Skip to comments.Deny the HIV to AIDS connection and you'll be attacked, crushed, and ruined
Posted on 07/22/2008 9:56:23 AM PDT by thinkingIsPresuppositional
click here to read article
The reference isn’t with me, it’s in a book on my bookshelf about 6,00 miles from where I am, but I’m sure I can dig up a web reference. Give me a few hours to get this done. You can be sure I am absolutely accurate in my statement, though.
Really? Who woulda thunk?
Most important, Mr. Baker is utterly wrong to see the pharmaceutical industry as the cause of the trouble; rather, it's the government itself that is the center of the problem. I believe that Ronald Reagan said something like: government is not the solution, government is the problem. It is tragic that his Secretary of HHS did not take these words to heart.
The mention of Ryan White reminds me: did nobody but me think it paradoxical that nobody blamed the government for stigmatizing this young man as carrying a deadly and contagious disease, while a local school board was vociferously blamed for believing it?
Yep, the last bastion of trust in our society—namely, blind trust in the motives of those who wear white lab coats—is about to vanish once the truth about AIDS and Global Warming come out. This is what happens when the power of government gets involved in almost any human endeavor. The sooner we get government out of the science business the better!
Thanks for the ping!
You are quite right. The government is most certainly at the center of the AIDS fraud. But secondarily, many key players in the pharmaceutical industry played along, cashed in, used their power and influence to add to the hysteria and squelch debate, conducted fraudulent drug trials, and concocted AIDS chemotherapy drugs that continue to maim and kill the poor unsuspecting souls who take them.
HIV entry to host cells begins with binding of the viral envelope protein to CD4 molecules on the host cell surface. This binding initiates conformational changes in the envelope protein that result in binding to a coreceptor (CCR5 or CXCR4), exposure of a previously hidden domain in the viral protein, insertion of a viral fusion peptide into the host-cell membrane and fusing the viral and cell membranes. Each of these steps provides an opportunity for intervention to prevent viral entry, and a number of agents targeting these steps are in development. Studies of coreceptor inhibitors and fusion inhibitors have indicated the presence of host and viral factors that can result in variability of antiretroviral effect. Improved understanding of these factors will help to guide clinical use of these new agents. This article summarizes a presentation by Robert W. Doms, MD, PhD, at the International AIDS Society-USA course in Chicago in May 2004.
The fact that some healthy individuals, who were repeatedly exposed to HIV infection but remained uninfected, were found to be homozygous for a 32-bp deletion in the CCR5 gene (20, 42, 52) triggered the search for CCR5 antagonists as potential anti-HIV agents.
CCL3L1, the gene identified in the new study, makes a protein that also binds to CCR5. Ahuja suggests that people with extra copies of this gene are more resistant to HIV because they make more CCL3L1, and cuts the amount of CCR5 around for the virus to attach to and therefore prevents it from entering white blood cells.
It's an interesting press release and thread. Here's the title of the original article and abstract, i.e. a brief summary.
Immunoglobulins (Igs) in uninfected humans recognize residues 421-433 located in the B cell superantigenic site (SAg) of the HIV envelope protein gp120 and catalyze its hydrolysis by a serine protease-like mechanism. The catalytic activity is encoded by germline Ig variable (V) region genes, and is expressed at robust levels by IgMs and IgAs but poorly by IgGs. Mucosal IgAs are highly catalytic and neutralize HIV, suggesting that they constitute a first line of defense against HIV. Lupus patients produce the Igs at enhanced levels. Homology of the 421-433 region with an endogenous retroviral sequence and a bacterial protein may provide clues about the antigen driving anti-SAg synthesis in lupus patients and uninfected subjects. The potency and breadth of HIV neutralization revives hopes of clinical application of catalytic anti-421-433 Igs as immunotherapeutic and topical microbicide reagents. Adaptive improvement of anti-SAg catalytic Igs in HIV infected subjects is not customary. Further study of the properties of the naturally occurring anti-SAg catalytic Igs should provide valuable guidance in designing a prophylactic vaccine that amplifies protective catalytic immunity to HIV.
Here are the questions if HIV does not cause AIDS:
How did large numbers of people in China get it after they donated blood? 23 August 2001
The Agence France Presse (AFP) reported that China admitted for the first time that tens of thousands of its citizens have been infected with the AIDS virus. Deputy Health Minister Yin Dakui stated, A large number of blood sellers have been infected with HIV due to illegal blood plasma. The illegal blood collection stations usually collected and pooled blood from poor farmers, separated the plasma, and then returns the contaminated blood back to the donators. Yin said, that "so far the problem of HIV infection caused by blood donations had only affected several provinces in central China.
How do you explain the drop in new HIV/AIDS cases after blood was screened for HIV before transfusion of blood and blood products?
Why does giving antiretroviral drugs to HIV positive pregnant women just before and around the birth of their children reduce the rate of HIV positive children being born?
Why do HIV negative children breastfeeding from HIV positive mothers get AIDS and die from it?
Why do the highly active antiretroviral therapy(HAART) drugs decrease mortality and increase longevity?
As far as I'm concerned, Peter Duesberg has only one valid question - the diagnostic accuracy in Africa, but he ignores all of the good outcomes from using antiretroviral drugs there. He's fixated on homosexuals using amyl nitrate "poppers." Other than being a mind altering substance and less inhibited about being promiscuous, I don't see an explanation from Duesberg for why homosexuals get AIDS.
The same goes for intravenous drug abusers. They don't get AIDS if they use clean needles and don't share.(PERIOD!) And yes, they do exist. Not everyone is your typical junkie. Chronic alcoholics are more readily recognized for being immunocompromised. Check the abstract with this link. I almost forgot it.
P.S. If the CDC is such an all powerful entity, then why aren't HIV positive people who have spread it to more than one person quarantined?
But they're not. It's not much, but it's enough to sustain the prevalence outside their cohort through heterosexal contact and intravenous drug abuse.
Let it kill them all, especially if it’d drug use.
I suggest you volunteer to help with that.
People who are HIV positive and have developed AIDS die less now on anti-retrovirals than before there was any medicine for them, so how could it be the medicine that is killing them?
Amazing claims need good evidence. You have supplied none.
You are right, and as I explained I am thousands of mile away from my reference materials. But my assertions are true, never fear. I will post references in due course.
AIDS is the Global Warming of human illness. A complete and total fraud. An invention, a construct. A disease of definition.
I am one of those whow would have been will to be intentionally infected with HIV to prove the point, but it will never happen, for many reasons. But it still doesn’t change the fact that HIV is a harmless passenger virus and there is not a single piece of evidence to the contrary. If there is, show it to me, please.
And don’t direct me to wordy but meaningless self referential papers. Show me one that demonstrates causality.
Immune deficiency was almost unheard of in human populations until your “harmless passenger virus” made it into the human population. It bears a striking resemblance in genetics and mode of action to S.I.V. which causes AIDS in monkeys. Amazingly HIV,this “harmless passenger virus”, seems to cause AIDS in humans exactly as SIV causes it in monkeys.
Amazing too how those with no other risk factors than exposure to HIV from occupational sources or blood transfusions suddenly got AIDS after exposure to this “harmless passenger virus”. Amazing how it swept through the hemophiliac community as well. Are hemophiliacs suddenly risk prone for AIDS due to IV drug use and homosexuality? And why did hemophiliacs never seem to get AIDS before we started detecting HIV in human populations?
You have nothing but your own paranoid delusions of a conspiracy among those who are working diligently to find cures and treatments for disease.
Do you agree with Rev. Wright that AIDS was invented by the US government to kill blacks? Seems you are reading from the same “wackadoo” page.
Now that is the best question raised so far!!!
OK, after spending many hours reading both sides of this debate I think it's safe to say that HIV plays a very major role in AIDS, although we do not full understand how it does it.
==Unwelcome guests with master keys: how HIV enters cells and how it can be stopped.
If HIV is not the cause of AIDS, then they might as well be talking about how any number of harmless retroviruses bind to their host.
==Inhibition of Human Immunodeficiency Virus Replication by a Dual CCR5/CXCR4 Antagonist
Again, if HIV is not the cause of AIDS, this information is worthless.
==Gene fights off HIV
==Pathologists Believe They Have Pinpointed Achilles Heel Of HIV
==Catalytic antibodies to HIV: Physiological role and potential clinical utility.
More on your remaining questions later.
Heterosexual sex does not spread AIDS.
Homosexuals don’t want this info known since it might affect their funding and sympathy.
I have an idea. All known HIV infected individuals should have to register with a national database so that people could scrutinize their sexual partners IN ADVANCE. I’m sure that will happen.
Thanks for the link, but the title is misleading after reading the story.
This was your assertion:
“But they’re not. It’s not much, but it’s enough to sustain the prevalence outside their cohort through heterosexal contact and intravenous drug abuse.”
The article (and many others) refutes that:
From the article:
“Whereas once it was seen as a risk to populations everywhere, it was now recognised that, outside sub-Saharan Africa, it was confined to high-risk groups including men who have sex with men, injecting drug users, and sex workers and their clients.”
From your link (Comment section):
“Sex: From 2003 through 2006, the estimated number of HIV/AIDS cases increased approximately 5% among males and decreased 6% among females (Table 1). In 2006, males accounted for 74% of all HIV/AIDS cases among adults and adolescents. In 2006, rates were 33.8 per 100,000 among males and 11.5 per 100,000 among females (Table 5b).
Transmission category: From 2003 through 2006, the estimated number of HIV/AIDS cases increased among men who have sex with men (MSM) and remained stable among adults and adolescents with HIV infection attributed to high-risk heterosexual contact (heterosexual contact with a person known to have, or to be at high risk for, HIV infection) (Table 1). The estimated number of HIV/AIDS cases decreased among injection drug users (IDUs), MSM who were also IDUs, and among children. MSM (49%) and persons exposed through high-risk heterosexual contact (33%) accounted for 82% of all HIV/AIDS cases diagnosed in
Those numbers do not support “sustaining the prevalence” ofAIDS through heterosexual transmission.
They do support making public who has the disease so heterosexuals can avoid having sex with those individuals.
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