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The first small step, as I understood it, was to examine if there are cases that fit the description of AIDS without HIV.

Just one single confirmed such is enough to expose the name trickery that made HIV part of AIDS as an a priori matter.

First, I'd like to say that your recent contributions to this blog have been nothing short of excellent, Pope.

As a living example of a confirmed case of HIV-negative AIDS, it was the "HIV part of AIDS as an a priori matter" that first caused me to take a second look at HIV=AIDS. Had my doctors confidently diagnosed me as an ICL patient and had they competently explained the difference between ICL and HIV/AIDS, I would have continued to accept the consensus opinion, I suppose. That of course did not happen. In fact, the very opposite was the case. As I've noted previously, my experience suggests that patients in similar situations are more likely to encounter imcompetence rather than confidence, and that's due largely to the insufficient explanatory value of the HIV model of causation.

Other worthy comments from you that I would like to see "believers" such as Chris Noble and DT address are:

"The rethinkers are asking for an HIV particle - a whole particle directly from a patient. They don't need, as DT suggests, to kill a patient in order to get enough material to propagate the thing in cell lines. Just one particle, from a purified selection for obvious reasons." -- Pope

This really is the crux of HIV's undoing. If we continue to allow HIV researchers carte blanche in claiming that it is unreasonable to expect a whole HIV particle to be cultured directly from an afflicted patient, the question of HIV's infectivity will forever remain a predetermined mystery. Contrast that with the high standards demanded by research associated with other, less politicized, public health concerns, and you'll see why accountability is seriously lacking in HIV research. For example, the predicative value of our knowledge regarding the pathogenesis of various bacteria demonstrates perfectly where our knowledge of the same phenomenon in viral agents is exponentially inferior. To say it another way, the clinical symptoms of an acute bacterial illness can very easily be verified by their subsequent resolution with appropriate antibiotic treatment. We can even demonstrate mutations in the organism, without appealing to mysterious and esoteric explanations as in the case of HIV. The demonstration of bacterial mutations can even be narrowed to resistance to particular antibiotics. HIV's supposed mutations are fanciful illusions, by comparison. We are no where near that level of sophistication in our understanding of retroviral pathogenesis, and the most obvious indication of this failing is captured by observing how the clinical presentations of HIV/AIDS often conflicts with the clinical predictions we've relied upon to direct our inquiries. That is an unacceptable state of affairs.

I'm not saying science should ignore any correlation, that's one of the main points. It may be that there is a correlation between HIV and the clinical symptoms of what you call AIDS. I happen to doubt the correlation is as good as you apparently think. I certainly disagree that the correlation is good enough to hand out death sentences by.

Very well said.


Barry A's excellent contributions are equally appreciated by most of the bloggers here, as well, I would think, except for perhaps Chris Noble, DT, and Dale. How else does one explain their avoidance of Barry A's very astute characterizations of the most logical beginnings for evaluating HIV as both a necessary and a sufficient cause of AIDS. So, I hope no one minds that I try to get this conversation back on track by revisiting Barry's insightful additions to this discussion:

First, let's look again at the two competing claims...

Scientific Claim 1:

A retrovirus, named HIV, transmitted primarily through blood or semen, attacks and destroys CD4 cells, by an unexplained mechanism. This disabling of a critical component of the immune system leads to opportunistic infections and death, if untreated.


Scientific Claim 2:

The causal link between the retrovirus => CD4 cell decline => opportunistic infections => death is unproven. Many different things cause CD4 cell decline; many different things cause opportunistic infections. Focusing narrowly on the retrovirus, to the exclusion of other possible factors of pathogenesis, is a mistake.

Now, I'm very curious to hear from the usual suspects over in Camp Apology as to whether or not they agree that both claims have merit, as presented. I happen to agree with Barry:

I think we can all now agree, based on the science, that CD4 cell depletion is not a result (effect) unique to HIV (purported cause).

If anyone disagrees that these two claims fail to capture the clinical picture, then the onus is on you to explain why. What say you, Camp Apology?


Source : http://scienceblogs.com/aetiology/2007/02/21/while-all-the-hiv-dissidents-a/

While all the HIV “dissidents” are milling around….
The long shadow of smallpox