Grounds to Validate with Rezz

[Guest guest]

Yes Lynda,

 

"Grounds to validate?" I love this choice of phraseology. Tony Robbins and Deepok Chopra are two scholars that I am well familiarized with, yet I do not see them on the same levels. Deepok, in my experience, is much more polished in his applied knowledge and insights. These are but a mere two gurus of reference. Dr. Afrika, Dr. Jewel Pookrum, Gary Null, Dr. Sebi, Steve Cokely, Brother Phil Valentine, Bobby Hemmit, Ashra & Merira Kwesi, Shekem Ur Shekem Ra Un Nefer Amen, Krishnamurti and many other scholars, griots & gurus are aware of this massive hoax on the people. The knowledge goes further indeed. Think more carefully.

 

Our perceptions of terminology and verbiage cannot be overstated. When we mention things like, "people are dying", then we have created a reality for this conceptualization called "death." If you truly innerstand the teachings and insights of gurus like Deepok Chopra, then you can see that there is no such a thing as "death" or "dying." If we accept the definitions of our downpressors, what then is our most immediate avenue for Uhuru Sasa? Wisdom lays in the silence of a firm meditation. Unspoken words/language are ultimately confusion and latent regress. We must be the wiser of our Self.

 

Now, here is my insight on the science of it all. A foreign material enters and/or attaches to the body. Our body's immunological response is to search its genetic composition, expel it or

quarantine this material in the circadian rhythms of our physiology and histological make up. As soon as the body determines the nature of the material is toxic [to whatever degree], all of the "defenses" will attempt to neutralize this material. If this material is allowed to overwhelm the bioelectric charge {nerve/brain purity} of the body's blood & lymph circulations, then it can proliferate [set infection anywhere] in the body. If this material is "identified" to be a so-called virus, then this naming aught to be indicative of the nature of its toxicity and the degree of proliferation in the body.

 

Further, to call the foreign material an Human Immunodeficiency Virus(es) is such a hook for those of us that do not take it further in thought before verbiage. The knowledge goes on. . .

 

 

 

 

 

 

Acquisition of HIV Infection [sourced from the University of California at San Francisco]

{see http://hivinsite.ucsf.edu/InSite?page=kb-02 and take special

notice of the 4th bullet point line from the top, no link, hiv plural?}

 

 

 

 

In most infectious diseases, a number of factors contribute to the risk of acquisition of infection and to the occurrence of illness after exposure to a pathogenic organism. These include the nature of the exposure (eg, the route, the size of the microbial inoculum), the "virulence" of the microbe, and the nature of the host susceptibility to infection. The nature of the exposure clearly determines the risks of infection. Parenteral exposure to blood infected with HIV carries a substantial risk of infection. Among individuals transfused with blood of HIV-infected persons before screening of blood donors was practiced, the risk of infection approached 100%.(1) Transmucosal infection risks vary according to the site of exposure, with risks of transmission through rectal exposure exceeding the risks of transmission through vaginal exposure and both of the above exceeding

the risks of transmission across oral mucosa. Mucosal inflammatory disease tends to enhance the risk of transmission particularly if associated with ulceration. Though firm data are lacking, epidemiologic evidence of seroconversion after accidental needlestick injuries (2) or sexual contact with infected persons with different levels of plasma HIV RNA suggest that the magnitude of the inoculum also contributes to the risk of infection.(3,4) Similarly, mother-to-infant transmission of HIV is enhanced among women with high levels of plasma HIV RNA, even after taking into account other known predictors of transmission,(5-7) and the intensity of exposure to contaminated

antihemophilic factor concentrates has been shown to predict the risk of HIV infection among hemophiliacs.(8) Insight gained from persons at high risk for infection yet who persistently remain seronegative indicates that certain genetic loci can dramatically affect risk for acquisition of HIV infection. Specifically, persons homozygous for a 32-base-pair deletion (the so-called delta-32 mutation) in the C-C motif chemokine receptor 5 (CCR5) open reading frame that results in failure of surface expression of this key viral coreceptor are protected from acquisition of HIV infection.(9-11) In the rare instances when such persons have been found to be infected, they appear to acquire infection with viruses that may be capable of entry using the CXC motif chemokine

receptor 4 (CXCR4) coreceptor.(12-14) In addition, persons with the -2459G polymorphism in the CCR5 promoter that may result in diminished CCR5 expression also may have a somewhat lower risk of infection than do persons with the alternative -2459A nucleotide at this site.(15) One other rare polymorphism in the CCR5 gene, characterized by a point mutation at position 303, introduces a premature stop codon in the elongating product chain and prevents the expression of a functional CCR5 coreceptor when associated with the delta-32 deletion, also conferring virtually complete resistance to CCR5-using viruses.(16)

 

 

As these studies have been performed among groups at risk for infection by both parenteral and mucosal routes, these observations suggest that acquisition of infection is highly dependent upon expression of the HIV coreceptor CCR5. The location of this critical "bottleneck" that requires CCR5 expression remains to be determined. One model proposes that CCR5-receptor availability is critical at the level of the mucosal dendritic (Langerhans) cells, which express CCR5 but much less CXCR4 or other C-type lectin receptors to which HIV may bind to facilitate cellular entry. On the other hand, a nonmucosal location for this bottleneck is suggested by the high prevalence of the CCR5 delta-32 homozygous state among seronegative hemophiliacs who otherwise appear to be at high risk for parenteral acquisition of infection.(17) Importantly however, among HIV seronegative

cohorts at very high risk of either parenteral or transmucosal infection, only a minority (eg, 16% in a group of hemophiliacs at >95% risk of infection according to treatment history) are homozygous for the delta-32 mutation,(17) indicating that other mechanisms determine risks for and protection from HIV infection in these settings. Of note, members of several high-risk, HIV-seronegative cohorts have demonstrated immunologic "memory" of HIV exposure. Specifically, mucosal immunoglobulin A (IgA) capable of cross-clade HIV binding and neutralization has been found in genital secretions of some high-risk uninfected persons,(18) and low levels of CD8+ T cells reactive to HIV peptides have been found in circulation in other groups of high-risk

seronegative individuals.(19,20) It is not yet clear whether these immune defenses are actually responsible for protection against infection or, alternatively, are a reflection only of exposure while protection is mediated by some other mechanisms that remain to be defined.

Researcher For Life!

 

~Rezz

 

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