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AIDS (hah)

You never considered that a virus can be completely harmless and just propagate itself? Without causing its hosts any harm?

What evidence do you have that HIV acts in this way? None, of course.
 
Can't believe that we're arguing with an idiot that named himself 'W' after Cheney's monkey.

What a sleaze.
 
You never considered that a virus can be completely harmless and just propagate itself? Without causing its hosts any harm?

Sure. It happens all the time. Again, with HIV, the proof is largely in the cell biology. And the epidemiology. I totally understand that the people who are killed quickly by HIV often have other issues, so the epidemiology on it's own is questionable. But then there are things like the people (and there are lots of them) who are brought back from the brink of death with antiretrovirals. Others, of course, who die from the meds, too. More...many more...who are kept alive longer, though, than those who completely abstain from medication.

Then there are the children who are born with HIV who almost inevitably die without treatment. Seriously look into that group and most of the "HIV doesn't cause AIDS" theories start to crumble. What do you think Christine Maggiori's daughter died from? Do you think the coroner faked the autopsy? Was he "in on" the conspiracy? Then there was Cuba, where a draconian quarantine was imposed on all HIV positive people at the beginning of the epidemic. They now have no HIV and no AIDS in the country. On and on and on.
 
It is almost impossible to get the HI Virus by sexual contact.

The problem that you probably don't understand, is, the HIV tests, and how they are performed, are complete ****.

Have to say, you've picked a doozy here. Your evidence so far is fairly comprehensive, however. People like Kary Mullis can't be swept away like a Behe. He may not necessarily be right, but his opinion has to be respected.

quote from a pm I just received from troll Dab --

I raise my bet to 2000 posts.

I'd take that double and raise you to 4K that he isn't.

I see someone posting a highly controversial point, but with evidence. Trolls never do that. Well, not with respectable evidence, anyway.

Kary Mullis is an interesting guy. Loves to surf. Loves to get high--weed and acid, mostly. Loves to be a contrarian. He's had some good ideas, but isn't right if he thinks HIV doesn't cause AIDS.

When, along with getting high, he has time to win a Nobel Prize, take the award for R & D scientist of the year, plus other sundry honours, I suspect those homours say more about him than his having the occasional spliff. Sagan used to smoke dope, I believe? Is Cosmos bunkum?


Fascinating stuff so far, Dabljah. (Mind if I just call you Dubbya? Your way is a pest to type.)

Not related to John Hewitt are you?
 
Can't believe that we're arguing with an idiot that named himself 'W' after Cheney's monkey.

What a sleaze.

Well, until someone can post adequate refutation of his position, I'll continue to not consider him a complete idiot or troll. I see lots of assertion masquerading as fact in effort to refute him, but none of it's worked so far.

Is there a doctor or microbiologist in the house? Has anyone refuted Mullis' position? Seems to me Dab has taken Mullis' position on board - if that's been refuted, we can put him to bed right now.
 
People like Kary Mullis can't be swept away like a Behe. He may not necessarily be right, but his opinion has to be respected.

I'd disagree with you. Everyone from Shermer to Penn & Teller to Randi have commented that very intelligent people can fall into the woo at least as easily as anyone else. And, once they do, they use their intellect to construct very complex and elaborate rationalizations for the woo... making it more difficult to bust through.

Or, more simply: I respect Newton's work in physics, but the man was a moron when it came to religion... just 'cause someone's sharp as a tack doesn't mean they can't also be an idiot.
 
Is there a doctor or microbiologist in the house? Has anyone refuted Mullis' position? Seems to me Dab has taken Mullis' position on board - if that's been refuted, we can put him to bed right now.

Seems like we've seen some pretty good evidence, plus the evidence points towards a "conspiracy theorist crackpot" mindset... not conclusive, but really damned solid.
 
more on Kary Mullis

HIV / AIDS Controversy
Mullis has also drawn controversy for his past association with Peter Duesberg and his skepticism about the evidence for the idea that HIV causes AIDS. (For more on this topic, see also AIDS reappraisal and the interviews listed below.) As the recipient of a Nobel Prize for the PCR technique that is used to measure viral load in people with AIDS, he has often been cited by people within the AIDS dissident movement as someone who supports their views.
[edit]Global Warming
Mullis is skeptical about the concern over global warming, disagreeing with the scientific consensus that it is caused by humans, and with the idea that CFCs (chlorofluorocarbons) cause ozone depletion.
[edit]Authorship

Dr Mullis wrote the 1998 autobiography "Dancing Naked in the Mind Field", which gives an account of his initial invention of PCR, as well as providing insights into the opinions and experiences of the author. Several examples of supposedly atypical behavior for a scientist, including the use of LSD, belief in astrology, and the belief in an extraterrestrial encounter, are also chronicled within the book. These accounts have made Dr. Mullis a controversial figure within the scientific community.


I'm saying his love of being a contrarian goes beyond the occasional spliff.

This doesn't discredit him, any more than his belief in E.T. encounters.
 
Can anyone (W?) verify that Mullis still disbelieves that HIV causes AIDS?
The most recent quotes I can find are from 1998.
And there's this:

http://www.aidstruth.org/Nobel-Denial.pdf

Incidentally, it is not at all clear that Mullis still objects to the use of PCR to detect viral nucleic acids. In an exchange with HIV expert Peter McDonald in the context of the Adelaide trial of Chad Parenzee (an Australian HIV-positive man who was accused and convicted of knowingly endangering the lives of his sexual partners), Mullis wrote that PCR appears to work well and correctly observed that the validity of the technique is not dependent on his opinion, anyway. While this does not necessarily mean that Kary Mullis has entirely rejected HIV/AIDS denialism, it does suggest that denialists should be more careful when formulating his supposed pronouncements on the value of PCR.
In conclusion, apart from Kary Mullis—a dubious authority at best, and whose position seems to have changed over the years—no Nobelist denies that HIV causes AIDS

A LOT of research has been done in the past 10 years. I can almost see how in 1998 it might have still been just a wee tiny bit "open".
 
Mullis isn't even the most important AIDS critic. I'd say the most important one is Duesberg, who is a tenured professor and expert on retroviruses. His most important book is "Inventing the AIDS Epidemic"

Mind you: Intelligent people do make honest mistakes, but these mistakes are very rarely of the type where they lose their jobs over controversial opinions. Because for those type of controversial opinions and statements, you want to double-check you didn't just make a mistake somewhere in your logic.

Remember, Duesberg is the guy who first had the suggestion to look for retroviruses as a cause for cancer. A year later, he retracted that, figuring he was wrong about that. Didn't stop the cancer researchers of course. He's not the type of guy who stays on a wrong course when he knows its wrong. Kary Mullis neither does have any financial or economical reason to criticize the medical establishment for the HIV-AIDS hypothesis.

On the other hand, there's a multi, multi multi billion industry based on the HIV->AIDS assumption. Every single one of them has a good, financial reason to dismiss any evidence that point away from HIV causing diseases, and instead overstressing the threat that AIDS supposedly causes.

Conspiracy? I think you have the wrong impression of what's going on. Gallo was famous for blaming all sorts of diseases, such as alzheimers, parkinsons, and others on retroviruses, and none of his theories ever held up to the scientific scrutiny of real scientists like Duesberg in the journals. The process of science does not prevent bad science from being published, what it does is, it allows for the bad science to be eventually corrected.

1983 or so, Gallo got to talk with the president of the health department, and simply convinced her with his small presentation that the cause for the AIDS disease had been found in this retrovirus Montagnier discovered a few months earlier. The Health Department's President simply announced this to the public, and from then on, everyone went with it. Billions upon billions were granted on AIDS research, and those people would have been stupid to suddenly come out and say "Hey, HIV probably isn't the cause for this AIDS thing"

Well, only Duesberg and a few others were stupid enough. Now that is some serious scientific integrity and courage, for which I believe Duesberg should get a medal or something. Mind you, the NIH or the CDC aren't interested in disproving the AIDS myth either: They both would get much less money if infectious diseases were understood to be less of a danger.

And Africa? In africa, AIDS is just a way to get world health organization funding for old tropical diseases such as malaria. Malaria causes diarrhea, fever, and by itself can satisfy the Bangui AIDS definition. But with Malaria, the doctors, the country, and the individual do not receive as much money, as when they claim another AIDS case.

Children die to malnutrition and poor sanitation every day in the third world, but thanks to the AIDS definitions, instead of poverty, these deaths can now be attributed to a disease.
 
http://garlan.rethinkingaids.info/Cases/Parenzee/McDonald-Mullis.html

Kary Mullis said:
I will not try to convince anyone that PCR can be used successfully to specifically make multiple copies of any nucleic acid sequence that can be uniquely defined by two “primer target sequences” comprising the termini of the sequence of interest. The veracity of this no longer has anything to do with me. I think this has been confirmed by a huge number of laboratories around the world. The rapid spread of this simple technology would not have occurred had it been ineffectual or flawed in any persistent way.

The matter which you are considering, if I understand it correctly, is that the presence or absence of a given nucleic acid sequence, as determined by PCR, can be used as a reliable marker for a living organism in a biological sample. This is done quite often in scientific studies, but that does not mean there could never be exceptions. Remember scientific studies are done with the understanding that findings will be subject to scrutiny from colleagues. A nucleic acid segment very similar in size and terminal base could easily, in a cursory examination, be mistaken for the sequence in question. If this happened in the course of a normal scientific finding, somebody would finally notice it. Papers are retracted all the time. I am not aware of the nature of the evidence you are considering, but when it comes to legal issues, retractions don’t necessarily make up for the original mistake, and if I were to offer advice to the courts system of Australia, I would plead that they realize that the AIDS/HIV issue is what is not settled scientifically, not the effectiveness of PCR.
Mullis agrees that PCR is good for finding the HIV virus, but is iffy on if the HIV virus causes AIDS.

Anyway, W....do you now agree that PCR is useful for finding the HIV virus?
 
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I'd disagree with you. Everyone from Shermer to Penn & Teller to Randi have commented that very intelligent people can fall into the woo at least as easily as anyone else. And, once they do, they use their intellect to construct very complex and elaborate rationalizations for the woo... making it more difficult to bust through.

Or, more simply: I respect Newton's work in physics, but the man was a moron when it came to religion... just 'cause someone's sharp as a tack doesn't mean they can't also be an idiot.

Agree entirely. I chat to a bloke on a christian forum who's a PhD Theoretical Neuroscientist and he's unquestionably one of the smartest blokes on the planet.

He's also a raving Roman Catholic.

That said, Mullis' Nobel was in his specialist subject, which is very close to what he talks about.

Like KellyB, I'm a bit concerned that everything he raises in "evidence" is a decade old. The has certainly been an enormous amount of money spent and research into AIDS/HIV during that time, while I doubt Mullis has done much more.

Bloody interesting, though - I'd been discussing the Karposi's Sarcoma/AIDS business just a few days ago, wondering why it wasn't seen as a symptom of AIDS any longer, and how the disease/syndrome seems to keep changing shape - metaphorically speaking, from our humble human perspective. I'm no doctor, but I spot inconsistencies in stuff. Why I'm an atheist, really.

Seems like we've seen some pretty good evidence, plus the evidence points towards a "conspiracy theorist crackpot" mindset... not conclusive, but really damned solid.

Fair. Plus, it isn't as though drug companies don't feature in conspiracy theories. Unfortunately, drug companies do not have a squeaky clean image. Thalidomide, anyone?

more on Kary Mullis

Mullis is skeptical about the concern over global warming, disagreeing with the scientific consensus that it is caused by humans, and with the idea that CFCs (chlorofluorocarbons) cause ozone depletion
(bolding mine)

AGW, the jury may still be out, but only for a quick ciggie break before returning a guilty verdict, but I understand that CFC/ozone depletion was a simple chemical reaction which is well-documented? I'm no chemist either, but I recall the link being nothing else.

belief in astrology

Not good.

belief in an extraterrestrial encounter, are also chronicled within the book.[/B] These accounts have made Dr. Mullis a controversial figure within the scientific community.

I'm saying his love of being a contrarian goes beyond the occasional spliff.

Hmm. All he needs is a touch of homeopathy and he could go for the full house.

A LOT of research has been done in the past 10 years. I can almost see how in 1998 it might have still been just a wee tiny bit "open".

Agree entirely.

Looking at it dispassionately, I've seen a great deal of animosity, lack of agreement and dis/misinformation around the disease since it was first discovered.

Take this early post!

Without treatment, HIV cuts a population's average life expextancy in half. (source).

So, the current world average life expectancy is about 67 years old. (source) Without treatment, a population's average life expectancy is 33.5 years.

Debunked.

Get back under your bridge.

Now, this is statistic mining of the worst kind.

From that same page, I will mine a few things:

what is the life expectancy of someone with HIV? We don't know exactly

Well, if you don't know, you don't know... How then does that back up an assertion that HIV cuts life expectancy in half?

What we are starting to see is that deaths among people with HIV are now caused more and more by things like injuries and heart attacks, rather than by AIDS

Not all that compelling, but gets worse with:

Heart disease may be related to HIV or its treatments,

So let's make our first guess that the AIDS or the treatment is causing it? Don't we ask first and decide second? They may well be right, but it would be nice to put the data before the hypoethesis.

More:

but it seems that if people have their cholesterol monitored and take medication to lower it as needed, stop smoking, and take care of other risk factors like high blood pressure, the risk of heart attack should be greatly reduced.

Very good, positive changes in diet and smoking and other dangerous habits will make you live longer! This is new?

Cut to the chase:

Dabjah:

Do you have any hard data to back up your position, other than the out-of-date stuff by Mullis?

Anyone else:

Why is Kenya's AIDS rate dropping so quickly? HIV/AIDS prevalence was 6.7 percent in 2004, down from about 10 percent in the late 1990s

Given that the AIDS rate - blamed for most of Africa's ills - is dropping so quickly, it should have an immediate impact on life expectancy.

Funny how Kenya's is still decreasing:

Average life expectancy
2004 47.5 years UNDP - Human Development Report 2006
2003 47.2 years UNDP - Human Development Report 2005
2002 45.2 years UNDP - Human Development Report 2004
2001 46.4 years UNDP - Human Development Report 2003
2000 50.8 years UNDP - Human Development Report 2002

link

Why do some people have vastly reduced CD4 cells and not contract AIDS?
 
From a CIA plot/accident (HIV was supposedly a mutant version of smallpox vaccine) to HIV hasn't really been "proved" as the cause of HIV-AIDS....the human psyche is so bizarre. There must be some sort of neurosis that affects people like Behe (irreducible complexity) and Mullis, some as yet inexplicable desire to be 'the one' who went against the establishment and was vindicated. Trouble is, a few people actually had evidence such as Darwin or Wegener (plate tectonics), but people like Behe and Mullis only have a fantasy. Yet the fact they have some university degree or Nobel Prize gives people who are looking for reinforcement of denial or of some anti-establishment conspiracy belief a cause celebre.

Here are a few debunking web sites of this particular nonsense and Dabljuh's twisted logic.

AIDS Denial is Pseudoscience is a very thorough web site with multiple links including this one: AIDSTruth.org.

AIDSTruth has a list of most of the most prominent AIDS Denialists and addresses their unsupported claims.
Pareto's Law would predict that 20% or fewer of the denialists would account for 80% or more of the denialist activity. Below are some of the more notorious members of the first category.


THE AIDS DENIERS, (By Jim Nelson; GQ Sept. 2001), is an interesting short story, non-fiction, about a couple of HIV Denialists that are now both dead from HIV-AIDS. One died in 2004 and one just this year according to aidstruth.org's list of AIDS Denialists that have died of AIDS.
Michael Bellefountaine - A member of the denialist ACT UP/San Francisco, Michael Bellafontaine died on May 10, 2007. He was 41. His Bay Area Reporter obituary said that "According to Andrea Lindsay, a friend and fellow activist, Mr. Bellefountaine died of a sudden systemic infection, though the exact cause has not been determined." (http://ebar.com/obituaries/index.php?sec=ob&article=252)

David Pasquarelli - David Pasquarelli, a leader of the denialist group "ACT UP San Francisco" developed PCP, anemia, thrush, meningitis, mycobacterium and disseminated CMV before he died in March of 2004. He was 37. (http://www.davidpasquarelli.com)


Mother Jones had an article on The Foo Fighters front man Dave Grohl, another AIDS Denialist with a public microphone, (Feb 2000).

And here's a skeptical review of Mullis' "Dancing Naked in the Mind Field".

And as for Duesberg, the following excerpts are from a review in Nature of his 1996 book, Inventing the AIDS Virus. A decade more has not led to any supporting evidence for this tripe.
According to Bryan Ellison, who co-wrote with Peter Duesberg an earlier version of Inventing the AIDS Virus, the U.S. Central Intelligence Agency (CIA) tried to suppress the publication of this book. I can't think why they would want to bother. But conspiracy theories so pervade the book and that I shouldn't be in the least surprised if Oliver Stone does the movie.

Duesberg's central thesis is that the human immunodeficiency virus (HIV) is a harmless virus, and that life-style (especially recreational drug use) is the principal reason why people die of AIDS. The use of AZT as an AIDS therapy is blamed for exacerbating the problem. In the first section of his book, Duesberg tells the story of an obscure syndrome (SMON) that was present in Japan from the 1950s to the 1970s. Despite persistent theories of a viral cause, SMON was found to be a toxicological problem caused by anti-diarrhoea drugs sometimes used to treat SMON symptoms. Duesberg draws an analogy from these events to AIDS, with AZT analogous to the anti-diarrhoea drugs. An interesting tale, but documenting this and a few other old medical mistakes scarcely proves that AZT causes AIDS and that HIV is a mere passenger virus. But according to Duesberg, "No fatal viral disease is known to cause death in nearly all infected people -- except the paradoxical 'AIDS virus'." Try telling that to those who came across Ebola-Zäire; their mortality rate was about 80 per cent, for this virus is literally more lethal than a bullet in the head.
Rabies is close to 100% fatal in humans and the only known survivor was treated with Rabies Immune Globulin very early on. And the AZT hypothesis is so ridiculous since it wasn't even used until HIV-AIDS was well into a full blown pandemic, not to mention all the people in third world countries with HIV-AIDS who haven't had access to any anti-retrovirals, ever.

The review goes on to say
The book contains no new revelations on the 'non-link' between HIV and AIDS since September 1995, when the US National Institute of Allergy and Infectious Diseases released its 61-page document on The Relationship Between the Human Immunodeficiency Virus and the Acquired Immunodeficiency Syndrome. This contains all the facts, and I strongly recommend people to read it. Of course, seeing that it was written by government scientists, it will no doubt be dismissed by Duesberg's sympathizers as part of a continuing cover-up. For according to Duesberg, the AIDS epidemic became the "salvation" of the Centers for Disease Control (CDC). The Epidemic Intelligence Service (EIS) of the CDC is described as the "medical CIA" and ex-members are said to "have obtained prominent positions in the media". One even edits a scientific journal. How sinister! Whatever next? Essentially, Duesberg's case is that the fundamental purpose of the CDC is to invent medical emergencies for the National Institutes of Health to resolve - anything is justified so long as the tax dollars just keep on rollin'. Implicit, and often explicit, is that tens of thousands of health-care professionals and research scientists are either too stupid to realize that HIV is not the cause of AIDS, or too venal to do anything about it for fear of losing income from the government or drug companies.

Duesberg mounts an assault on the virology "establishment", with special emphasis on the tumour virologists of the 1960s and 1970s. Researchers mistakes, real and opined, are gleefully documented - a veritable virological Who's Who is castigated. And the trend continues when the HIV section is finally reached. There, all the 'big name' retrovirologists of the 1980s are targeted, and the early scandals of AIDS research are picked over yet again. So many scientists and so many of the "mistakes" are listed that I was eventually reminded of the old joke about the brigade of guards on parade, with one little guardsman horribly out of step. When the drill sergeant bawls at him, an old lady attacks him with an umbrella saying: "Leave him alone, my boy Peter is in step, it's all them other so-and-so's what are the problem!" All this ancient history is very entertaining, but it hardly seems central to the purpose of the book. Or is it?

Although some vengeance might be expected from a virologist whose eminent career was ended by the AIDS epidemic, one might have wished for a better understanding of modern virology from Duesberg. One of his main complaints about HIV and other 'slow' viruses is that they "violate the laws of virology". But what are these laws? Was it carved in stone that the Lord God spake unto the retroviridiae and commanded: "Thou shalt not kill"? The great beauty of biology - indeed, of science in general - is that as knowledge advances, so paradigms shift; if HIV acts differently from the viruses Duesberg grew up with, what of it? And herein, I suspect, lies the basic problem: Duesberg clearly has an outstanding knowledge of the relatively simple avian leukaemia viruses with which he made his professional reputation. But he draws his views on how HIV 'should' behave from his early research experience; he has never published any papers based on his own work with HIV at the laboratory bench. Reading the AIDS literature can take one only so far: experimenting gives active researchers a whole new dimension to their knowledge.

I can list here only a few of the more egregious examples of Duesberg's misunderstanding of HIV virology. He states that "retroviruses do not kill cells". This assertion is not even correct for all avian leukaemia viruses, and anyone who has cultured HIV can attest to its prominent cytopathic effects. HIV is not a leukaemia (onco)virus; it is a lentivirus, and behaves distinctly differently from the oncoviruses both in vivo and in vitro. To extrapolate from avian leukaemia virus to HIV is like asserting that because one can stroke a pussy-cat with impunity, it is perfectly safe to put one's head in a lion's mouth. Duesberg sees a fatal paradox in the fact that HIV can be grown in permanently infected, immortal T-cell lines in vitro, yet is supposed to cause AIDS by killing T cells in vivo. There is no such paradox. When a chronically infected cell culture is started, clones of cells relatively resistant to the cytopathic effects of HIV are gradually selected for and eventually take over the culture. There can also be some adaptation of the cells (and virus) to the culture conditions. The principal phenotypic change in the cells is a partial reduction in the surface expression of the HIV receptor, which reduces the extent of cell-killing in the culture. But the HIV produced in these cultures is still highly cytopathic when plated back onto unadapted primary T cells. And sadly, HIV produced from permanent cell lines is pathogenic in vivo – it is today causing disease in at least one accidentally infected laboratory worker.

Duesberg writes: "Only rare luck … can extract HIV from an antibody-positive person". Perhaps I should get the technicians in our laboratory to buy my lottery tickets; they succeed in isolating HIV almost every time they try. Many of Duesberg's problems with the pathogenic effects of HIV seem to lie in his belief that HIV is dormant in vivo, that HIV-infected people "never have more than one in every 10,000 T-cells actively producing copies of the virus". This old canard, derived from research in the mid-1980s, has long since been proved incorrect. In the early days of HIV research, analytical techniques were obviously more primitive than they are now, so why still rely on them? The true figure for the frequency of infected cells is more like 1 in 100, although there is a wide range, depending on the state of disease progression. The documented loss of more than a hundred million T cells a day as a result of the generation of more than a billion virus particles a day attests to the virulence of HIV.

...

Duesberg believes that HIV is essentially not a sexually transmitted virus; indeed, the very cover of his book states that "AIDS is not sexually transmitted". Instead, he argues that "HIV has been passed along from mother to child for many centuries". The first statement ignores the entire body of data on the epidemiology of HIV spread in the United States and Europe, whereas the second ignores the death rate among children infected by HIV from their mothers; only a tragically small proportion of these children survive long enough to have the chance of having children of their own. How could transmission from mother to child permit sustained HIV spread under these conditions?

....

Duesberg wraps together his twisted facts and illogical lines of argument to create a tangled web to trap the unwary, desperate or gullible. But however much he attempts to gild his writings with philosophies of scientific truth, the reality is that his premises are based not on facts but on faith: faith that he is right, and that everyone else is wrong. This was his position long before AIDS appeared, as tumour virologists know well.

Duesberg ends by detailing his ostracism by the virology community, his inability to get research funding, the personal snubs he has suffered. The advent of HIV has clearly been a personal tragedy for a once highly respected retrovirologist, but one's sympathy must of course be tempered by thoughts of those for whom AIDS has been a rather greater personal tragedy. Three years ago, I likened Duesberg to the Black Knight from "Monty Python and the Holy Grail". This character had his limbs hacked off one by one, but the game little torso tried to bite the knee-caps from his assailant. The events of the past few years have extracted the Black Knight's teeth, leaving him with the sole recourse of spitting at those whose views of virology have differed from his over the past two decades. But where the spittle lands is on the graves of those millions of people killed by HIV, and on those it has yet to slaughter. How sad, and how ultimately pathetic.
Looks like a pretty agenda/sour grapes driven mentality.

What's your beef, Dabljuh? Denying your own HIV? Have some anti-establishment conspiracy belief underlying your attraction to pseudoscience?

As someone who grew up during a war 'against the establishment', I'm really annoyed that so many people think mainstream science is the equivalent of the 'establishment'. That's an image we need to change if we are ever going to reach some of these conspiracy theorists.
 
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Bloody interesting, though - I'd been discussing the Karposi's Sarcoma/AIDS business just a few days ago, wondering why it wasn't seen as a symptom of AIDS any longer, and how the disease/syndrome seems to keep changing shape - metaphorically speaking, from our humble human perspective. I'm no doctor, but I spot inconsistencies in stuff. Why I'm an atheist, really.

Let's you and I play a game, shall we? You seem bright, skeptical, and also intuitive enough to follow along with the general sort of path my mind takes. So, let's dissect an area of the HIV/AIDS issue.

Unless it kills it's host slowly.
If HIV had emerged in a way that led to a quick death for it's host, it, too, would have probably killed itself off. Or attenuated itself over time to become less lethal.
It survives because it acts slowly, though.

Except, of course, that AIDS did NOT "act slowly" in the early 1980s. Once you developed Kaposi's Sarcoma, you were dead in under a year, 99.999% of the time. The fact that suppression of the HIV virus also slows the mortality of KS is yet another bit of proof of the HIV/AIDS connection. Further, the fact that the advent of AIDS treatments has reduced the occurrence of KS can be seen as a coincidence only by the most die hard of HIV/AIDS denial crackpots.

Let's look more closely at the claim made by kellyb, that HIV/AIDS didn't burn itself out by killing its hosts because it "killed slowly". That is false, based on the evidence. However, there are two ways a virus can survive and thrive within a population: kill slowly, or spread quickly. HIV had a perfect host population among the gay/IV drug user populations. it could kill relatively quickly, because each host could spread the disease to dozens before showing any outward symptoms.

This also explains the "changing shape" you've noticed. The virus has gone from spreading rapidly/killing rapidly to spreading slowly/killing slowly.... so we can logically expect a significant shift in the way it presents.
 
The Atheist said:
Anyone else:

Why is Kenya's AIDS rate dropping so quickly?

http://www.medicalnewstoday.com/medicalnews.php?newsid=54309

HIV prevalence in Kenya has declined to 5.9% this year from 6.1% last year, and HIV prevalence among women in the country is 7.7%, compared with 4% among men, according to statistics released Wednesday by Kenya's National Aids Control Council, the East African Standard/AllAfrica.com reports (Mwai, East African Standard/AllAfrica.com, 10/12). NACC Acting Director Alloys Orago speaking Wednesday in Kenya's capital, Nairobi, attributed the decrease to several initiatives, including voluntary HIV testing and counseling and programs to prevent mother-to-child HIV transmission
http://209.85.165.104/search?q=cach...+AIDS+Strategic+Plan&hl=en&ct=clnk&cd=3&gl=us

HIV/AIDS continues to be a major challenge to our socio-economic development. Since the first case was discovered in 1984, it is estimated that over 1.5 million people have died due to AIDS-related illnesses, resulting into 1.8 million children left as orphans. It is also estimated that 1.4 million people are living with the HIV today.

However, there is hope, as we have noted a decline in the HIV prevalence which reached a peak of 14 percent in 2000, and which has fallen to 7 percent in 2004, due to successful multi-sectoral responses including the fact that HIV/AIDS has now become everybody’s concern. The scale up in condom uptake, voluntary counselling and testing services, antiretroviral therapy, and increased co-ordination among stakeholders is expected to result into a further reduction in HIV prevalence.

Basically, a more complete understanding of how HIV "works" and the suggested interventions are obviously having a positive effect. Not great, mind you. But better than nothing.

Given that the AIDS rate - blamed for most of Africa's ills - is dropping so quickly, it should have an immediate impact on life expectancy.

Funny how Kenya's is still decreasing:

Average life expectancy
2004 47.5 years UNDP - Human Development Report 2006
2003 47.2 years UNDP - Human Development Report 2005
2002 45.2 years UNDP - Human Development Report 2004
2001 46.4 years UNDP - Human Development Report 2003
2000 50.8 years UNDP - Human Development Report 2002

The UNICEF link explains it. They've had a long drought, and a lot of war. They're dying from starvation and violence, and a small decrease in HIV prevalence isn't going to eclipse that. Also, a lot of HIV infected individuals are dying, and apparently no longer quite replacing themselves with one or more new infections there so quickly before death.
Make sense?
 
There must be some sort of neurosis that affects people like Behe (irreducible complexity) and Mullis, some as yet inexplicable desire to be 'the one' who went against the establishment and was vindicated.
My current bet leans towards the sort of Joseph Campbell "hero monomyth", most currently seen in the Matrix movies, where each conspiracy theory nutball sees himself as the next "Neo", fighting unseen malevolent forces in order to bring the truth to the brainwashed masses.
 
Joe said:
Except, of course, that AIDS did NOT "act slowly" in the early 1980s. Once you developed Kaposi's Sarcoma, you were dead in under a year, 99.999% of the time. The fact that suppression of the HIV virus also slows the mortality of KS is yet another bit of proof of the HIV/AIDS connection

Compared to most viruses, that's still slow. Very slow. Many or most deadly viruses, if they're going to kill you, do it within a matter of weeks. Sometimes days. Any time you're talking about a virus that takes more than a year...with a looooog asymptomatic phase where you can infect who knows how many people before you show any symptoms, it's slow for a virus.
 
Viruses don't have a metabolism on their own. But they can infect cells and have them produce toxins. I don't know the details of the hepatitis viruses, I simply assumed that the destructive process was more toxic than mechanical in nature.

Maybe I can help you out here... :wackynah:

Hepatitis viruses replicate in the liver cells. The real damage is a result of the immune reaction of the body against the virus, which also destroys the liver cells (carrying the antigens of the virus). The transformation into HCC (hepatocellular carcinoma) is slightly different from that: it's the incorporation of viral DNA and mutagenesis of the cellular DNA leading to cancer.

If you give someone with Hepatitis corticosteroids, the liver damage will decrease, but the viral load will increase dramatically and infect more and more cells, so you will end up dying anyway from the viral load that eventually will trigger a response with disastrous effects. Therefore, we never give corticosteroids.

Getting rid of one type does not always protect you from another type. Hepatitis B is often found with C in chronic infections. Often the chance to have the other when you have one of them is greater (same risk groups). Reduced immunity (not vaccinated), may make you more vulnerable...etcetera...

You see many roads (immune reaction, additional infection, viral load) lead to the same end result: you die from the virus.
That's why the definitions are often rather complex for chronic infections with viruses.

Feel free to ask any question, but I really have more important things to do then fight conspiracy believers. Glaxo-Wellcome has done less then admirable things in Africa, maybe that is your problem or maybe you are one of the few that honestly believe or wish to believe that HIV and AIDS are something else then what current science says they are. I think you are missing the point that science is something that evolves and is led by evidence that usually convinces most of the scientists in time after careful consideration.

It's not democratic rule nor a popularity contest, your preference or mine for a specific "truth" or outcome are completely irrelevant, they bare no weight at all.

SYL :)
 
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....Bloody interesting, though - I'd been discussing the Karposi's Sarcoma/AIDS business just a few days ago, wondering why it wasn't seen as a symptom of AIDS any longer, and how the disease/syndrome seems to keep changing shape - metaphorically speaking, from our humble human perspective. I'm no doctor, but I spot inconsistencies in stuff. Why I'm an atheist, really.
This article sheds some light on your questions about the changing pattern of Karposi's epidemiology. HHV-8 and Kaposi's Sarcoma: Epidemiology, Transmission, and Therapy
Alexandra M. Levine, MD

The etiology of Kaposi's sarcoma (KS) is complex and multifactorial.[1] Underlying immunosuppression clearly increases the risk of KS; thus, the incidence of KS in organ transplant recipients receiving immunosuppressive therapy is 400-500 times higher than that in the general population. Genetic factors related to various immune functions may also play a role.[2,3]

Aside from immunosuppression, infection by human herpesvirus type 8 (HHV-8; also known as Kaposi's sarcoma-associated herpesvirus [KSHV]) is required for the development of KS in humans.[4] Genomic material from HHV-8 is found within tissues from virtually all types of KS, including AIDS-KS, classic Mediterranean KS, endemic KS from Africa, and transplantation-associated KS. A number of HHV-8-encoded gene products have been identified which have the capability to induce the multiple aberrations found microscopically within KS tissues and macroscopically within affected patients.
Transmission of HHV-8

Several studies of men who have sex with men (MSM) have shown that HHV-8 may be transmitted sexually.[5] Thus, increasing numbers of sexual partners, history of a sexually transmitted disease, and presence of underlying HIV infection are all risk factors for HHV-8 infection among MSM.[6,7] Deep kissing, sex with a partner with KS, and use of inhaled nitrites or amyl nitrite capsules are also risk factors for HHV-8 infection among HIV-negative MSM without KS.[8] Increasing numbers of heterosexual partners is a risk factor for HHV-8 infection among heterosexual persons studied in Africa.[9]

Recent data have also identified infected saliva as a potential source of HHV-8 transmission.[8,10] Investigators at the University of Washington, Seattle, looked for the presence of HHV-8 in various anatomic sites and secretions from a group of 50 HHV-8-infected men without KS.[8] Of interest, saliva was the secretion that was the most consistently infected over time, with HHV-8 detected in 34% of oropharyngeal samples, 0.3% of urethral swabs, 1% of anal swabs, and 5% of semen samples. Furthermore, the titers of HHV-8 in mucosal pharyngeal swabs and saliva were 2-3 logs higher than those found in semen, prostatic secretions, or anal-rectal swabs.

The discovery that HHV-8 may be transmitted by infected saliva may explain the increased risk of KS among MSM who engage in deep kissing[8] or oroanal sexual contact,[11] and may also explain the widespread epidemic of KS among children in Africa. In this regard, Sitas and colleagues[12] have shown a relationship between maternal HHV-8 infection and HHV-8 infection among their children, with no statistically significant relationship to the father's HHV-8 status. These children appear to acquire HHV-8 infection at some stage after birth, with increasing rates of infection over time. Sexual or parenteral routes of HHV-8 transmission would be most unlikely in these children. Salivary transmission is possible, however. In resource-rich areas of the world, the weaning of children from milk to solid foods is accomplished with the use of commercially available blended baby foods. Such products are not available in resource-poor regions, where mothers commonly premasticate the food for their infants, depositing this food, admixed with maternal saliva, into the baby's mouth. It is possible that the epidemic of KS in African children may have evolved from this practice.
New Data on HHV-8 Transmission

In an attempt to study the transmission of HHV-8 from mothers to their children, Phiri and colleagues[13] studied 3136 mother-infant pairs from Zambia, Africa. The overall seroprevalence of HHV-8 in the mothers at time of delivery was 40% (1259 of 3136), and 30% were HIV-1-seropositive. HIV-1-infected mothers were more likely to be infected with HHV-8 than were HIV-1-seronegative women. A cohort of 494 mother-infant pairs was studied again 12 months after delivery. The HIV-1 seroconversion rate in the mothers was 3% during the year, and the HHV-8 seroconversion rate was 10% during the same period. Among the infants, 20% developed new HHV-8 infections and 8% seroconverted to HIV-1. HHV-8 transmission was more likely in infants whose mothers were coinfected with both HIV-1 and HHV-8. All infants in the study had been breast-fed, although information was not available regarding presence of HHV-8 within breast milk per se. It is of interest that the infants were more likely to develop HHV-8 infection (20%) than HIV-1 infection (8%) during their first 12 months of life. Furthermore, HHV-8 infection appears quite prevalent among Zambian women and their children.

Webster-Cyriaque and colleagues[14] from the University of North Carolina at Chapel Hill studied the presence of the HHV-8 genome within throat washings, peripheral blood, and buccal scrapings from a group of immunocompetent, HIV-negative, HHV-8-seropositive patients in the United States, who did not have clinical evidence of KS. Presence of HHV-8 latency-associated nuclear antigen (LANA) was detected in the majority of buccal epithelial cell specimens of these individuals, indicating that the saliva may be a potential source of HHV-8 transmission within the general population of immunocompetent individuals.

The prevalence of HHV-8 infection among 192 healthy blood donors in the United Kingdom was studied by Kumar and colleagues.[15] This study differed from previous studies in that both serologic methods and direct PCR of peripheral blood mononuclear cells were employed. A nested PCR method was used to amplify a 172-base-pair fragment of ORF 26 and a 246-base-pair fragment of the VR1 region of K1. A total of 16% (31 of 192 individuals) tested positive for the presence of the HHV-8 genome, with subsequent confirmation by sequencing. A total of 34% were seropositive for HHV-8, while 42% were seropositive for cytomegalovirus, 87% for Epstein-Barr virus, 21% for herpes simplex virus (HSV) type 1, and 1% for HSV-2. This study again demonstrates the fact that healthy, immunocompetent individuals may be infected by HHV-8, without clinical illness.

Epidemiology of KS in the Era of HAART

One of the most fascinating outcomes of the widespread use of highly active antiretroviral therapy (HAART) in the United States and Europe has been the remarkable decline in Kaposi's sarcoma. Thus, in the Multicenter AIDS Cohort Study (MACS) of MSM, rates of KS fell by 66% when comparing the periods 1989-1994 and 1996-1997, coincident with the period in which HAART use increased substantially.[16] In the Swiss HIV Cohort Study, Ledergerber and colleagues[17] demonstrated a substantial reduction in incident cases of KS, with a relative risk of 0.08 when comparing data from 1992-1994 with data from July 1997 to June 1998, after the introduction of HAART. Similar data were reported from a large international collaborative study that evaluated cancer incidence data from 23 prospective studies, including 47,936 HIV-infected individuals from North America, Europe, and Australia.[18] In this study, the adjusted incidence rate for KS declined from 15.2 per 1000 person-years in 1992-1996 to 4.9 per 1000 person-years in 1997-1999, representing a rate ratio of 0.32.

The remarkable decline in the incidence of KS in the era of HAART could be explained by the ability of potent antiretroviral therapy to inhibit HIV replication and ameliorate HIV-induced immunosuppression. An alternative possibility, however, is that HHV-8 prevalence and transmission rates may have fallen within the same time interval. To address this issue, Osmond and colleagues[19] recently studied the prevalence of HHV-8 infection among MSM in San Francisco, California, over time, using blood samples acquired in 1978-1979, 1984-1985, and 1995-1996. Of interest, the prevalence of HHV-8 infection was 26.5% in 1978-1979 and remained essentially unchanged over time. In contrast, the prevalence of HIV infection declined from 49.5% in 1984-1985 to 17.6% in 1992-1993. With regard to sexual behaviors, the rates of unprotected oral intercourse remained relatively constant over time (60% to 90%) but the proportion of men practicing unprotected receptive anal intercourse decreased from 54% in 1984 to 11% in 1993. These data would suggest that the decline in KS documented in the HAART era is not due to any significant decrease in the prevalence of HHV-8, or to any change in the sexual behaviors (oral-anal contact) that are thought to be operative in terms of HHV-8 transmission. Instead, the recent decline in KS is likely to a consequence of the improved immune function and decrease in HIV-1 viral load induced by HAART.

Use of HAART to Treat KS

In light of the significant decline in KS incidence coinciding with the widespread use of HAART,[17,18] and the known importance of the HIV tat gene and its protein product in the pathogenesis of AIDS-related KS, the efficacy of HAART as a specific treatment for KS has been entertained. At this time, no prospective trials addressing this issue have been completed. However, there are several anecdotal reports of KS regression in patients receiving HAART alone.[20-22]

A recent study of 78 patients with AIDS-related KS, who had previously received therapy for KS, sought to determine the time to treatment failure both before and after the initiation of HAART therapy.[23] The median time to KS treatment failure before starting HAART was 6 months. In contrast, the median time to KS treatment failure from the start of HAART was 1.7 years (P < .001). Of interest, loss of HIV viral control (defined as HIV-1 RNA levels > 5000 copies/mL) was associated with a statistically increased risk of requiring therapy for KS, but change in CD4+ cell count was not.

Several new studies of the impact of HAART on KS were presented at the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies. To illuminate the ability of specific types of antiretroviral agent to treat known KS, Bower and colleagues[24] reported their experience with a cohort of 8640 HIV-infected patients cared for at the Chelsea and Westminster Hospital in London, United Kingdom. Of these patients, 1204 were diagnosed with KS, including 198 cases diagnosed after 1996 when HAART became widely available. The incidence of KS within the cohort was as high as 30 cases per 1000 person-years of follow-up from the 1980s through 1995, then fell to 7.6 cases per 1000 person-years during 1995-1996, when dual antiretroviral therapy was commonly administered. Most recently, the incidence fell to 0.03 cases per 1000 person-years between 1997 and 2001, when HAART was routinely administered. With regard to the characteristics of the underlying HIV-1 disease, no differences between the pre-HAART and post-HAART era were observed in terms of nadir CD4+ cell counts or CD4+ cell count at the time of KS diagnosis; however, patients with KS diagnosed in later time periods were statistically more likely to have KS as their first AIDS-defining diagnosis. Univariate and multivariate analyses were performed to determine the factors associated with the diagnosis of KS since 1996. Factors included in the model were age, gender, ethnic origin, nadir CD4+ cell count, most recent CD8+ cell count (as a surrogate for presence of cytotoxic T lymphocytes), and antiretroviral drug exposure. In the multivariate analysis, the factors that were statistically associated with an increased risk of Ks were age (2% increased risk of KS per year older at entry into the cohort), a nadir CD4+ cell count < 150 cells/mm3, and lack of antiretroviral drug exposure. Of interest, the rate ratios for KS were statistically decreased for all types of antiretroviral drug use, as shown in Table 1.
This study is of importance in defining the factors associated with KS in the era of HAART. It is clear that the majority of these patients have simply not been receiving HAART, and among those who are treated, development of KS is associated with virologic and immunologic treatment failure. This study thus emphasizes, once again, the importance of effective antiretroviral therapy in preventing the development of KS. Moreover, apparently any effective antiretroviral regimen will likely be efficacious in preventing KS.
Update: Therapy of AIDS-Related KS
Phase 3 Study of IM 862

Several papers were presented regarding treatment options for patients with AIDS-related KS (AIDS-KS). Ariela Noy[25] presented data from the National Cancer Institute (NCI)-sponsored AIDS Malignancy Consortium regarding IM 862, a compound initially isolated from extracts of the thymus glands of cows in Russia and used as an immune adjuvant in that country. Initial work by Gill and colleagues indicated that this dipeptide had antiangiogenic properties, and a subsequent randomized phase 2 trial[26] in 44 patients with advanced AIDS-KS documented a response rate of 36%, following administration of a fixed dose of 5 mg given intranasally either every other day or in 5-days-on, 5-days-off cycles. In an attempt to ascertain the potential value of IM 862 in patients with AIDS-KS, Noy and colleagues[25] initiated a phase 3 study of IM 862 (5 mg intranasally every other day) vs placebo. A total of 202 patients were enrolled between December 1998 and February 2001. Eligibility criteria included biopsy-proven KS with 5 or more measurable lesions on skin or mucus membranes in patients who were not believed to require systemic chemotherapy. Antiretroviral therapy was required to be unchanged for at least 8 weeks before enrollment, to exclude the possibility that any effect might have been due to effective HAART. The baseline characteristics and results are summarized in Table 3.


References

1. Antman K, Chang Y. Kaposi's sarcoma. N Engl J Med. 2000;342:1027-1038.
2. Lehrnbecher T, Foster CB, Zhu S. Variant genotypes of Fc gamma RIIIA influence the development of Kaposi's sarcoma in HIV infected men. Blood. 2000;95:2386-2390.
3. Nagy K, Kemeny B, Horvath A. HIV co-receptor mutation affects course of Kaposi's sarcoma in HIV/HHV8 positive patients. Program and abstracts of the 1st IAS Conference on HIV Pathogenesis and Treatment; July 8-11, 2002; Buenos Aires, Argentina. Abstract 274.
4. Chang Y, Cesarman E, Pessin MS, et al. Identification of herpesvirus-like DNA sequences in AIDS-associated Kaposi's sarcoma. Science. 1994;266:1865-1869.
5. Gao S-J, Kingsley L, Hoover DR, et al. Seroconversion to antibodies against Kaposi's sarcoma associated herpesvirus-related latent nuclear antigens before the development of Kaposi's sarcoma. N Engl J Med. 1996;335:233-241.
6. Martin J, Ganem DE, Osmond DH, et al. Sexual transmission and the natural history of human herpesvirus 8 infection. N Engl J Med. 1998;338:948-954.
7. Grulich AE, Olsen SJ, Luo K, et al. Kaposi's sarcoma-associated herpesvirus: A sexually transmissible infection? J Acquir Immune Defic Syndr Hum Retrovirol. 1999;20:387-393.
8. Pauk J, Huang-M-L, Brodie SJ, et al. Mucosal shedding of human herpesvirus 8 in men. N Engl J Med. 2000;343:1369-1377.
9. Sitas F, Carrara H, Beral V, et al. Antibodies against human herpesvirus 8 in black South African patients with cancer. N Engl J Med. 1999;340:1863-1871.
10. Brodie SJ, Johnson A, Vieira J, Coelle D, Wald A, Corey L. Oral shedding and propagation of HHV8 in pharyngeal lymphoid tissues: Potential cofactor role of HIV. Program and abstracts of the 5th International AIDS Malignancy Conference; April 23-25, 2001; Bethesda, Maryland. Abstract 48.
11. Grulich AE, Kaldor JM, Hendry O, et al. Risk of Kaposi's sarcoma and oro-anal sexual contact. Am J Epidemiol. 1997;145:673-679.
12. Sitas F, Newton R, Boshoff C. Increasing probability of mother-to-child transmission of HHV8 with increasing maternal antibody titer for HHV8. N Engl J Med. 1999;340:1923.
13. Phiri S, Brayfield B, Muyanga J, et al. Kaposi's sarcoma associated herpesvirus (KSHV/HHV-8) and HIV-1 infections in a cohort of mother/infant pairs in Zambia. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 18.
14. Webster-Cyriaque J, Quinlivin EB, Kendrick K. Detection of KSHV in the saliva of immunocompetent and immunosuppressed individuals. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 25.
15. Kumar N, Porter SR, Teo CG. Prevalence of HHV-8 in healthy blood donors. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 39.
16. Palella FJ Jr, Delaney KM, Moorman AC, et al. Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. N Engl J Med. 1998;338:853-860.
17. Ledergerber B, Telenti A, Effer M. Risk of HIV related Kaposi's sarcoma and non-Hodgkin's lymphoma with potent anti-retroviral therapy: Prospective cohort study. BMJ. 1999;319:23-24.
18. International Collaboration on HIV and Cancer. Highly active antiretroviral therapy and incidence of cancer in human immunodeficiency virus infected adults. J Natl Cancer Inst. 2000;92:1823-1830.
19. Osmond DH, Buchbinder S, Cheng A, et al. Prevalence of Kaposi's sarcoma associated herpesvirus infection in homosexual men at beginning of and during the HIV epidemic. JAMA. 2002;287:221-225.
20. Tavio M, Nasti G, Spina M, Errante D, Vaccher E, Tirelli U. Highly active antiretroviral therapy in HIV related Kaposi's sarcoma. Ann Oncol. 1998;9:923.
21. Lebbe C, Blum L, Pellet C, et al. Clinical and biological impact of antiretroviral therapy with protease inhibitors on HIV related Kaposi's sarcoma. AIDS. 1998;12:F45-F49.
22. Conant MA, Opp KM, Poretz D et al. Reduction of Kaposi's sarcoma lesions following treatment of AIDS with ritonavir. AIDS. 1997;11:1300-1301.
23. Bower M, Fox P, Fife K, Gill J, Nelson M, Gazzard B. Highly active antiretroviral therapy prolongs time to treatment failure in Kaposi's sarcoma. AIDS. 1999;13:2105-2111.
24. Bower M, Portsmouth SD, Mandalia S, Nelson M, Gazzard BG. HIV-1 related Kaposi's sarcoma n the highly active antiretroviral therapy (HAART) era. Nonnucleoside reverse transcriptase inhibitors are as effective at preventing KS as protease inhibitors. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 4.
25. Noy A, Gill P, Scadden D, et al. Angiogenesis inhibitor IM 862 is ineffective against AIDS-KS in a randomized, placebo controlled trial. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 5.
26. Tulpule A, Scadden DT, Espina BM, et al. Results of a randomized study of IM862 nasal solution in the treatment of AIDS related Kaposi's sarcoma. J Clin Oncol. 2000;8:716-723.
27. Gill PS, Wernz J, Scadden DT, et al. Randomized phase III trial of liposomal daunorubicin (DaunoXome) versus doxorubicin, bleomycin, vincristine (ABV) in AIDS-related Kaposi's sarcoma. J Clin Oncol. 1996;14:2353-2364.
28. Northfelt DW, Dezube B, Thommes JA, et al. Pegylated liposomal doxorubicin versus doxorubicin, bleomycin and vincristine in the treatment of AIDS related Kaposi's sarcoma: Results of a randomized phase III clinical trial. J Clin Oncol. 1998;16:2445-2451.
29. Little RF, Aleman K, Pluda JM, et al. Preliminary results of combination liposomal doxorubicin and interleukin-12 (IL12) followed by chronic IL-12 maintenance therapy in advanced AIDS related Kaposi's sarcoma. Program and abstracts of the 6th International Conference on Malignancies in AIDS & Other Immunodeficiencies; April 22-24, 2002; Bethesda, Maryland. Abstract 6.
Edited, I put most of the article here sans the tables and last couple paragraphs since the link wants you to log in. When I found the article via Google, no log in was required. (I am not registered with Medscape myself.)

....Why is Kenya's AIDS rate dropping so quickly? HIV/AIDS prevalence was 6.7 percent in 2004, down from about 10 percent in the late 1990s

Given that the AIDS rate - blamed for most of Africa's ills - is dropping so quickly, it should have an immediate impact on life expectancy.

Funny how Kenya's is still decreasing:

Average life expectancy
2004 47.5 years UNDP - Human Development Report 2006
2003 47.2 years UNDP - Human Development Report 2005
2002 45.2 years UNDP - Human Development Report 2004
2001 46.4 years UNDP - Human Development Report 2003
2000 50.8 years UNDP - Human Development Report 2002

link
There should be a lag time. I don't know why you would think the life span would increase immediately when the disease has such a long incubation period.

Why do some people have vastly reduced CD4 cells and not contract AIDS?
Well this article was made to order in answering your question.

Viral Load and T-Cell (CD4) Counts: Why They Matter
May 11, 2001
Note: This article is part of our series answering the AIDS denialists, who say that HIV does not cause AIDS and who often urge patients to reject medical advice. Writer Bruce Mirken prepared this simple-language version to help agencies prepare materials for their clients....

...While there have been a few medical reports of people who seemed healthy even though they had very low CD4 counts, these cases are rare. Research overwhelmingly shows that people with low CD4 counts are much more likely to get sick than people who have a normal amount of CD4 cells.

The AIDS denialists who claim that CD4 counts are meaningless often point to a study of AIDS patients called the Concorde study, in which people who had a small increase in CD4 counts did not live longer than those whose CD4 counts stayed the same. But that study was done nearly 10 years ago, before modern combination therapy, and the CD4 increases were very small. Newer studies with more potent treatments show that a big boost in CD4 cells almost always lowers the risk of getting seriously ill.

For example, the deadly pneumonia called PCP occurs much more often in people with very low CD4 counts. In one study with over 1,000 patients, almost everyone who got PCP had a CD4 count below 200. Study after study has shown the same thing: The lower your CD4 count, the greater your chance of getting PCP or other serious infections.

The AIDS denialists leave out these important facts. ...
 
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Compared to most viruses, that's still slow. Very slow. Many or most deadly viruses, if they're going to kill you, do it within a matter of weeks. Sometimes days. Any time you're talking about a virus that takes more than a year...with a looooog asymptomatic phase where you can infect who knows how many people before you show any symptoms, it's slow for a virus.

You're right, and I had considered this point the very moment after posting. I was immediately struck by how fast ebola acts, or how quickly necrotizing fasciitis can spread. However, it is still short compared to how the disease behaves when treated by drugs... drugs designed based on the facts of the disease that people like Dabljuh aggressively deny.
 

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