HHV-6 University

http://www.washingtonpost.com/politics/cdc-says-20-percent-of-us-children-have-mental-health-disorders/2013/05/19/8c316b42-c0b3-11e2-8bd8-2788030e6b44_story.html?hpid=z3

http://www.ncbi.nlm.nih.gov/pubmed/23535036

http://www.ncbi.nlm.nih.gov/pubmed/17276366 If HHV-6 is the real cause of AIDS, here are some of the implications: 1. HIV is a massive scientific fraud. Something akin to a Ponzi scheme. Scientists who challenged the HIV theory of AIDS (the ones who have been thuggishly censored and silenced) turn out to be on the money. 2. Chronic Fatigue Syndrome and Autism (and many other so-called HHV-6 related mysterious epidemics) are part of the so-called AIDS epidemic.  Chronic Fatigue Syndrome and Autism both are clearly the results of the ravages of HHV-6. 3. AIDS and Chronic Fatigue Syndrome has been artificially and politically separated into two epidemics. We are living in a period of CFS/AIDS apartheid. So-called AIDS patients have to sit in the back of the HHV-6 epidemic bus while the befuddled HHV-6/CFS patients and HHV-6/Autism victims sit up front. Nobody is well-served. 4. AIDS is not a sexually transmitted disease. That paradigm has set a scapegoating and ant

In the June 26, 1989 issue of New York Native Neenyah Ostrom covered CFS research pioneer Dr. Paul Cheney’s testimony to Congress concerning the CFS epidemic. Cheney told Congress that [chronic fatigue syndrome] might have a relationship with the AIDS epidemic. Cheney told Congress, that one informal "survey of patients in [CFS] groups from 35 states shows an exponential rise in cases produced each year since the 1970s. This curious temporal and case production relationship with the AIDS epidemic has prompted some researchers to project CFS as an AIDS epiphenomenon. Indeed, the new human herpes virus HHV-6 may be amount the most important co-factors shared by both AIDS and chronic fatigue syndrome." If HHV-6 is the real cause of AIDS, here are some of the implications: 1. HIV is a massive scientific fraud. Something akin to a Ponzi scheme. Scientists who challenged the HIV theory of AIDS (the ones who have been thuggishly censored and silenced) turn out

Human herpesvirus-6 entry into the central nervous system through the olfactory pathway Abstract Viruses have been implicated in the development of neurodegenerative diseases, such as Alzheimer's, Parkinson’s, and multiple sclerosis. Human herpesvirus-6 (HHV-6) is a neurotropic virus that has been associated with a wide variety of neurologic disorders, including encephalitis, mesial temporal lobe epilepsy, and multiple sclerosis. Currently, the route of HHV-6 entry into the CNS is unknown. Using autopsy specimens, we found that the frequency of HHV-6 DNA in the olfactory bulb/tract region was among the highest in the brain regions examined. Given this finding, we investigated whether HHV-6 may infect the CNS via the olfactory pathway. HHV-6 DNA was detected in a total of 52 of 126 (41.3%) nasal mucous samples, showing the nasal cavity is a reservoir for HHV-6. Furthermore, specialized olfactory-ensheathing glial cells located in the nasal cavity were demonstrated

The HHV-6 Paradox Blumberg BM, Mock DJ, Powers JM, Ito M, Assouline JG, Baker JV, Chen B, Goodman AD. BACKGROUND: Progressive multifocal leukoencephalopathy (PML) and multiple sclerosis (MS) are demyelinative diseases of the central nervous system (CNS). PML occurs mostly in individuals with AIDS-impaired immunity and is thought to be caused by JC polyoma virus (JCV). In MS a neurotrophic virus trigger is suspected, but the precise etiology remains unknown. Human herpesvirus 6 (HHV6) is a ubiquitous, commensal and usually benign beta-herpesvirus. Some researchers have found evidence for HHV6 infection in MS plaques and sera. We recently demonstrated a high frequency of cells containing HHV6 genome in PML lesions, as well as co-infection of oligodendrocytes by JCV and HHV6. This suggests that HHV6 may be a co-factor in the etiology of PML, and raises questions about its role in other demyelinative diseases. OBJECTIVES: To determine the prevalence and cellular localizati