throughout the United States. Appropriate statistical tests, including mean, median, Z test, multivariant analysis, and Chi-square test, were used. This information was compared to national statistical Information on animal interaction compiled by the American Veterinary Medical Association.

One hundred twenty-seven (127) criteria-met CFIDS patients completed questionnaires on their animal Interactions- There were 114 females and 13 males in the study. All respondents were Caucasian with the exception of one Native American. The mean age of the CFIDS patients was 42.4 years with a median age of 43 years. 61.4% of the respondents were married; 311.6% were either single, divorced, or widowed.

The most striking result of this study was the association between CFIDS patients and animals (usually indoor pets) and the number of animals per CFIDS patient. 97% of the CFIDS patients had animal contact [expected normal contact: 57.9% (4)], with only 2 males and 2 females not reporting animal contact. Reported dog ownership per household for CFIDS males was 9.5 and for CFIDS females was 7.9 (expected national average: 1.52). Reported cat ownership per household for CFIDS males was 6.1 and for CFIDS females was 8.7 (expected national average: 1.95). 106 of the respondents (83.5%) reported that their animals (pets) had atypical diseases with signs and symptoms which mimicked CFIDS in humans. Of these 106 CFIDS patients 100 (94.3%) either were the primary caregiver for the sick animals or had intimate contact (sleeping with, being bitten or scratched by, or kissing the animal). The next most common animal contact was birds (parakeets and ducks were mentioned most often), followed by horses, cows, rabbits, goats, and guinea pigs. Two (2) CFIDS patients had contact with primates. The reported mean age of the dogs was 6 years (median = 6 years); of the cats was 6.2 years (median = 5 years); and of other types of animals was 3.2 years (median = 0.4 years).

All of these differences between expected and observed values were found to be statistically significant (p>001) including a statistically significant higher (.02
Finally, of equal importance were the CFIDS patient's comments. These comments were often voluminous and detailed the interaction between the animals and the CFIDS patient. It is very clear that the CFIDS patients, in general, are "animal lovers" even though frquently the patient comments spoke of allergies to animals. Simliarly, the respondents gave excellent descriptions of their animal's(s') CFIDS-like signs from time of onset to ultimate temination.Respondents also noted that the animals were often the "living being" most consistently in close contact with the CFIDS patient.

The conclusion of this study was that CFIDS patients not only have pets, but that there is a significant animal interaction and that a large number of these animals have atypical or unusual diseases which at least mimic CFIDS.

In the second study, the CFIDS patients reported on a total of 463 animals: 115 healthy animals (which served as a control group for the study) and 348 animals which showed signs of either dysfunction or disease. The control group was comprised of 51 dogs (44%), 39 cats (34%), and 25 animals that were grouped together as "others". The "others" group was predominantly large animals: horses, cows, goats, and pigs. All the control animals were still living and well at the time of the survey or had died of either traumatic or natural causes.

The group of animals which showed signs of either dysfunction or disease were made up of 189 dogs (54%), 144 cats (41%), and 15 animals that were grouped together as "others". This "others" group was predominantly small domestic pets: birds, hamsters, and guinea pigs. The mean age of the dogs in this study was 6.5 years (median 6 years); of the cats was 6.2 years (median = 5 years); and of other types of animals was 3.2 years (median = 0.4 years).

The distribution of signs of the animals showing either dysfunction or disease are as follows: 137 animals (59 cats; 64 dogs; 14 others) were classified as having "General Signs." 36 animals (15 cats; 14 dogs; 7 others) of the general signs category were classified as being "Sick NOS" because the animals were clearly Ill, but no diagnosis could be or had been rendered by a veterinarian. The "Sick NOS" animals were often described as having the same types of clinical signs as their owner. 26 animals (9 cats; 9 dogs; 7 others) in the general signs category died suddenly of unexplained causes. 26 animals (11 cats; 15 dogs) of the general signs category had a variety of altered immune conditions. including allergies, skin rashes, hair loss, systemic lupus erythematosus, and sneezing. 20 animals (3 cats; 17 dogs) developed Parvo or other viral Infections. 11 animals (9 cats; 2 dogs) transmitted their conditions to other animals either by birth or direct contact. 10 animals (9 cats; 1 dog) were listed as having eaten mice, rats, or other wild animals. 9 animals (3 cats; 6 dogs) had non-viral infections.

122 animals (41 cats; 81 dogs) had "Neurological" signs. 32 animals (17 cat.; 15 dogs) of the neurological category had lethargy, weakness, or sleep disorders. 30 animals (9 cats; 21 dogs) in the neurological category had seizures, tremors, or tail twitching. 19 animals (4 cat:; 15 dogs) demonstrated hind limb dragging, myalgia, arthralgia, or Bell's palsy. 16 animals (6 cats; 10 dogs) were anxious, depressed, moody, or demonstrated inappropriate behavior, including urination and defecation outside their litterbox. 15 animals (4 cats; 11 dogs) had photophobia, ocular discharge, or blindness. 10 animals (1 cat; 9 dogs) had deafness, ear sensitivity, or loss of balance.

36 animals (21 cat.; 15 dogs) demonstrated "Gastrointestinal" signs. 13 animals (9 cats; 4 dogs) in the gastrointestinal category had inflamed gingiva, mouth odor, tooth loss, or drooling. 10 animal, (4 cats; 6 dogs) in the gastrointestinal category had diarrhea or abdominal distention. 9 animals (5 cat.; 4 dogs) demonstrated anorexia. 3 animals (2 cats; I dog) had increased appetite without weight gain. 1 cat had hard stools.

33 animals (18 cats; 14 dogs; 1 other) showed "Reticuloendothelial or Blood Disorders". 12 animals (3 cats; 8 dogs; 1 other) of this category demonstrated bleeding or blood disorders. 10 animals (9 cats; I dog) in this category developed leukemia. While all of the leukemic cats were positive for feline leukemia virus [FLV], 5 of the cats had been vaccinated against FLV prior to the onset of their feline leukemia. 7 animals (5 cat.; 2 dogs) died of either feline AIDS or canine immune defidency (AIDS). 2 dogs showed massive and generalized lymphadenopathy. 1 cat and 1 dog died of lymphoma (lymphosarcoma).

Excluding leukemia and lymphoma, 15 animals (3 cats;12 dogs) developed tumors ("Neoplasia"). 8 animals (2 cats; 6 dogs) in this category had either fatal and/or multiple tumors which were not further classified, but which resulted in euthanasia of the animal. 4 dogs of this category died from malignant tumors of epithelial origin (3 squamous cell carcinomas and 1 transitional cell carcinoma), while 1 cat developed perianal adenomas, but was still living at the time of the survey. 1 dog died of a functional pituitary tumor and 1 dog died of melanoma.

Only 5 animals (2 cats; 3 dogs) were reported to have "Endocrine Disorders". 2 cats and 2 dogs in this category had thyroid hyperplasia or thyroid nodules and 1 dog has pituitary hyperplasia.

Of equal importance, 113 of the 127 patients 89%) stated that their own CFIDS symptoms directly related their interaction with animals. Specifically, 79 of the respondents (71%) stated that they either had contact with multiple animals, were farmers, or were caretakers of multiple animals. 18 of these CFIDS patients (16%) note that the onset of their CFIDS symptoms were temporarily associated with the obtaining of a new pet, while 2 CFID patients (1%) noted that their CFIDS symptoms improved after the pet left or died. 9 respondents (8%) stated the other family members also contracted CFIDS in such manner as to implicate the pet as being possibly a common link in etiology. 3 CFIDS patients noted that the onset their CFIDS symptoms directly followed a flea bite episode and 2 CFDS patients reported that the prior owner of the home in which they contracted their CFIDS was inhabited by both CFIDS patients and sick animals.

As was noted in the first study, CFIDS patients care deeply for their animals. This observation can be understood by the detail and thoroughness with which the CFIDS patients filled out the information concerning the symptoms, laboratory results (such as blood count., blood chemistries, biopsy reports, etc.) and the courses of the animal's(s') condition. For the most part, it was the CF1DS patient who filled out the questionnaire. It must be remembered that these patients usually have severe fatigue and for them to have given such attention to detail was a major task.

Both studies also noted what an important role the pet plays in the CFIDS patient's life. An analysis of the comments by the CFDS patients demonstrates unequivocally that the pet was often the CFIDS patient's major contact with a living being. While it is imperative to consider the results of this study, it is equally imperative not to isolate CFIDS patients from their pets Rather, prevention of intimate contact, such as sharing food or kissing between the CFIDS patient and the pet, should be encouraged.

While the results of this study have certain subjective elements, such as reliance upon CFIDS patient and fault observations or the possibility of "symptom transference" (e.g., arthralgia in a pet is more likely to be noted by an arthralgic patient than a person free of joint pain), the recurrent finding of certain symptoms that may be common to both the CFIDS patient and the animal warrant attention It is important to consider the possibility that CFIDS may be transmitted from human to animal and/or from animal to human. If one considers the symptom of lethargy in the animals, the 32 CFIDS patients who observed this symptom all noted that the lack of energy was different than they had observed before in either the affected animal or in other animals in the same household who did not demonstrate the symptom. The seizure disorders and sudden unexplained deaths were more dramatic and objective signs of possible transmission of an agent that affects the nervous system. While seizure disorders and sudden unexplained deaths are not accepted features of CFIDS in humans, others have noted anecdotally a higher than usual number of seizure disorders and even sudden unexplained deaths in CFIDS patients.

While this study demonstrates the multiplicity of CFIDS-like signs in the animals, it is this same multi-organ involvement in the CFIDS patients that makes CFIDS so difficult to diagnose in humans. As with CFIDS in humans, the animals usually showed no laboratory evidence of a specific disease entity. There was, however, a predominance of neumlogic, neuromuscular, and rheumatologic symptoms in the animals just as there are in CFIDS patients. The result of these studies need to alert the veterinary profession of the need to inquire as to the health of the animal owner and their family. Conversations with a number of clinical veterinarians have pointed out that they are commonly confronted with conditions in domestic animals which do not fall into well established disease patterns. The most common of these deal with neurological and infectious diseases. These two areas were the most often reported as the pet signs found by CFIDS patients. Somewhat confounding was the low number of animals demonstrating endocrine disease. This under-reporting may be more of a lack of testing than a lack of disease as these tests are expensive and CFIDS patients are often financially unable to afford their own diagnostic tests., much less their animal's(s').

The results of these studies also need to alert the veterinaray profession that should there be a possibility of animal to human transmission of CFIDS, veterinarians might want to consider the wearing of protective clothing, gloves, eyewear, and masks when examining animals. We have received a number of reports from veterinarians around the country, especially from female veterinarians, that they have had to substantially limit their practices due to fatigue and other CFIDS-like symptoms. Similarly, precautions need to be taken to prevent CFIDS from being transmitted from one animal to another.

The conclusions of the second study were that animals of CFIDS patient. demonstrated a wide range of disease and dysfunctional signs, similar to their CFIDS owners. The interactions between the animal and the CFIDS patients was often intimate. The study showed that the course of CFIDS in the animals varied widely, but after more thorough analyses of the data and of subsequent data, it appears that the animals have two distinct courses: 1. Their CFIDS signs produce progressive deterioration and the animal dies or 2. The animals appear to completely recover, usually after about five years.

In closing, both of the above studies had one common conclusion: animal interaction is a very important part of CFIDS patients' lives'. I am often asked by CFIDS patients, knowing what I do about the CFIDS patient/animal interaction, if I would recommend that CFIDS patients have pets. While there is no way for me to survey animals, from my interaction with my own pet. and with the way CFIDS patients love their pets' I would say that any pet would willingly run the risk of contracting CFIDS for the love, care and attention they will receive from CFIDS patients.


1. Ostrom, N. 50 Things You Should Know About the Chronic Fatigue Syndrome: New York: That New Magazine, 1992: pp 25, 26, 36, 37

2. Ostrom, N. What Really Killed Gilda Radner? New York: That New Magazine, Inc., 1991 pp. 159-164, 345-352

3. Cotran, RS., Kumar, V., Robbins, SL. Robbins Pathological Basis of Disease, 4th ed. Philadelphia: W. B. Saunders Co., 1989; pp. 309-310

4. Wise, JK. The Veterinary Sevice Market for Companion Animals. Schaumburg, IL; American Veterinary Association, 1992; pp. 5-65.

AUTHORS NOTE: This article is the first of three articles on my experiences with Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS; aka CFS). The first article deals with the interaction between CFIDS patients and their animals. The second article will deal with the actual autopsy findings of sick animals owned by CFIDS patients, the transmission of the CFIDS infectious agent to healthy animals, and the autopsy results of these animals. The third article will deal with the oral and head and neck manifestations of CFIDS, a lip biopsy of minor salivary glands for the confirmation of CFIDS, and some interesting therapy for the head and neck pain so often experienced by CFIDS patients [The second and third articles by Dr. Glass will he published in the next two consecutive issues of MPWC News - Ed. note.] In the early 1990's, the following studies were conducted on CFIDS patients and their animals. The articles were sent to a number of both medical joumals and veterinary medical journals. The response from the editor of the medical journals was that while the articles were well-written, thorough and timely, they were better placed in veterinary medical journals. The veterinary medical joumal editors agreed with the medical journal editors in terms of the validity of the studies; however, they felt that if they published the articles, they might jeopardize the entire practice of veterinary medicine as small animals comprise the largest segments of such practices.

This article appeared in the Spring 1998 Vol 3 Number 2 Edition of the
Medical Professionals With CFIDS (MPWC) News

" . . .there is every likelihood that it may be HHV-6 but we need those studies that confirm that"

Monday, August 17, 1998 
[NOTE: The following is a transcript of the Sunday, August 16 broadcast of the CFS Radio program, hosted by Dr. Roger Mazlen. The guest is Dr. Tom Glass, who is discussing his research into CFIDS patients and their pets.  This transcript is provided by Carolyn Viviani, who has given her permission to reproduce it as long as her name and email address are not removed from the end of the transcript. You can view transcripts of past CFS Radio, find links to audio versions of the shows and to Dr. Mazlen's home page at

Sadly, Carolyn tells me that this may be the last CFS Radio broadcast for some time. Dr. Mazlen has been funding the broadcasts himself, but is no longer able to do so; until a sponsor is found for the show, there will be no further CFS Radio broadcasts. Dr. Mazlen is hopeful of resuming
broadcasts in the fall, but no date has been set.]

DR. MAZLEN: Today we have a very important distinguished scientist as our guest. We have Dr. R. Tom Glass who's a dental surgeon and a Ph.D. and a Professor Emeritus of Pathology at the University of Oklahoma, Health Sciences Center in Oklahoma City. In fact he was one of the people who participated in forensic work on the Oklahoma City bombing victims but today we're talking about Chronic Fatigue Syndrome and we're talking about animals and earlier in a show that we had in May where we had Neenyah Ostrom as a guest, she had spoken about the work of R. Tom Glass, but today, excitingly enough, we have Dr. Glass here to talk about it himself. Welcome to the show, Dr. Glass. Welcome, Tom.
DR. GLASS: Thank you, Dr. Mazlen. It's good to be here. and greetings to New York City.
DR. MAZLEN: Thank you. I think we should start and let you tell us about how you got into this area because this is a little different from some of the things you've done in the past.
DR. GLASS: Well, it is and it isn't, Roger. I have really spent most of my career in search of transmission of disease issues and so this was rather along that same line. But what happened was a number of the patients that I was seeing who had Chronic Fatigue Syndrome talked about a relationship between their animals, either a relationship where the animal appeared to become ill in some way and then the patient developed Chronic Fatigue Syndrome or the patient developed their Chronic Fatigue Syndrome and subsequently their animal developed the signs that the patient thought
looked very much like their own disease process.

So we began an investigation of this and first looked at the experience that Chronic Fatigue patients had with animals and we basically looked at 125 people who had Chronic Fatigue Syndrome-that would be the criteria-diagnosed Chronic Fatigue Syndrome - also called Chronic Fatigue and Immune Dysfunction Syndrome - and asked them some questions about their animals. Did they have animals?  If so, what kind of animals? If they had animals, what was their role in terms of caring for the animals?
And the results of that study were very, very revealing. First of all, it's clear that people with Chronic Fatigue Syndrome are animal lovers. Almost 97% of the people had animals. More than having just one animal, many of these people had multiple animals and most of them gave a history of their animals having some kind of undiagnosed or inappropriate illness, inappropriate behavior, this sort of thing. And so that set up a stage then for the next study.
DR. MAZLEN: So, where did you go from there, basically?
DR. GLASS: Well, from there where we go is to asking these patients with the severely ill animals if they would allow us, since the animals were going to undergo euthanasia, asking if we might autopsy those animals. And so we set up a protocol as you have to do with research and had this pass by
both the committees that reviewed research in the human arena and the committees that review research in the animal area and both committees passed our protocol.

So we began a series of autopsies on these animals and the findings from the first autopsy I think were so significant. The first animal had gotten into a situation where it was constantly seizing and
because of these seizures the pet owner was unable to maintain the animal in any kind of health. Well, when we looked at the result of the autopsy, when we looked under the microscope at all the tissues that we had gained from the autopsies, the interesting and consistent finding in all the tissues was
that there was nothing wrong. There was absolutely nothing we could see at first blush that was going on with these animals.

Well, as part of that first autopsy we also had drawn blood from this animal and had injected a healthy animal to see if whatever it was that was making this animal seize could be transmitted and as we were reviewing the slides and were viewing the slide the healthy animal became sicker and sicker. Very much the same symptoms as the one that we had performed the autopsy on.
DR. MAZLEN: Well, that suggests a transmissibility of some sort.
DR. GLASS: It's a transmission of some sort and so we were rather convinced by this. Meanwhile we went back to the microscope a second time and looked at all the tissues and again came up with the same conclusion. While this animal clearly had unusual neurologic signs and a lot of other signs, that had kidney problems, that had GI problems, while this animal had these problems I could not document anything under that microscope in terms of traditional medical disease processes. In other words, this animal didn't have a brain tumor. The animal didn't have what appeared to be a bacterial
infection in the brain. The animal had no real cause for the symptoms and signs that were showing.

And so it was the third time that we looked at the slides that all of a sudden it began to be clear that what we were looking at was not a disease process as we ordinarily think of disease processes, but the individual cells were swollen and they contained a lipid material that made them look foamy under the microscope and at first blush you would have missed it because all of us who make these diagnoses mainly go to the brain center of a cell, that would be the nucleus of a cell, and if the nucleus is fine, there's not much more we can say about the cell.
But if we looked at the basically functioning part of the cell, the cytoplasm of the cell, what we found was that the cytoplasm was changed. So the cell would therefore be changed. And the functioning of that cell would therefore be changed. Well, with this in hand we were beginning to accrue more and more animals in our study, both dogs and cats and interestingly enough these animals showed this same change.
Now the first place we looked, of course, was the brain but as we began looking elsewhere, we found that a lot of the tissues showed these same type of changes. The tissues of the liver, the
tissues of the kidney, the tissues of even the salivary gland. We went so far as to look at the paw beds and the claws of these animals because, once again, a cat would project its claws and it projects its claws through a sleeve that has an oil, a lubricant and it was from that that we were able
to understand that not only was this organism affecting cells in the brain, but affecting cells throughout the entire body.

DR. MAZLEN: Including the paws.
DR. GLASS: Including the paw beds.
DR. MAZLEN: And I heard previously and I just want to slip this in that some of these animals are noticed to lick their paws a lot or frequently?
DR. GLASS: Exactly. They lick their paws, they also have that ability to lick themselves all over so they may run the risk of placing the organism at a variety of different places on their bodies.
DR. MAZLEN: Well, I'm glad I asked you that then. That does complicate it a
little bit.

DR. GLASS: It does complicate it. The largest involvements we found were in the animals' salivary glands. The salivary glands were showing this type of dysfunction but the interesting thing was that so many of the pictures as we began to study them produced some paradox from what we normally would have thought of in traditional diseases and therefore traditional diagnoses.
DR. MAZLEN: I want to ask you since you mentioned some foamy cells whether or not there's also been the finding of stealth virus in any of these animals because stealth virus shows in culture a type of foamy cell vacuolization in certain cells.
DR. GLASS: Roger, let me answer that question. Almost conversely in the sense that at the time we were doing the autopsies on the chronic animals I ran across the research of and met John Martin, who had isolated what he determined was the stealth virus. John sent me vials of the stealth virus
and, once again, under the protocol with the animals we injected this stealth virus into a series of animals and, in fact, produced the same condition. So, the stealth virus is at least one of the agents that is responsible for the kind of changes that we see in the animals. The answer we see is yes.

DR. MAZLEN: I wanted you to say it because a lot of people ask questions about stealth virus and I'm not really the person who's qualified to answer them specifically.
DR. GLASS: Well, you know, Roger, I think the name-and John and I have worked on the idea of this name-the reason I like the term "the stealth virus" is because in the Chronic Fatigue Syndrome the virus seems to be able to infect cells and yet not destroy the cells. The fancy word we use is "cytopathic". It doesn't have a cytopathic or cell destructive process and so it can basically go undetected by the body. Now we are beginning to understand what happens if the virus is detected by the body and that may be an even worse scenario but having the stealth virus, having it make the
cells dysfunctional, somehow the body is not able to recognize this virus as being harmful.

DR. MAZLEN: You know that leads obviously to problems which make it possible for the virus to persist in tissues and possibly even to spread, as you pointed out, to other tissues.
Talk about, as you had mentioned, because I want to at least put some balance in this situation, the point about animals being important for Chronic Fatigue Syndrome patients and that they shouldn't panic and do anything rash.
DR. GLASS: This is, I think, something that we have stressed from the very beginning of our research in the fact that when we did our initial survey of Chronic Fatigue patients, it was so apparent that Chronic Fatigue patients really are animal lovers. They're people that have a great deal of
interaction with their animals and when we did the analysis I remember one of my Chronic Fatigue patients saying, "My gosh, Dr. Glass, you mean I shouldn't have an animal." And that gave me such pause because on one side the animal for many Chronic Fatigue patients is so important in terms of
their own well being, that is to say that the animal is there, the animal accepts them in their limitations and is such an important factor that we do not want Chronic Fatigue patients to disown their animals.

I think the key is and what I admonish Chronic Fatigue patients to do is to be careful with their animals. They want to avoid close contacts. Let someone else feed the animal. Don't get down under the animal's face, don't let the animal lick you. I would be better if the cats were declawed so that they could not absorb any kind of body fluids in their claw beds. It would be better not to have the animal bite you. You know, play with a string and a ball on it as opposed to playing with your hands. These kinds are very practical aspects, Roger, of the things that I admonish my Chronic Fatigue patients to do.
DR. MAZLEN: I am very happy that you went through that list. I want to just quickly take this caller, Charles Ottlieb because he's the publisher of a newspaper. Charles are you there?
CHARLES: I was the publisher of the New York Native which published Neenyah Ostrom for 10 years and I just wanted to ask DR. GLASS about the possibility that this stealth virus is actually the virus that has been linked to Chronic Fatigue Syndrome over and over again which is called HHV-6 and whether there is any chance we can resolve rather quickly whether or not these viruses are related or the same thing?
DR. MAZLEN: OK, Tom it's your question.
DR. GLASS: Well, that's a great question and I think that, not to beg off, I just don't think we have enough information to say "yea" or "nay" on that. It looks like there are some very real possibilities from not only my work but from some of the other work that's being published at the present time
that HHV-6 is a very important factor and may in fact be the stealth virus. It's just at this juncture we don't have that data that's strong enough to really come down on that. But it's certainly an area that needs extensive investigation and certainly may well do it. The nice part about it is we have the animal model, we have the pathology and I would love to see a study where we infected animals with the HHV-6 and see if we get the same kind of cellular patterns. I think that is a way of answering that question.

DR. MAZLEN: And fulfilling Koch's postulates.
DR. GLASS: Exactly. Once again, fulfilling Koch's postulates which say you have to be able to identify an agent causing a disease remove that agent, grow it in a culture of some type, infect another system and produce the same disease. And so, yes, to answer your question, there is every
likelihood that it may be HHV-6 but we need those studies that confirm that.

DR. MAZLEN: I wanted to say Tom in terms of the ongoing research, I know you are also looking at therapies. You want to say a brief word about that?
DR. GLASS: Well, before I do that, let me talk just a little bit about some of the applications we made into the human population in terms of making or at least adding to the diagnosis of Chronic Fatigue Syndrome. From our studies with the animals the involvement of the salivary glands were so
pronounced that we then set up a study to look at salivary glands in humans.

And what we found is that while Chronic Fatigue Syndrome very often is associated with a condition known as xerostomia or dry mouth, these people really seemed to have a different picture microscopically of their xerostomia as opposed to the dry mouth we see in autoimmune conditions like Sjogren's or like Mikulicz where the body is actually reacting against it's own salivary glands.
To make a long story short, what we've begun to do and have studied this now for about six years, we make a small incision in the patient's lip and take out 4 minor salivary glands. By looking at these
microscopically we can confirm Chronic Fatigue Syndrome. It's a real excellent test and it's not terribly invasive. It's very reliable. And so, one of the things that we're doing now as an ongoing study is we're still seeing patients and having these salivary glands biopsies so that we can confirm their diagnoses of Chronic Fatigue Syndrome.

DR. MAZLEN: That's very exciting. We certainly want to pick up on that in a minute. I want to make a point here that this is a typical example of how important these shows are. Unfortunately we did have our original sponsor withdraw from the show recently and for that reason there won't be another show until later in the fall, I'm not sure exactly when. In the interim we'll be pressing our efforts to find a new sponsor and also when we resume notices will be posted on the Internet because we want to continue this type of exciting and important work about scientific discovery, about Chronic Fatigue Syndrome and all of its aspects.
Dr. Glass' office number in Tulsa, Oklahoma is 918-747-4760 if you like to call and request further information or materials. Tom, what do you want to tell us in the way of wrapping this up for now. Obviously, there's a lot more to come.
DR. GLASS: Well, two things, Roger. Number one, I heard the break and I am so disappointed that your sponsorship has been cancelled because shows like this certainly are so invaluable to getting the word out to the people who are infected by these conditions.
The second thing is the positive aspect. Once we have the animal model we're able to introduce therapies. And that's so so important. Not only therapies in humans, but therapies in animals and
we're able to talk about vaccination. One of the things that we did as part of an entire protocol is we attenuated - that is to say we destroyed the virus that we were injecting into animals - and we injected that destroyed virus into animals. Not only did it not produce the disease, it produced
protection. Because we followed that with two insults with live virus and the animal never got sick.

DR. MAZLEN: So, we're talking about vaccinations for your animals, we're talking about vaccinations for family members and we're talking about good therapies. Because the therapies here have to be very very carefully applied. If the body is allowed to recognize this agent then more ominous things can occur so I am so impressed with the idea that we have everything available and like you what researchers such as myself and John Martin need is funding and we do not have the funding. Well, we're going to work on that. That something we're going to both be working on as members of stealth virus task force and as individual scientists. We're not going to give up.
DR. GLASS: Exactly, we're not going to give up.
DR. MAZLEN: Now, I think this information about the vaccine is exciting and at least it offers promise so that people can take that back to their friends and to people who know people with Chronic Fatigue Syndrome who have animals. There is hope on the horizon for this.
We want to thank Dr. Glass because he's obviously a person with a lot of responsibilities, he's busy,
he's got his research but he's really enthusiastic about coming on this show. He told me in previous conversations that he really wanted to relate this information and we all owe him a vote of thanks.

Obviously there will be more about this. You can write or call Dr. Glass. I'll also give you an
address which is 2105 East 21st Street, Tulsa, Oklahoma 77114. Tom, thank you
so much for being with us today. We're very privileged to have had you as our guest. We look forward to talking with you some more and hopefully we will get another sponsor.

DR. GLASS: Well, Roger, it's been a pleasure and keep up the work. I mean, you feel sometimes in this work like you're working by yourself and all of us need to know that we're not.
DR. MAZLEN: Yes, and you've emphasized that and I am grateful for your efforts on behalf of caregivers and care providers and health care personnel like myself because you're making the headway that we need to make. Now we just have to work with the funding aspect, which hopefully we'll make some progress with.
We'll be back in the fall hopefully and when we do we'll be back on the Internet to let you know when and where you'll be able to reach us. So, stay tuned for another show in the future and it's been a privilege to be here to be your host and I look forward to being your host again for this important show. 

"Case in point, Dr. Thomas Glass' studies on our pets. This was a transmission study. He had to abandon these very important studies because he had no research monies. Our federal health officials would not grant him any money. This is what scientists DO in labs to research diseases like ours. They STUDY animals. How many of you have seen studies like this with our disease? How many of you have seen federal grants for such important and routine studies? Dr. Glass, also, was "mysteriously" banned from "respected" research journals, even though, these journals praised him for the high quality of scientific methods he had used. He went to a prominent, inter/national support group and waited three years to get his important findings published in their journal, and they turned him away, too. I had to track Dr. Glass down, and our small newsletter finally published his important research. Patients who had donated the bodies of their beloved pets, with all the other things they had lost, had been waiting for years to see his research."

 In collaboration with Dr. Tom Glass of the University of Oklahoma, we observed the virus-induced transformation of healthy cats to reclusive, pained, irritable creatures creating bald spots on their heads from constant rubbing. Again, there was no inflammation in the brains or other tissues of these animals, only the foamy, lipid-filled cells that were being seen in the viral cultures.

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