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SadunKal
August 26th, 2009, 05:56 AM
Here's something fun and necessary:
http://www.theperthgroup.com/REJECTED/AIDScausesHIV.pdf


"Abstract: We present data that the accepted cause of the acquired immune deficiency syndrome (HIV) precedes its claimed causitive role (acquired immune deficiency)in producing this syndrome.

HIV Infection the cause or the effect of Acquired Immune Deficiency?

Bradford Hill developed “nine viewpoints [that] can bring indisputable evidence for or against a cause and effect hypothesis”,1. They include strength of association, dose-response relationship, biological plausibility and temporality, that is, the logical necessity for cause to precede effect. Although these criteria have been the subject of some controversy over the years,2 it is generally accepted that temporality, although not sufficient, is absolutely necessary to prove causation. According to the HIV infection hypothesis of AIDS, acquired immune deficiency (AID = low numbers of T4 cells) follows HIV infection.

However,

1. In 1985 Montagnier stated "This [clinical AID] syndrome occurs in a minority of infected persons, who generally have in common a past of antigenic stimulation and of immune depression before LAV [HIV] infection".3 That is, Montagnier recognised that in the AIDS risk groups AID appears before HIV infection. More recently, Montagnier seems to be an apologist of our long standing hypothesis4 that both HIV expression, that is, detection of the phenomena which are considered to prove HIV infection as well as AID, are the result of oxidation induced by the many oxidative agents and conditions to which the patients belonging to the AIDS risk groups are exposed. Although Montagnier has never published his view about the oxidative agents proposed by us, he accepts one of them—in Africans the cause of oxidation and thus the decrease in T4 cells is malnutrition.5

2. In a prospective study published in 2003, researchers of the Amsterdam Cohort study, analysed "CD4 and CD8 T cell activation marker expression in 102 individuals with known seroconversion data, before and after seroconversion. They concluded “This study demonstrated for the first time that low preseroconversion numbers of CD4 T cells and increased levels of immune activation were associated with an increased risk to develop AIDS after seroconversion...In conclusion, our data show that chronic immune activation and the size of the CD4 T Manuscript cell pool are critical factors in HIV-1 pathogenesis, even when measured before seroconversion".6. In the MultiCenter AIDS Cohort Study seropositive gay men were divided into two groups: Group A, who developed AIDS and group B, who did not develop AIDS five years post seroconversion. Unlike other sexually transmitted diseases, the authors found that: "receptive anal intercourse both before and after seroconversion with different partners was reported more frequently by men with AIDS...When group A was stratified by development of AIDS within 30 months and within 30-60 months and compared to matched controls, a greater proportion of highrisk sexual activities postseroconversion was noted in the group progressing to AIDS most rapidly. The differences were statistically significant 12 and 24 months post seroconversion". It was concluded "These data then suggest that greater sexual activity following establishment of HIV-1 infection leads to exposure to promoters or co-factors that augment (or determine) the rate of progression to AIDS".7 Hence, HIV experts have published evidence showing there are non-HIV factors which act both pre and post seroconversion that induce AID and “augment (or determine) the rate of progression to AIDS" (emphasis ours).

3. In a study of IV drug users in New York it was shown that "The relative risk for seroconversion among subjects with one or more CD4 count <500 cells/uL compared with HIV-negative subjects with all counts >500 cells/uL was 4.53".8

4. A similar study in Italy showed that "low number of T4 cells was the highest risk factor for HIV infection".9

5. Numerous reports from many well known researchers of AIDS in haemophiliacs have shown that T4 cell depletion precedes "HIV infection".10-13

6. The same has been reported in recipients of “Transfusions of Blood-Derived Products”.14

7. One of the principal major signs of the Bangui AIDS definition is loss of body weight. However, in a study of Rwandan women, over a 24 months period it was reported that nutritional status assessed by loss of body weight "was a significant predictor of eventual HIV seroconversion…In addition to those findings for measured weight loss during follow-up, reported weight loss before enrolment was also a risk factor for subsequent seroconversion".15 That is, weight loss preceded HIV seroconversion by many months or even years.

The above evidence from all the main AIDS risk groups shows that, contrary to the HIV infection theory of AIDS, HIV infection follows, does not precede AID. Thus HIV can be its effect but not its cause."

HansSelyeWasCorrect
August 26th, 2009, 09:28 PM
Hans Selye was the first person (AFAIK) to articulate a "stress" notion of "disease," and it seems as though this is not just true for people (or animals and plants generally) but also for bacteria, which becomes "clingy" and prompts an inflammatory response (and that causes the symptoms of the disease). In the case of viruses (real ones), there is an inflammatory response to the particles, which is also true if you get asbestos in your lungs, for example. The amount of virus, the place of exposure, etc. play roles in how nasty the "disease" is. In any case, a key point for me is not to be taken in by abstract constructs, but rather to stay focused on undeniable facts. Both "HIV" and "AIDS" are constructs that are simply not worth even thinking about in the "disease" context (if we define "disease" precisely), except of course for the people being killed off by idiocy and conflicts of interest.

Demarque
August 27th, 2009, 08:39 AM
Here my view of "HIV"

cdm
August 27th, 2009, 11:31 AM
As far as I know, friend demarque, there is no evidence that the CD4s are destroyed anywhere during infections coupled with or without expression of Gallo antibodies. They are only changing place during their circulation. Under some circumstances they return and we observe fluctuations even during the period of one day. So this destruction of lymphocytes is a myth, that we must put aside.
I challenge you and anyone else to give such evidence.

G Man
August 27th, 2009, 03:45 PM
cdm, And don't the CD4's also get replaced and regenerated by the body periodically? I'm not sure how often.

Point is, if HIV is supposedly killing these cells or messing with them so they can't function, the body renews them every so often anyway and that would render HIV harmless.

I need to look into this more, but I think that would be a nail in the coffin for the theory that HIV takes 10 or 20 years to kill you.

moonchild493
August 27th, 2009, 05:40 PM
I believe the orthodox take on it is that HIV destroys CD4s faster than the immune system can replenish them, ultimately leading to extreme loss of CD4 cells and serious illness. I'm sure you can find some detailed accounts of this,, but I'm afraid I don't know where to look. Perhaps others can chime in.

G Man
August 27th, 2009, 05:57 PM
yeah, but if that's true that it kills the CD4's faster than they can be replenished, then it shouldn't take 10 (or 20!) years to kill a person. The person should be dead within days, weeks, or months at the latest, as is the case with every other "killer" virus.

moonchild493
August 27th, 2009, 06:03 PM
I'm only reporting what they say. They keep moving the goalposts when things don't behave like they should. Supposedly, it can take a long time for things to get so out of balance that really ill health occurs. Hey, it's not my idea, just another one of their crazy theories cloaked as fact.

HansSelyeWasCorrect
August 27th, 2009, 08:13 PM
Right, it's either got to kill quickly by that logic or else the body, if all else is fine, will be able to adapt, as it can to all kinds of real insults and traumas. What "HIV/AIDS" teaches us is that the highest medical authorities can generate the most ridiculous ideas, not even worthwhile in the realm of science fiction.

cdm
August 27th, 2009, 11:43 PM
The lifespan of thymus derived lymphocytes is a controversial issue. Practically they live for ever, although they have at least one to maximum three phases. First, after having succeeded in passing the exams of recognizing only the external antigens and not the internal, they are allowed to get into the circulation as naive cells. If they encounter a foreign antigen that is in their individual span of recognition, they become activated for a few days -second phase- and later on they become effector cells -third phase- committed to a special task. How long do they stay in this effector state and if they abolish it, I have not heard of it. To me it seems probable that they can abolish the effector state and regain their naivity. The only reason for their apoptosis is when they make mistake and misinterpret the internal antigens as foreign, although this is not the case in the course of the so-called autoimmune diseases.
Regeneration of lymphocytes probably does not follow strict rules, as is the case of erythrocytes and neutrophils who show an accurately measured lifespan. Actually they are not regenerated periodically. They must be replaced in a mysterious way after living a life of a random carrier. Not having a huge place of production -like the bone marrow- is a sign they are relatively produced in small numbers. Thymus is said to sub-function or not function at all, during the adult life, so regeneration is impossible in large numbers.
We must not forget that they are cells of the lymph, that means the most of them are not in the blood circulation but outside of it. This is their natural inhabitation while the lymph glands are like castles or strategic offices where they make exchange of information with their comrades, lymphocytes or dendritic cells. Being in the blood is only in terms of a fast traffic means, and so they do not have another practical reason to be in it. In accordance to special needs they may probably be in the blood in only small numbers, in order to be in larger numbers into tissues where they are most needed. This is reversed sometimes after a few hours, or a few days. When the acute inflammation markers subside they begin to reappear in the blood. There is a negative correlation between the acute inflammation markers -ie CRP -and lymphocytes. There is no killing of them my friend demarque.
And all these thoughts are derived from the classic teachings of conventional immunology. I do not support them all definitively.

cdm
August 27th, 2009, 11:57 PM
The lifespan of thymus derived lymphocytes is a controversial issue. Practically they live for ever, although they have at least one to maximum three phases. First, after having succeeded in passing the exams of recognizing only the external antigens and not the internal, they are allowed to get into the circulation as naive cells. If they encounter a foreign antigen that is in their individual span of recognition, they become activated for a few days -second phase- and later on they become effector cells -third phase- committed to a special task. How long do they stay in this effector state and if they abolish it, I have not heard of it. To me it seems probable that they can abolish the effector state and regain their naivity. The only reason for their apoptosis is when they make mistake and misinterpret the internal antigens as foreign, although this is not the case in the course of the so-called autoimmune diseases.
Regeneration of lymphocytes probably does not follow strict rules, as is the case of erythrocytes and neutrophils who show an accurately measured lifespan. Actually they are not regenerated periodically. They must be replaced in a mysterious way after living a life of a random carrier. Not having a huge place of production -like the bone marrow- is a sign they are relatively produced in small numbers. Thymus is said to sub-function or not function at all, during the adult life, so regeneration is impossible in large numbers.
We must not forget that they are cells of the lymph, that means the most of them are not in the blood circulation but outside of it. This is their natural inhabitation while the lymph glands are like castles or strategic offices where they make exchange of information with their comrades, lymphocytes or dendritic cells. Being in the blood is only in terms of a fast traffic means, and so they do not have another practical reason to be in it. In accordance to special needs they may probably be in the blood in only small numbers, in order to be in larger numbers into tissues where they are most needed. This is reversed sometimes after a few hours, or a few days. When the acute inflammation markers subside they begin to reappear in the blood. There is a negative correlation between the acute inflammation markers -ie CRP -and lymphocytes. There is no killing of them my friend demarque

G Man
August 28th, 2009, 01:25 AM
Ok, so in layman's terms are you saying that most of the CD4's live in the lymphatic tissue and not in the blood? If that's the case, then the t-cell test results they get from a blood sample isn't really an accurate interpretation of a person's CD4 level. And that would mean that the number they give HIV patients to determine whether to label them as having AIDS is not accurate either.

cdm
August 28th, 2009, 07:05 AM
I am saying that nobody is allowed to postulate that, because their number is small, the Cd4s have been "killed". That has never been proven. It is a matter of circulation most of all. There is no need for them to regenerate or die automatically, likewise as the other white blood cells normally do. The theory of HIV/AIDS is a false theory because it has never adopted the central dogma of immunology that lymphocytes -all of them, not only CD4s- are practically immortal. Most of them live a silent life. It has long been recognized that they are inert for years, before being activated and be effector-cells. The HIV/AIDS theorists say that the CD4s are killed by the so-called virus, but do not explain how ART reconstitutes their number, if they are not capable of multiplying in large numbers. The only reason for multiplying, especially of B- lymphocytes, is the encounter with specific antigens, and this applies only to a certain specific lymphocyte, according to the official and dominant theory.
There might be a use in measuring the number of CD4 by tests. I am not against the use of the test, and no one can predict what will be the use of this test in the future. I am, actually, against the easily made explanations.
But as long as this theory (of T-cells being killed) dominates, it is better for the Gallo positives not to take the test, except if they are powerful enough to challenge the doctors' arrogance and ignorance. It is a useless and dangerous test at the moment, because there is an obsession with this "terrible" number of CD4s.
Science is think hard, try hard, realize the total icon of reality and do not explain anything swiftly, in terms of causation. Be modest. The cause of things is not seen by humans because we -humans- look at the surface. At the surface there is correlation, not causation.

T.rex
September 2nd, 2009, 05:12 PM
IThe HIV/AIDS theorists say that the CD4s are killed by the so-called virus, but do not explain how ART reconstitutes their number, if they are not capable of multiplying in large numbers.

i just wanted to say that i took your challenge on that, and posted that question on thebody.com a few days ago. I wanted to see if the respected doctors there could elicit what process is happening in the body that allows for the ARTs to replenish CD4 count.

He didn't answer that question... One of the first times, he didn't at least try to spoonfeed some type of rehearsed response to one of my questions. That was 3 days ago... if he still tries to answer it, i'll post it here.

Mike_Stewart
April 13th, 2011, 04:26 PM
Here my view of "HIV"

Demarque,

I took a closer look at the schematic you posted.

To wit:

http://www.ncbi.nlm.nih.gov/pubmed/12084618

Would appreciate your comment on L Soderberg's findings.

Dr. Haverkos, et. al.:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1567358/pdf/envhper00406-0056.pdf

jonathan barnett
April 13th, 2011, 04:35 PM
I hope Demarque see this, Mike, but this is a pretty old thread and Demarque has not been a frequent contributor here since last Fall. You might see if he allows messages to be sent to him from your user control panel.

If you click on a user's name in a post, one of the choices is "view all posts.." This will give you a sense of member's posting history, though that doesn't mean they have not been here, or don't follow along quietly.

Just thought you and others might find this info helpful, if you didn't already know it.




Would appreciate your comment on L Soderberg's findings.