The Story behind The Lady Upstairs

Monday, January 19, 2015

Do pets get Non-HIV AIDS from their owners and vice versa?

Dr. Thomas Glass on Chronic Fatigue Syndrome and pets. Did he inadvertently establish the first animal model for Chronic Fatigue Syndrome and HHV-6? If the agent responsible for the illness in both people and their pets is HHV-6, we may have definitive proof that HHV-6 is the cause of Chronic Fatigue Syndrome. And that could be just the beginning of the HHV-6 story.

Glass, R. 2000. Abnormal signs found in animals of myalgic encephalomyelitis/chronic fatigue syndrome patients: A look at 463 animals. Journal of Chronic Fatigue Syndrome 6:73-81.

Glass, R.T. 2000. The human/animal interaction in myalgic encephalomyelitis/chronic fatigue syndrome: A look at 127 patients. Journal of Chronic Fatigue Syndrome 6:65-72.

Glass, R.T. 1998. Autopsy findings of chronically ill animals of patients with chronic fatigue and immune dysfunction syndrome and autopsy findings of acutely ill animals who receive the agent which produces chronic fatigue and immune dysfunction syndrome. Medical Professional/Persons with CFIDS News 3:1-4.

Glass, R.T. 1998. The human/animal interaction of chronic fatigue and immune dysfunction syndrome: A look at 127 patients and their 463 animals. Medical Professional/Persons with CFIDS News 3:2-4, 15.

Martin, W.J. and Glass, R.T. 1995. Acute encephalopathy induced in cats with a stealth virus isolated from a patient with chronic fatigue syndrome. Pathobiology 63:115-118.

Gallo on HHV-6 and AIDS

Is HHV-6 the real AIDS Virus? Is it also the cause of Non-HIV AIDS???


The Name War

myalgic encephalomyelitis, aids, cfs, chronic fatigue syndroem, julian lake, gay, epidemiology

Gut-Brain Dysfunction: One of HHV-6's 50 Shades of Non-HIV AIDS

Autonomic nervous system dysregulation in irritable bowel syndrome

http://onlinelibrary.wiley.com/doi/10.1111/nmo.12512/abstract

Conclusions & Inferences

IBS subjects display a significant reduction in α index, an established marker of cardiac baroreflex. ANS dysfunction appears to be involved in the pathophysiology of IBS and its assessment may open new perspectives for clinical management of patients suffering from IBS.

Immunomodulation and immunosuppression by human herpesvirus 6A and 6B

http://www.futuremedicine.com/doi/abs/10.2217/fvl.13.7

Lorenzo Dagna Joshua C Pritchett & Paolo Lusso

Vol. 8, No. 3, Pages 273-287 , DOI 10.2217/fvl.13.7
(doi:10.2217/fvl.13.7) 
 
"Like other members of the Herpesviridae family, human herpesvirus (HHV)-6A and HHV-6B have developed a wide variety of strategies to modulate or suppress host immune responses and, thereby, facilitate their own spread and persistence in vivo. Long considered two variants of the same virus, HHV-6A and HHV-6B have recently been reclassified as distinct viral species, although the established nomenclature has been maintained. In this review, we summarize the distinctive profiles of interaction of these two viruses with the human immune system. Both HHV-6A and HHV-6B display a tropism for CD4+ T lymphocytes, but they can also infect, in a productive or nonproductive fashion, other cells of the immune system. However, there are important differences regarding the ability of each virus to infect cytotoxic effector cells, as HHV-6A has been shown to productively infect several of these cells, whereas HHV-6B infects them inefficiently at best. In addition to direct cytopathic effects, both HHV-6A and HHV-6B can interfere with immunologic functions to varying degrees via cytokine modulation, including blockade of IL-12 production by professional antigen-presenting cells, modulation of cell-surface molecules essential for T-cell activation, and expression of viral chemokines and chemokine receptors. Some of these effects are related to signaling through and downregulation of the viral receptor, CD46, a key molecule linking innate and adaptive immune responses. Increasing attention has recently been focused on the importance of viral interactions with dendritic cells, which may serve both as targets of virus-mediated immunosuppression and as vehicles for viral transfer to CD4+ T cells. Our deepening knowledge of the mechanisms developed by HHV-6A and HHV-6B to evade immunologic control may lead to new strategies for the prevention and treatment of the diseases associated with these viruses. Moreover, elucidation of these viral mechanisms may uncover new avenues to therapeutically manipulate or modulate the immune system in immunologically mediated human diseases."

Cockamamie study on HHV-6 and AIDS

http://www.ncbi.nlm.nih.gov/pubmed/24555113

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