Parkinson’s disease and Avian Flu H5N1 Viral Load

Avian influenza can cause a predisposition to Parkinson’s disease, according to research published this week in the Proceedings of the National Academy of Sciences.

This is very interesting research that would cause you to want to take exposure to flu more seriously!  First, let’s stay healthy so we do not get flu or colds with all that I discuss from Immuni-T 2 and 3 to long term detoxification, as in FIGHT program. Then since for many that is too rigorous a requirement, so let’s have an EMERGENCY SUPPORT PACKAGE in the homes of anyone that realizes who important this new research is!  Have BioE’nR-G’y C, ACS 200, and high dose D AND A available to immediately begin at the first sign of active infections.

What if their vaccines turn out to be as wrong for stopping H1N1, as MMR has been shown to be for compromised children? After MMR in autistic kids the live virus from the vaccination later has been shown to be growing in the CSF of these children.  Will the current testing of the new swine flu vaccines even attempt to look for how many receiving the vaccines actually wind up being infected with the virus instead of being protected against the virus, as they are not able to launch an immune response to the vaccine?

It appears that the virus accesses the neuron through the axons in the GI tract and lung. This sets the stage then for loss of Dopamine secreting cells over time.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
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Recent studies have suggested that the currently circulating strain of avian influenza has similar pathology to the 1918 flu. Though the subtypes of the viruses are different (Spanish flu shares the H1N1 subtype with the current H1N1 swine flu, whereas avian influenza has an H5N1 subtype), both viruses appear to enter the central nervous system (CNS) and can cause encephalitis, or inflammation of the brain.

Highly pathogenic H5N1 influenza virus can enter the central nervous system and induce neuroinflammation and neurodegeneration
http://www.pnas.org/content/early/2009/08/07/0900096106.abstract

1.       Haeman Janga,b,
2.       David Boltzc,
3.       Katharine Sturm-Ramirezc,1,
4.       Kennie R. Shepherda,2,
5.       Yun Jiaoa,
6.       Robert Websterc and
7.       Richard J. Smeynea,3

+Author Affiliations
1.       Departments of aDevelopmental Neurobiology and
2.       cInfectious Diseases/Virology, St. Jude Children’s Research Hospital,
262 Danny Thomas Place, Memphis, TN 38105-3678; and
3.       bIntegrated Program in Biomedical Sciences, University of Tennessee
Health Science Center, Memphis, TN 38163
1.      1Present address: Fogarty International Center, National Institutes
of   Health, 16 Center Drive, Room 202, Bethesda, MD 20892.
2.      2Present address: Department of Environmental and Occupational
Health, Rollins School of Public Health and Center for
neurodegenerative Disease, Emory University, Whitehead Biomedical
Research Building, 5th Floor, Room 575.1, Atlanta, GA, 30322.

Abstract
One of the greatest influenza pandemic threats at this time is posed by the highly pathogenic H5N1 avian influenza viruses. To date, 61% of the 433 known human cases of H5N1 infection have proved fatal. Animals infected by H5N1 viruses have demonstrated acute neurological signs ranging from mild encephalitis to motor disturbances to coma. However, no studies have examined the longer-term neurologic consequences of H5N1 infection among surviving hosts. Using the C57BL/6J mouse, a mouse strain that can be infected by the A/Vietnam/1203/04 H5N1 virus without adaptation, we show that this virus travels from the peripheral nervous system into the CNS to higher levels of the neuroaxis. In regions infected by H5N1 virus, we observe activation of microglia and alpha-synuclein phosphorylation and aggregation that persists long after resolution of the infection. We also observe a significant loss of dopaminergic neurons in the substantia nigra pars compacta 60 days after infection. Our results suggest that a pandemic H5N1 pathogen, or other neurotropic influenza virus, could initiate CNS dis