Outtie

As I mentioned here, I’m heading to Ohio in the morning. I have two brand-new nephews to meet. My sister gave birth to her first child back on January 24th, and a sister-in-law just had her first on Valentine’s Day. (And the baby boom ain’t over yet–another almost-sister-in-law–my brother-in-law’s girlfriend–is due in May). So, the positive: I get to spend the weekend playing with babies and then give them back to their mommies when they puke, poop, and generally do all that nasty stuff that babies do. The negative: 8+ hours (looks like bad weather, so potentially up to 10) in a car with just me, my two kids, and the dog, likely with much of that taken up by my daughter complaining when we listen to “boy music,” and my son likewise complaining about every “girl song.”

Anyhoo, I’ll be back next week (or maybe even over the weekend, if I get bored of family stuff) with more on the AIDS issue, and hopefully some more original research analyses. I’ve been a bit short on those lately because of time–alas, despite what was claimed by one of the more active responders on the Bethell AIDS thread, I don’t make a living blogging, and I’m not paid by Tony Fauci to discuss these things.

Comments

#1 john
February 17, 2006

I wouldn’t let a woman who plays with viruses all day come see my babies, even if you were my little sister! I’d bring up your blog, point to your picture and say, “There’s Auntie! Say Hi”!
#2 Harvey Bialy
February 17, 2006

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding family affairs, preparing your promised answers to Anon II, your analysis of the Padian paper for Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water these days, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me “an utter waste of time” so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great “Breakdown” blog.

Whenever *you* do get around to it, *we* wil be anxiously waiting.

Pase un buen fin de semana

B. Ali
http://bialystocker.net/files/pipedream.pdf
#3 Roberto Stock
February 17, 2006

Dr. Bialy asked me to attempt to post this because his own comments are suddenly held for moderation. I thought his comments thus far here are absolutely moderate, for anyone, ket alone him!

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding matters, preparing your promised answers to Anon II, your analysis of the Padian paper with Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me �an utter waste of time� so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great �Breakdown� blog.

Whenever *you* can get around to it, *we* will be anxiously waiting.

Pase un buen fin de semana

B. Ali
http://bialystocker.net/files/pipedream.pdf
#4 Roberto Stock
February 17, 2006

Dr. Bialy asked me to attempt to post this because his own comments are suddenly held for moderation. I thought his comments thus far here are absolutely moderate, for anyone, let alone him!

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding matters, preparing your promised answers to Anon II, your analysis of the Padian paper with Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me �an utter waste of time� so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great �Breakdown� blog.

Whenever *you* can get around to it, *we* will be anxiously waiting.

Pase un buen fin de semana

B. Ali
http://bialystocker.net/files/pipedream.pdf

fyi tara

roberto is real and he asked me to try to put it through for him because he is actually busy with an *experiment*
#5 Darin Brown
February 17, 2006

It received an email from Harvey Bialy recently, indicating that he had attempted to make a post to this thread, but his IP address was blocked. So, here I am going to relay what he attempted to post:

—

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding matters, preparing your promised answers to Anon II, your analysis of the Padian paper with Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me “an utter waste of time” so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great “Breakdown” blog.

Whenever *you* can get around to it, *we* will be anxiously waiting.

Pase un buen fin de semana

B. Ali

http://bialystocker.net/files/pipedream.pdf
#6 Orac
February 17, 2006

Well that explains a lot. Learning of your impending absence, it would appear that Hank Barnes has decided to come over to my blog to start causing trouble.
#7 Darin Brown
February 17, 2006

I received an email from Harvey Bialy recently, indicating that he had attempted to make a post to this thread, but his IP address was blocked. So, here I am going to relay what he attempted to post:

—

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding matters, preparing your promised answers to Anon II, your analysis of the Padian paper with Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me “an utter waste of time” so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great “Breakdown” blog.

Whenever *you* can get around to it, *we* will be anxiously waiting.

Pase un buen fin de semana

B. Ali

http://bialystocker.net/files/pipedream.pdf
#8 George Kaplan
February 17, 2006

I got this strange message in my email this afternoon, asking me to post it at this blog. I have no idea what this is all about, but what the heck…

—

Hi Tara,

Just in case you can squeeze the time in between all these delightful sounding matters, preparing your promised answers to Anon II, your analysis of the Padian paper with Mr. Barnes, and all the other things a young assistant professor must do to keep her head above water, you might be able to refute the bold *claim* made here:

http://www.rethinkingaids.com/graphs.htm

I know that you consider conversations with me “an utter waste of time” so I will not even think of offering myself as a target of your piercing intellect, and instead offer a young assistant professor from someplace in New Mexico, named Darin Brown, that I encountered on your great “Breakdown” blog.

Whenever *you* can get around to it, *we* will be anxiously waiting.

Pase un buen fin de semana

B. Ali

http://bialystocker.net/files/pipedream.pdf
#9 anony mouse
February 17, 2006

Keeping a tally
Not of science but of sally
There is nary a doubt
The pundits will tout
The clear winner must be Hank B. Ali
#10 Darin Brown
February 17, 2006

The link to the pdf file was apparently misspelled (mis-capitalised). This link should work:

http://bialystocker.net/files/Pipedream.pdf
#11 Darin Brown
February 17, 2006

>> Heh. Am I supposed to comment on every HIV paper written over the past 20 years?

No, of course not. I don’t expect you to be familiar with every paper written on HIV over the past 20 years. I doubt there’s a single person in the world who is familiar with EVERY paper.

But the Ho/Shaw papers are not just ordinary papers. They became the basis for a supposedly new understanding of AIDS. More importantly, they were the basis for announcements at the time (1995) that Duesberg had finally been answered. In other words, these were the papers that were supposed to shut Duesberg up for good. To quote straight from John Maddox in Nature on 19 January 1995, he said the papers “should be an embarrassment for Duesberg” and he finished by saying “Now may be the time for them [the Duesbergs of this world] to recant.”

That by itself makes the papers tremendously important. But the papers were also used as the justification for initiating HAART therapy. Now, regardless of what conclusion you reach about whether HAART has worked or not, or has been beneficial or not, it seems that it should be a matter of great principle whether these landmark papers really justified HAART AT THAT TIME. In fact, it seems to me that such papers should have been held to even HIGHER standard, if they were used to justify new treatment regimes.

So, no I don’t expect you to be familiar with every paper written on HIV over the past 20 years. These were major papers, though. They attracted a lot of media attention. And as I mentioned above, you must be familiar with them, if you’ve really read all of Infectious AIDS and Duesberg’s papers, because there are critiques of the papers in Infectious AIDS, and even more extensive critiques available in the Genetica book.

>> I don’t have much to say about them, anyway. Yes, I’m quite familiar with them, and with both the critiques by Duesberg et al. and with the responses to the critiques and responses to the critiques of the critiques etc. etc.

I’m curious about these papers you refer to. I’m not familiar with every paper on HIV in the literature, either, and it seems I must have overlooked these myself. I would very much like to read the opposing viewpoints and responses (“responses to the critiques” as well as “responses to the critiques of the critiques”). Could you provide some references to the specific papers or articles to which you refer?

>> In the end, I think the proof is in the pudding, and the drug cocktails have largely worked. Does this mean Ho et al. were correct? I can’t say, but again, that paper was 11 years ago, and the field has progressed since then.

But if fundamental problems slipped by peer review 11 years ago, then the natural question arises: How do we know that fundamental problems are not *currently* slipping by peer review? If it happened once, it could happen again. In my opinion, it would seem incumbent upon the scientific community to re-examine these papers, and if major errors are found, do some long, hard, soul-searching about how this could have happened. Mistakes as grievous and consequential as these should make any scientist pause for a moment and ask whether the current institutions need to be reformed.
#12 Hank Barnes
February 17, 2006

Well that explains a lot. Learning of your impending absence, it would appear that Hank Barnes has decided to come over to my blog to start causing trouble.

Orac, could you please stop being a weenie, for god’s sake?

I had no idea you even existed until your little personalized hit-and-run snark from the other day:

Oh, goody, Tara. You know you’re really hitting a nerve when trolls like Hank Barnes (a regular fixture on Dean Esmay’s blog and an annoyance that MUSC Tiger had to slap down a while back) start showing up and making pests of themselves.

–Orac the great, 2/14/06

There’s 2 good rules of thumb, I learned growing up in Chicago:

1. Don’t cross the street to pick a fight
2. Don’t bring a knife to a gun fight.

You, my friend, are an intellectual poseur. On surgery, you may know a bit; but on infectious disease and AIDS, you don’t know squat. And I’d be happy to educate you.

Hank Barnes

p.s. Also, for the record, while I share the same initials as Dr. Harvey Bialy, we ain’t the same fellow. He was editor of Nature/BioTechnology — a prestigious medical journal. Assuredly, I was not:)
#13 Darin Brown
February 17, 2006

Given that there’s been a lot of discussion over the Ho/Shaw papers recently here, it seems to me it would be a good idea to make available the following link:

http://www.virusmyth.net/aids/data/pdmaddox.htm

As Harvey states, this series of internal communications between Duesberg, Harvey, and Maddox illustrates how journalistic manipulation and suppression can occur without invoking any kind of “conspiracy theory”, as many (even Tara) have implied.

I would invite everyone reading this thread to please read the link above. Not only does it contain the FULL text of Duesberg and Harvey’s response to the Ho/Shaw papers, it also shows how that response never made it to print. Let me reiterate some of the things I mentioned in the above, just to put this in context for people:

1. These papers were used as a basis for saying that Duesberg had finally been answered. In other words, they were announced, in the pages of Nature, as a direct challenge to him. Whenever any kind of journal makes an editorial statement claiming that a number of papers have answered specific challenges of someone, that person should have an even GREATER right of reply than would be usual.

2. These papers were about HIV dynamics. In other words, they were dealing with what everyone agrees is an extremely important public health issue, as Richard Strohman put it, “an issue of great scientific and human importance”. Especially, given the fact these were going to be the basis for initiation of HAART, it seems obvious that every possible voice, claim, dissent, suggestion, criticism, comment, and challenge should have been given a wide opportunity for the scientific community to hear. This is not just a humane decision, it is plain common sense.

Keeping these 2 points in mind, read the ROR documents, and tell me honestly that Maddox met his obligations.
#14 Darin Brown
February 18, 2006

“The ‘HIV-hypothesis’ is much simpler [than Duesberg/Bialy's assembled references]: HIV causes AIDS, in some manner not understood; most of those infected will develop the disease.”

This is one of my favourite Maddox quotes. If you’re interested in seeing the context, click under “Maddox’ response to our commentary” at the ROR.

This is an AMAZING quote. More than any other quote I can think of, it exposes the intellectual bankruptcy of the HIV/AIDS hypothesis in striking fashion. Here, we have the editor of the most prestigious scientific journal in the world, offering a version of the “HIV/AIDS hypothesis” which contains almost no real content, and which is virtually worthless in terms of predictive or explanatory power. It would be one thing if daf9 or Orac or someone said something as silly, vacuous, and useless as this, but this is a quote from John Maddox. He should be able to do better.
#15 Darin Brown
February 18, 2006

Dale,

Your post in response to Liam is truly a masterpiece of mathematical ignorance. Normally, this may not be a problem for you, but unfortunately, you tried to slip this flim-flam into a thread where a real live ph.d. in mathematics happened to be reading. Guess it wasn’t your day.

Liam, The Padian paper contains two pieces of data relevant to HIV heterosexual transmission rates. Also the Padian paper can’t be interpreted in isolation from the rest of the literature any more than any other single paper can. But just looking at Padian. No seroconversions in 3000 couple months means less than 1 per 250 couple years. Less than 1, not zero, because neither you nor Hank nor Dr. Padian can possibly know what might have happened in month 3001. Still that is a pretty low number. But there’s a second piece of a data.

Your point is true: of course, anything could happen in month 3001. That is the whole point of running experiments: We don’t know what will happen! If we knew what would happen, what would be the point of collecting emperical data?? So, your observation here is technically true, but completely trivial and irrelevant.

You appear to have a fundamental misunderstanding of the nature of statistical inference, which is a branch of mathematics which uses probability theory to infer conclusions about a given population from sample observations. (That’s really a gross over-simplification, but it will do for now.) The zero seroconversions in 3000 couple months is the sample statistic. From that, we make inferences about the overall seroconversion rate. No one is claiming that the seroconversion rate for the entire population is actually exactly zero.

So either several million people who all claim to have no risk factor other than a heterosexual relationship with an HIV positive partner are ALL lying, or heterosexual transmission occurs at some rate less than once per encounter but definately greater than zero.

Well, yes, that’s true, but again, trivially true. “Heterosexual transmission occurs at some rate less than once per encounter but definately greater than zero.” Think about what you’re saying, and why it’s trivially true.

And FYI, 3 seroconversions per hundred couple years doesn’t mean 1 serodiscordant couple can go at it in relative safety for 33 years; or to use your numbers, that an HIV negative individual can have 999 sexual encounters before running into a problem. It means if 1000 HIV negative individuals have one encounter each with an HIV positive individual, on average, one unlucky individual will end up HIV positive. To argue otherwise is like saying that because the odds of winning a lottery are less than one in 10 million and no one individual ever buys 10 million tickets then clearly no one ever wins a lottery.

Nice dodge. Unfortunately, what you say is completely wrong, assuming that the sexual encounters are identically and independently distributed, which would seem to be a fairly reasonable assumption in this case.

Have you heard of random variables? Expected value? The situation you’re describing is something studied in lower-division stats courses — it’s called the geometric distribution. You have a trial with 2 outcomes: success (probability p) and failure (probability q = 1 – p). The geometric distribution assigns to each positive integer n the probability of exactly n trials before success is reached. The situation you describe above is the case p = 1/1000.

Of course “3 seroconversions per hundred couple years doesn’t mean 1 serodiscordant couple can go at it in relative safety for 33 years; or to use your numbers, that an HIV negative individual can have 999 sexual encounters before running into a problem.” That’s not what is being claimed. What’s being claimed is a mathematical statement: that the expected number of sexual encounters before “success” is 1000 = 1/p. And, in fact, that is the case. A random variable with geometric distribution does indeed have mean equal to 1/p.

You are quite wrong with the lottery ticket analogy. It does not matter WHO buys the tickets, what matters is that the trials of buying a ticket to see if you win are identically and independently distributed. And this is true for lottery tickets, regardless of whether one person buys 1,000,000 tickets or 1,000,000 people each buy one ticket. The trials don’t give a hoot about who’s buying the tickets…why should they?
#16 Dale
February 18, 2006

Darin, Your post in response to my post on the other hand demonstrates a lack of understanding (or a masterpiece of ignorance if you prefer that term) of biology.

In particular your statement “assuming that the sexual encounters are identically and independently distributed, which would seem to be a fairly reasonable assumption in this case.”

That might be a reasonable assumption to a mathematician but no biologist would ever make such an assumption, particular as applied to human beings.

Human beings are not a homogenous population, neither genetically nor with regard to the environments they live in. Some are more susceptible to HIV infection than others. Sexual encounters are not all the same,some incorporate more risk factors for transmission than others. The viruses themselves also vary genetically and that too will affect transmission rates.

The identification of any individuals in whom sexual transmission of the virus has occured says the virus can be transmitted sexually and a hundred or a thousand population studies such as Padians will not determine the true probability of transmission for any given individual at any given sexual encounter.
#17 Darin Brown
February 18, 2006

The identification of any individuals in whom sexual transmission of the virus has occured says the virus can be transmitted sexually and a hundred or a thousand population studies such as Padians will not determine the true probability of transmission for any given individual at any given sexual encounter.

Well then, what’s the point in having population studies at all? You seem to be throwing in the towel on science altogether. I don’t claim to be an expert on the Padian study in particular (Hank?); I was merely pointing out some mathematical fallacies I saw in your post.

My comments on your first and second mistakes (if you can call them mistakes, they are not so much mistakes as they are trivial statements) still stand. Those issues have nothing to do with whether something is or is not independently or identically distributed.

My point with regard to the geometric distribution doesn’t actually hinge on whether the sexual encounters are *precisely* independently and identically distributed. I misspoke when I said that what you said was wrong, “assuming the sexual encounters are identically and independently distributed”. That’s an assumption that simplifies things, but your mistake doesn’t depend on that assumption.

My point was to show that you don’t seem to have a good understanding of the meaning of the expected value of a random variable, or how it should be interpreted. For instance, suppose someone *does* have a lot of risk factors which affect the transmission rate. Maybe they’re not independently distributed (probability of transmission on one encounter affects probability on future encounters) for instance. You’ll get a different distribution then, not exactly geometric (but fairly close), but it will still have a mean (expected value) and variance. Let’s say it made a drastic difference, that now the expected number of encounters before “success” was only 700 instead of 1,000. That still doesn’t mean you can use this argument which amounts basically to “Well, there’s no way of knowing that transmission might not happen BEFORE 700 encounters, so you can’t say the first 699 are risk-free.” But no one is saying that. It’s the same dodge.

Your analogy with the lottery ticket was comparing (correct me if I’m wrong) the situation where, given an HIV positive person, you’re considering the probability distribution for the number of encounters until transmission depending on whether (a) the HIV positive person was half of a serodiscordant couple, or (b) the HIV positive person had sex with 1,000 different HIV negatives. Unless having sex with the same partner 1,000 times somehow has a drastic effect on transmission, these are mathematically the same situation. That was what I meant by “The lottery tickets don’t give a hoot WHO buys them.”
#18 Darin Brown
February 18, 2006

I would also point out that the fatality rate in driving a car is about 1 per 75,000,000 miles driven. Does anyone doubt traffic accidents can be fatal because of that statistic? Would anyone seriously suggest that if you only drive 74,000,000 miles and then hung up the keys you’d be perfectly safe? That seems to be the argument some are making for HIV transmission via sex.

No, it’s a *misrepresentation* YOU’RE making. See the above post.
#19 Darin Brown
February 18, 2006

>>Darin Brown said:

>>HELLO! The claim at hand which Harvey was referring to was not the HIV/AIDS hypothesis, it was whether the HIV/AIDS remained an “open” question. And he provided an emperical, quantitative way of testing the hypothesis of whether such a question remained “open”. That is what scientists do — provide emperical tests of hypotheses.

And if that were the case, then we’d already be seeing the debate being played out in the literature and at scientific conferences. That’s what scientists do.

Right, if you don’t *see* something in print in the journals, it must not exist? See no dissent, hear no dissent, speak no dissent.

May I remind you that scientific peer review, as it is currently practiced in the journals, is a relatively recent process? (And not, as someone on the previous thread ignorantly described, “something which has worked for hundreds of years”.) It is basically a 20th-century invention. Science advanced, indeed mightily advanced, all through the 17th, 18th, and 19th centuries without anything resembling peer review as it is practiced today.

>>”Psuedo-debate” is exactly the perfecto description of the sorry state of affairs of the past 20 years. PSEUDO = FAKE.

Thank you Darin Brown for explicitly admitting that this petition has nothing to do with asking an honest and clear question, and everything to do with a public relations stunt. Harvey Bialy avoided this question for a reason.

I think you’re confused about what the word “pseudo-debate” is referring to. It’s not referring to a potential debate between Duesberg and Baltimore. It’s a description of the *alleged* debate that has supposedly taken place the past 20 years.
#20 Darin Brown
February 18, 2006

Indeed, they have been done in the past. They have been done with HIV. You don’t agree with them–fine and dandy. And I hate to point this out here, but as you said, you’re a mathematician. The HIV-AIDS link has been looked at by thousands of people with relevant expertise all over the world–microbiologists, virologists, epidemiologists, immunologists, geneticists, physicians, and on and on. Don’t you think, perhaps, there’s a reason why we accept it? Are we really just so “brainwashed,” stupid (or, if you really want to get into the conspiracy theory angle, paid off) to fall for the HIV causation angle?

Tara, I’m *so* glad you (you!) used the “C-word”! Besides being a dead giveaway that you have almost nothing left to fall back on, it allows me to pull out one of my favourite Serge Lang quotes, when he was responding to someone who was making a similar type of argument using the “C-word”:

“The main problems with the HIV/AIDS controvery have not been due to a ‘conspiracy’…Rather, these problems have included:

* The inability by many people, and especially influential people, in the scientific establishment to tell the difference between a fact, an opinion, a hypothesis and a hole in the ground.
* The refusal even to consider alternative hypotheses to the pathogenesis of HIV, notably drug use.
* Censorship and tendentious reporting in the scientific press, as well as in the press at large.”

— Serge Lang, 25 April 1995, letter to the National Academy of Sciences

You don’t need a “conspiracy” to explain HIV. Just imagine an army of daf9′s, Orac’s, Dale’s, wheatdogg’s, Dave S.’s, and Dr. Dumbass’s running around the CDC and NIH. Seems pretty easy to me to imagine how it happened.
#21 Dale
February 18, 2006

Darin, you appear to agree that Padian cannot be interpreted as saying that the rate of heterosexual transmission of HIV is zero and you further agree that it would be inappropriate to say that any encounter between a seropositive and seronegative is risk free. So what are we arguing about?
#22 Darin Brown
February 18, 2006

Dale,

Nothing in life is risk-free. Again, all you’ve demonstrated is a complete lack of understanding of the nature of statistical inference. As is apparent to anyone reading this thread who *does* have such an understanding.
#23 Hank Barnes
February 18, 2006

Hi Boys (& the lovely Dr. Smith!),

Dale is all wet about Padian. Darin Brown just adds to the fun by decimating Dale’s mathematical zigs, zags and circumlocutions. Dale, you are truly the Harry Houdini of the scientific blogosphere:)

Let’s rewind.

1.The year is 1985 — one year after the supposed “cause” of AIDS has been discovered — a virus called HTLV-III (now called HIV).
2. The thought is HIV is sexually transmitted.
3. The thought is once acquired, within 2 years, you die.
4. Most of the folks dying of AIDS are gay males. But, this is a bit nonsensical, since viruses don’t discriminate. They are real dumb and real small.
5. The thought is an infectious disease will likely move into the general population and kill a lot of people.

6. So, a buncha brilliant epidemiologists from San Francisco set out test the hypothesis: Find HIV+ people and observe what happens to their partners when they have a lotta sex. Clean. Easy. Crisp science.

7. So, the a priori hypothesis is this: We expect the uninfected partners of HIV+ people to become infected at some rate. 100%? 50%? Who knows? Padian does not say (for good reason).

8. We get a lotta $$ from the gov’t to fund this study. It lasts 10 years. We test a lotta people for HIV. We follow them for years. They have a lotta sex. We keep re-testing them. So, How many got infected? The answer is:

Zero. Zip. Zed. Nada. Nil. Nothing. Nobody.

NOT ONE SINGLE PERSON (175 discordant couples), after unlimited, abundant, (dare I even say wild and kinky?) sexual acts over 10 years contracts HIV. Not one.

Buried in the paper on pg 354 (“We observed no seroconversions after entry into the study”).

Those are the facts. So, what is one to conclude?

My conclusion is that the connection between sex and AIDS has been proven false. Some folks don’t like that conclusion. The ostrich crowd has emotionally invested in the wrong paradigm, and are unwilling to change their beliefs, despite the evidence. Not very scientific, mind you.

Myself, I go with the facts. NO SEROCONVERSIONS. You cannot have a sexually transmitted disease, where sexual activity is abundant, yet sexual transmission is non-existent.

So, put that in your pipe and smoke it!

Hammerin’ Hank Barnes

p.s. When will Dr. Smith return to give us her take on the Padian as she promised? She is an epidemiologist, and it is an epidemiological study (the longest one, I might add.) I would like her to show me if I have erred.
#24 Dale
February 18, 2006

Darin, You say above that no one is saying that the risk of sexual transmission is zero but I would put it to you that Hank Barnes does seem to be saying that. Over and over, ad naseum, I might add. Maybe you should be explaining statistical inference to him?
#25 Darin Brown
February 18, 2006

I suspect Hank is getting a little carried away and using a slight abuse of language. It’s pretty clear what he means.

I don’t know the exact methodology of the Padian paper. But in inference, you never know anything to be *absolutely* certain. You seem to take this innocuous fact and think that it’s a stinging indictment against the whole field of statistical inference. That’s what I meant “nothing in life is risk-free”.

When Hank says “sexual transmission is non-existent” there are 2 ways of interpreting this, which do not contradict each other. One is the staightforward interpretation that no seroconversions were observed in the sample. The other interpretation is that the *inference* you can make from this is the *actual* seroconversion rate in the entire population is very, very low. We don’t know for certain what it is exactly. That’s why inference exists. If we knew for certain, we wouldn’t have to have studies like Padian in the first place.

The best we can do with inference is make probabilistic conclusions about the general population. While I’m not familiar with this particular study, I would imagine the conclusion is that there is an extremely high probability that the transmission rate is extremely low (very, very low). A crude (and not misleading) way to state this is to say that “transmission is non-existent”.

You point out that we can’t with 100% certainty conclude the transmission rate of the whole population is exactly zero (a claim which on its face is almost absurd) and somehow use this as an indictment that the Padian study is worthless, that we can’t conclude anything from it, and that we can’t say anything about the risk involved in a single specific encounter. But Hank is not saying any of these things.
#26 Dale
February 18, 2006

Darin, Based on Padian even a non statistician such as myself would agree that there is a high probability that the HIV transmission rate was low during the conditions that prevailed over the course of this study. The issue is how far can one extrapolate that conclusion, especially since 15% of the couples entering the study were seroconcordant at the outset. That piece of data alone suggests that transmission rate may have been higher at some point during the partner relationships than it was during the 3000 months of the study itself. Furthermore, studies other than Padian carried out in other parts of the world have observed higher rates of seroconversion than Padian did. Again as a non statistician I don’t interprete that as saying Padian is worthless I interprete it as indicating that there are factors not identified in any of these studies that significantly affect heterosexual HIV transmission rates. You of course are free to interprete conflicting data in any way you choose.
#27 Darin Brown
February 18, 2006

That’s not what I’m saying at all–indeed, it seems that you missed or have forgotten my original point here. HIV fulfills all of Koch’s postulates as well as any other infectious disease does. I’m not just saying “HIV’s present at the scene of the crime”. I’m saying it’s there with a bloody knife, matching stab wounds in the victim and a dozen eyewitnesses.

Let’s see…we can barely find it — even at the last stages of clinical AIDS, when it’s supposed to be doing the most damage, it’s almost impossible to find without incredibly powerful machinery. Most every other virus (errr…excuse me, “non-postmodern virus”) is swarming in the body at the height of infection and clinical symptoms. It’s almost impossible to miss them.

Let’s see…HIV doesn’t do much. It just sits there. Despite all the viral markers, it’s difficult to find actual *infectious* virus, which is really the only type of virus which matters in a case like this.

Let’s see…even when HIV can be found, it can’t always be found in the affected (diseased) tissue which is supposedly suffering from a particular opportunistic infection. For instance, HIV isn’t always found in the tissue of Kaposi’s sarcomas, even if it’s found elsewhere. (Oh, that’s right…I forgot…HIV kills T cells (indirectly), which THEN causes a general state of immunosuppression, and this general state of immunosuppresion THEN allows another virus which supposedly causes KS, to flourish, and THIS virus then causes KS. So, on second thought, I guess it’s understandable why HIV might be nowhere found.)

Let’s see…HIV, like all other retroviruses, in not cytocydal and depends on its host for reproduction. Apparently this HIV is a hit-man who mistakes his boss for his mark.

Let’s see…even if, in spite of all the above, we were able to say with certainty that HIV caused AIDS, we still are at a complete mystery as to HOW, so not only is this a skilled hit-man, he’s able to cover up his tracks pretty well, too.

And finally, even if HIV is the hit-man, he appears to strike at unpredictable times, in unpredictable ways, and despite having only 9000 nucleotides, he can tell whether his mark is male or female, American or African.

It seems to me that this HIV guy is a lot less like O.J. Simpson and a lot more like Eve Kendall’s show at Mount Rushmore…maybe enough to fool the Vandamm’s of the HIV world.

Tara, your comparisons with Streptococcus pyogenes and Mycobacterium tuberculosis just don’t hold up. Contrary to what someone implied in the previous thread, I don’t think HIV is the first microbe claimed to become embattled with the immune system. I said HIV was the first microbe claimed to be an infectious cause of immunosuppression itself.

There is a difference between microbes which take advantage of a compromised immune system to cause disease, and genuine immunosuppression diseases. The former are very common, and they include e.g. the 2 examples you gave, as well as almost any other well-known infectious disease-causing agent.

These are not immunosuppresion diseases, however. The latter you can find in the Merck Manual. THESE are diseases which are claimed to attack the immune system itself, and these known immunosuppression diseases listed in the Merck Manual, if you choose to read it, are autoimmune diseases, genetic disorders, immunosuppresion caused by recreational drug use, and by malnutrition (esp. undernutrition). These are diseases whose underlying pathogenesis is some general impairment of the immune system. They are diagnosed using information from a variety of tests as well as clinical observation.

There are 2 things to notice about all these immunosuppression diseases — first, MOST of them have non-infectious causes, or are a combination of some non-infectious and infectious causes. Second, the mechanism of action of each of these is far more complex and complicated than anything as simple as HIV. Drugs, e.g. have power chemical properties, and malnutrition involves a wide variety of nutrients, chemicals, and their reaction with the human body. None of these (NONE) is remotely as simple as something like HIV.

But really, Tara, I don’t want to distract you with all these issues. I’m far more interested in the referenced, logically conherent replies you have promised to offer to anon II…*HIS* questions are really the most important ones that have been asked of you, and thus far, you are about as good at answering them as Dale is at math.
#28 Hank Barnes
February 18, 2006

Dale asserts:

HIV fulfills all of Koch’s postulates as well as any other infectious disease does.

First, Dale, if HIV does not satisfy Koch’s Postulates, are you prepared to say that HIV has not been shown to cause AIDS?

Second, Duesberg made the charge that HIV did not satisfy Koch’s postulates in the esteemed pages of Science in 1988.

The response by Gallo & Temin was quote:

They [Koch's Postulates] are a useful historical reference point, but were not regarded as rigid criteria by Koch himself and should not be so regarded today.

This is goal-post moving writ large.

So, Dale, gimme a cite as to what paper demonstrated that HIV fulfilled Koch’s postulates.

Hank B
#29 Darin Brown
February 18, 2006

Hank,

Sorry, I wasn’t clear who wrote that. It was Tara who wrote what I responded to, so your inquiries should be directed to her.

I will be more clear in the future to prevent further misunderstandings.
#30 Hank Barnes
February 18, 2006

Darin,

Not a problem. I’ll ask Tara those questions, then.

I’ve been wrestling with Dale now for over a year.

Hank Barnes
#31 Dave S.
February 19, 2006

Here’s a neat trick.

You simply take the comments from a thread that was closed and paste them in some other random thread and keep right on going.

You AIDS deniers are a funny bunch.
#32 JP
February 19, 2006

Dale–

What Darin Brown is trying to say is that, if we imagine that in each sexual encounter there is a probability p of “success” of transmission of the virus, if p is a constant, then theory will tell you the expected number of sexual encounters before transmission. He does neglect to mention, however, that for a small p, the variance is very large.

Darin Brown–
What Dale is saying is that p is not constant; that p itself if a random variable, dependant on host genotype (which has more than 9000 nucleotides), virus genotype, and stage of the virus, among other things. biology ain’t always as pretty as we’d like.

I know relatively little about this debate, so please no one ask me what I think about study X or paper Y.
#33 Darin Brown
February 19, 2006

Dave S. said:

Here’s a neat trick.

You simply take the comments from a thread that was closed and paste them in some other random thread and keep right on going.

You AIDS deniers are a funny bunch.

Tara was the one who said she would provide responses to all of the “AIDS deniers” at the very moment she closed the original thread, ostensibly because the debate had degenerated into “name-calling”. Anyone can go back to the original thread and judge whether the name-calling was threatening to overtake the discussion.

If she was planning to provide responses, why close the original thread in the first place? That seems funny.
#34 Darin Brown
February 19, 2006

JP said:

Darin Brown–

What Dale is saying is that p is not constant; that p itself if a random variable, dependant on host genotype (which has more than 9000 nucleotides), virus genotype, and stage of the virus, among other things. biology ain’t always as pretty as we’d like.

Great, then we should devise further studies to examine these other factors, not make fallacious red herring arguments that prey on people’s misunderstanding of random variables and expectation. As I said earlier, the dodges Dale was making don’t really depend whether the encounters are exactly independent or not.
#35 Hank Barnes
February 19, 2006

You AIDS deniers are a funny bunch

Dave S,

Well, humor makes the world go round, don’t it?:)

Myself, I’m not an AIDS “denier,” whatever that means. I prefer the term “healthy skeptic.” But, this applies to many things, besides AIDS.

I do think it’s kinda funny that people who call folks “AIDS Deniers” are some of the most remarkably ignorant people I’ve ever met.

Say, Dave S, one quick question:

1. Although I doubt you’ve read a peer-review, published paper on AIDS, if you do contend that HIV causes AIDS, what evidence would falsify this statement?

No, I don’t expect you to respond — I’ve slogged thru the quality of your work above

Hint: it ain’t too hot:)

Cheerio,

Barnes
#36 Darin Brown
February 19, 2006

J’ACCUSE
========

http://harveybialy.org

“Why “J’Accuse and Why “ahorra”?” (the “J’Accuse” is dynamically linked to the above page)

WHY THESE TWO?

Maddox and Koshland each had several opportunities to slow the inexorable acceleration of the HIV/AIDS shitball. Neither did, and worse each used the offices of their respective, very powerful journals to poison the very atmosphere in which normal scientific discourse had preceded for centuries.

(These propositions are demonstrated beyond any shadow of any doubt in my biography of Peter.)

WHY NOW?

It has been 5 academic generations since HIV has been loose in the world of science, and has done to its immune system over these “points in time” what it could never do to the physical bodies of any of the “scientists” who should have been lifelong vaccinated.

(This sad proposition was demonstrated to me finally and clearly by the transmission above, and i had no choice but to issue my indictment.)

—————-

The “transmission” referred to above can be read (and downloaded) here :: http://bialystocker.net/Pipedream.pdf .
#37 George Kaplan
February 19, 2006

J’ACCUSE
========

http://harveybialy.org

“Why “J’Accuse and Why “ahorra”?” (the “J’Accuse” is dynamically linked to the above page)

WHY THESE TWO?

Maddox and Koshland each had several opportunities to slow the inexorable acceleration of the HIV/AIDS shitball. Neither did, and worse each used the offices of their respective, very powerful journals to poison the very atmosphere in which normal scientific discourse had preceded for centuries.

(These propositions are demonstrated beyond any shadow of any doubt in my biography of Peter.)

WHY NOW?

It has been 5 academic generations since HIV has been loose in the world of science, and has done to its immune system over these “points in time” what it could never do to the physical bodies of any of the “scientists” who should have been lifelong vaccinated.

(This sad proposition was demonstrated to me finally and clearly by the transmission above, and i had no choice but to issue my indictment.)

—————-

The “transmission” referred to above can be read (and downloaded) here :: http://bialystocker.net/Pipedream.pdf .
#38 JP
February 19, 2006

Darin Brown–
Agreed. Dale isn’t a top-notch statistician.

On your suggestion that further studies be done to examine factors in HIV transmission, genetics is something I know a little about (as opposed to pathology), and a couple genetic factors are known to influence susceptibility to HIV infection– a mutation in the CCR5 gene (go to google scholar and search “CCR5 mutant HIV”) and possession of a low copy number of the gene CCL3L1 (gonzalez et al. 2005. Science 307: 1434-1440). In fact, the CCl3L1 mutant is thought to play a role in the progression of HIV to AIDS (assuming there is such a progression, of course).

The genetics of pathogen-human interaction is a fascinating area of research.
#39 Dale
February 19, 2006

Darin says “Great, then we should devise further studies to examine these other factors”

If you take a look at the HIV literature of the past ten years you will see that many such studies have and are being carried out. The question of heterosexual HIV transmission neither began nor ended with Padian.
#40 George Kaplan
February 19, 2006

Typo:

The “transmission” referred to above can be read (and downloaded) here:

http://bialystocker.net/files/Pipedream.pdf
#41 Hank Barnes
February 19, 2006

Dale writes:

The question of heterosexual HIV transmission neither began nor ended with Padian.

Please provide a cite for a 10-year study (or less, if you like) where uninfected folks did in fact become infected from heterosexual transmission of HIV.

Barnes
#42 Chris Noble
February 20, 2006

Please provide a cite for a 10-year study (or less, if you like) where uninfected folks did in fact become infected from heterosexual transmission of HIV.

OK I’ll bite.

Rates of HIV-1 transmission per coital act, by stage of HIV-1 infection, in Rakai, Uganda.

The Rakai cohort studies began in 1994.

While the researchers did not have the genitalia of the couples under an electron microscope at the time of transmission they did do sequence analyses to confirm transmission.

Note the strong dependence on the stage of infection upon transmission risk. This confirms earlier studies showing a relationship between viral load and transmission risk. It is also common sense. The risk of transmission of HSV is not constant. It varies with viral load and the amount of viral shedding.

The HIV+ member in Padian’s serodiscordant couples had been infected for a period of time before the start of the study. None were in the initial infection stage.

The HIV dissidents may be surprised that this is exactly what Duesberg has been saying – that the transmission of HIV should be highest during the initial infection stage.
#43 Chris Noble
February 20, 2006

I noticed that some HIV Deniers are posting the table from Duesberg’s latest paper that contains a set of strawman “predictions” of HIV/AIDS science.

The HIV-AIDS Hypothesis: 16 Predictions Versus the Facts

I have been trying to get a coherent answer from Harvey Bialy or any one else for some time.

Let’s start with
“Prediction” 10 AIDS spreads by infection of HIV.

“Fact” 10 But, contrary to the spread of AIDS, there is no spread of HIV in the US. In the US HIV infections have remained constant at 1 million from 1985 (29) until now (30), (see also The Durban Declaration and figure 1b). By contrast, AIDS has increased from 1981 until 1992 and has declined ever since (figure 1a).

The first thing an enquiring mind would ask is how it was that 1 million people were tested for HIV in 1985. The simple answer is they weren’t.

Reference 29. the data point for 1985 is The epidemiology of AIDS: current status and future prospects.

The first thing that is noteworthy is that the estimate is 0.5-1 million. For some reason Duesberg takes only the high end of the range and gives absolutely no clue about the uncertainty in the estimate.

The basis of the estimate comes from the San Francisco CDC cohort study with a total of 6875 subjects. In this cohort the seropositivity was found to have increased from 4% in 1978 to 68% in 1984.

In this group HIV prevalence increased from 4% to 68% in six years. Duesberg uses this study as evidence that “there is no spread of HIV in the US”.

Can anyone explain how someone can use a paper that presents a rapid increase of HIV prevalence in order to show that “there is no spread of HIV in the US”?

Now let’s look at “Fact” 7: Likewise, in 1985, only 1.2% of the 1 million US citizens with HIV developed AIDS (29, 30).

Again Duesberg cites this paper The epidemiology of AIDS: current status and future prospects. as a source of his claim.

If we look at how Curran et al came up with the estimate of 1 million for the prevalence of HIV in 1985 we find that they extrapolated from the SFCDC cohort with 6875 patients. The ratio of HIV-infected/AIDS-cases at this point in this sub-epidemic (the SFCDC cohort) was 28:1. Curran et al assumed that in the US as a whole the ratio of HIV-infected/AIDS-cases was higher – somewhere between 50:1 and 100:1. They then took the US cumulative number of AIDS cases ~10,000 and multiplied it by the magic number to get an estimate of between 500,000 and 1,000,000.

Thus the 1 million estimate comes from assuming that for 1985 the estimated 10,000 AIDS cases represent 1-2% of the total HIV infections.

Why does Duesberg act surprised that “in 1985, only 1.2% of the 1 million US citizens with HIV developed AIDS” when the estimate of 1 million was based on the assumption that between 1 to 2 percent of the US citizens with HIV in 1985 will get AIDS in 1985?

What about “Prediction” 13 – Viral AIDS “like all viral/microbial epidemics in the past” should spread randomly in a population

This is just a reiteration of Duesberg’s First Law of Epidemiology.

“Now, if we wanted to distinguish between infectious and not, here are the hallmarks of infectious diseases versus non-infectious diseases: All infectious diseases, zero exceptions, all of them, viruses, bacteria, fungi, you name it, are equally distributed between the sexes”

Talk By Peter Duesberg

If we look at the figures for 2003 we find that the male-to-female ratios for HIV and syphilis in the US are 2.7 and 5.2. Syphilis has a higher male-to-female ratio than HIV!

Using DFLE I can safely state that syphilis is not an infectious disease.

It’s amazing how many infectious diseases we can eradicate with dissident logic alone.
#44 Chris Noble
February 20, 2006

I see someone has cited Duesberg’s magic graph that completely lacks any error bars for the estimates of HIV prevalence. These estimates especially in the early years were extrapolations from a smaller number of tests primarily in high risk categories.

Could one of the dissident mathematicians put some error bars on the graph and explain Duesberg’s extrapolation techniques.

“On account of these tests, one million Americans were found to be HIV-positive in 1985 and one million Americans were found to be HIV-positive in 1992 and again in 1993. HIV is a totally long-established virus and on the grounds of this type of epidemio logy, you can extrapolate this curve back 200 years. It’s as solid as that. You can say the virus came with the immigrants 200 years ago to this country. It’s an old, long – established virus, but AIDS is a new disease. It’s not a good candidate for a new disease.”

Talk By Peter Duesberg

Here’s some more questions.

Can any mathematician explain how a virus can remain at a constant prevalence in a population when the perinatal transmission rate is less than 50%?

Can any mathematician extrapolate back 200 years based on perinatal transmission with 50% efficiency?
#45 JP
February 20, 2006

Chris Noble–

Interesting paper. For Darin Brown and Dale, here’s what it means: assuming the numbers can be trusted, p (the probability of transmission in a given sexual encounter) is highly dependant on the stage of the infection. But in any case, let’s take the p from early on (0.0082).

Darin Brown might invoke the geometric distribtion to say that the expected number of sexual encounters before transmission is about 122. pretty high. However, the variance is around 15000, which renders the expectation nearly meaningless in this case. Clearly, the geometric distribution isn’t the best way to model HIV transmission.

Dale’s instincts were right, even if his math wasn’t spot on.
#46 MissPrism
February 20, 2006

It seems everyone else has forgotten to say Congratulations…

Hope you had a splendid weekend. Your nieces and nephews are lucky to have such a cool science auntie!
#47 plunge
February 20, 2006

Dean gets in on the act:
http://www.deanesmay.com/posts/1140438935.shtml
#48 Orac
February 20, 2006

Yeah. Dean’s complaints about ad hominems buried the needle on my irony meter and caused the poor thing to explode, given how he’s questioned my honesty on more than one occasion. Tara didn’t deserve having collateral damage from his dislike of me.

I would point out, however, that anyone (like Dean) who enthusiastically accepts the conclusions of a report as shoddily reasoned and poorly supported (not to mention chock full of distortions) as the Al Bayati report as “proof” should be very careful about lecturing anyone about the nature of skepticism.
#49 Dale
February 21, 2006

MissPrism has made an excellent point. Congratulations on your new nephews!
#50 George Kaplan
February 21, 2006

Got another message from Harvey Bialy. Take a look:

—

Interesting stuff.

Just thought I would mention, regarding Duesberg/Baltimore debates real or hypothetical, that the last time the two titans of retrovirology squared off in the journals in a real debate was in the early 80s, and it was not about HTLV-III/LAV/ARV.

It was about the intermediates involved in retroviral integration. This highly technical and excellent debate , however, is neither easy to follow nor to reconstruct as it occurred in normal scientific fashion over a couple of years, and with the papers often in different journals. I had thought to collect and annotate this min-collection as a project at one time, but what with one thing and another….
#51 Hank Barnes
February 21, 2006

Chris Noble,

Your Ugandan study on heterosexual transmission is interesting, thanks.

But, it seems awful late in the game (published in 2005, regarding results in 1994)

By the mid-1980′s, the scientific community had already declared that HIV was heterosexually transmissible. Padian began her work 10-year study on this topic in 1985. I assert that her results, actually refuted the working-hypothesis.

The question is, What study of heterosexual transmission in the early 1980′s formed the foundation to support the scientific assertion that AIDS was a sexually transmitted disease? Your cite of Rakai is interesting, but dislocated from the historical development of the disease.

Barnes, Hank
#52 Darin Brown
February 21, 2006

Noble “ET AL” — You really must learn to read the body of scientific papers in addition to the abstracts, just like Hank has pointed out (n-times, n > 7). Because if you had read the body, you would know that overall transmission rate in the Rakai study was 1 in 856, over a whopping total of 6700 couple-months. That’s more than TWICE as many couple-months as Padian! They even admit in the discussion, “The overall rate of HIV transmission…is consistent with previous estimates from Rakai, Europe, and North America.” But since this would further confirm HIV can’t possibly cause a sexually transmitted disease, they had to hide this fact a few pages deep into the paper, and let all the lazy eyes glaze over “.0082/coital act within ~2.5 months after seroconversion” in the abstract, a ridiculous statement given the fact it’s only based on 10 couples who were only surveyed ONCE every TEN months…but wait, you would have to actually READ the paper to know that! Silly me.

Chris Noble said,

>Can any mathematician explain how a virus can remain at a constant prevalence in a population when the perinatal transmission rate is less than 50%?

The CDC says at the end of 2003, an estimated 1,039,000 to 1,185,000 persons in the United States were living with HIV/AIDS (which I’ll take that to mean “HIV positive”.) Take 1,112,000 as the average. Since HIV is equally distributed between the sexes, there’s 556,000 HIV positive females in the US in 2003. CIA factbook gives birth rate of 14.14 births/1,000 population and death rate of 8.25 deaths/1,000 population. This is 2.78% births/female, multiplying by 556,000 HIV positive females gives 556,000 * 2.78% = 15,446 births from HIV positive mothers. Assuming a 50% perinatal transmission rate, that’s 7,723 new HIV positives acquired by perinatal transmission. Multiply 1,112,000 HIV positives by the death rate to get 1,112,000 * .00825 = 9,174 deaths of HIV positives. We have to use the death rate directly, because AIDS death rates are screwed up by the fact all these people are taking all these wonderful antiretroviral drugs with proven toxicities.

The difference between the 2 numbers (7,723 and 9,174) can be explained by sexual and other routes of transmission.

Make sense?? Or do you need help with the arithmetic?

And while I have your attention, Chris, I’d like to direct you to the military recruit study in 1990:

Burke, D.S., Brundage, J.F., Goldenbaum, M., Gardner, M., Peterson, M., Visintine, R., Redfield, R. and Walter Reed Retrovirus Research Group (1990) Human immunodeficiency virus infections in teenagers; seroprevalence among applicants for the U.S. military service. J. Am. Med. Ass. 263: 2074-2077.

These are teenagers who have about as *LOW* a risk of acquiring HIV from behaviour as anyone. And they are in strong health overall. Most, if not all, of these teenagers must have acquired HIV via perinatal transmission. Yet they found 1 in 3000 of these teenagers were HIV positive. More striking, this percentage was found to be identical between the sexes! I have a simple question:

** If HIV is equally distributed between the sexes in this study, why does AIDS predominantly strike males in the US population? Simple damn question. I have an answer: HIV is a passenger virus, not the cause of AIDS.

Notice that this study was carried out between 1985 and 1990, so you are simply wrong, Chris, when you say that “the estimates especially in the early years were extrapolations from a smaller number of tests primarily in high risk categories”. But Chris, these were during exactly those early years, and the data were *NOT* taken primarily (in fact, not at all!) in “high risk categories”. Yet THE 1 in 3000 RATIO REMAINED CONSTANT THROUGHOUT THE FIVE YEARS IN BOTH SEXES. Please explain this.

And now that your silly distractions about the flat-line prevalence curve have been shown to be just distractions, I await your explanation of the flat-line curve. How did “AIDS” explode into the population at a time when the HIV prevalence is just sitting there?? Again, I have an answer: HIV is a passenger virus, not the cause of AIDS. What answers do *YOU* have??
#53 Darin Brown
February 21, 2006

J.P. said,

>Chris Noble–

>Interesting paper. For Darin Brown and Dale, here’s what it means: assuming the numbers can be trusted, p (the probability of transmission in a given sexual encounter) is highly dependant on the stage of the infection. But in any case, let’s take the p from early on (0.0082).

>Darin Brown might invoke the geometric distribtion to say that the expected number of sexual encounters before transmission is about 122. pretty high. However, the variance is around 15000, which renders the expectation nearly meaningless in this case. Clearly, the geometric distribution isn’t the best way to model HIV transmission.

>Dale’s instincts were right, even if his math wasn’t spot on.

You are correct to say the variance is about 15000, but oh so wrong to say that this “renders the expectation nearly meaningless in this case” and even more wrong to say “Dale’s instincts were right”. The 15000 variance doesn’t render anything meaningless. All it means is that when you’re focused on a rare event happening once, chance has a big part to play. That’s *ALL* it means. It’s a basic mathematical fact that’s used by good gamblers.

The reason I had to bring up the geometric distribution was because I had to play your stupid little game about “how long does it take a single couple to transmit HIV” and the associated rubbish arguments about lotteries and car crashes. When Dale goes on about, “we don’t know how long it takes until a couple transmits HIV”, that’s jibberish. We *do* know how long it takes *on average*, and we know there’s a great deal of chance involved. But that’s not what we’re talking about. We’re talking about what happens over a large population, a large number of trials. And we want to know how long until the population achieves a large number of successes. That’s not geometric at all. And you can be sure, as the number of desired successes goes up, the variance quickly goes down. There’s a bit of variance in how many times you have to roll a die before getting 6, but a lot less variance in how many times you have to roll a die before getting exactly 1,000,000 6′s. Think about it.

What you’re trying to say is “look, because we don’t know how long it will take before any particular person gets in a car crash, we have absolutely no idea how many car crashes will happen in the US next year”. That’s silly.

So, stop distracting and misleading people with single tosses of the die.
#54 Hank Barnes
February 21, 2006

Hi Chris,

Another thought that’s been bugging me. You write:

Note the strong dependence on the stage of infection upon transmission risk. This confirms earlier studies showing a relationship between viral load and transmission risk. It is also common sense. The risk of transmission of HSV is not constant. It varies with viral load and the amount of viral shedding.

I interpret this to mean that you believe a person is more likely to be infectious, and, therefore, more likely to sexually transmit the virus, at an early stage of the infection, rather than later stage.

So, the reason that Padian’s work unearthed no serconversions after 10 years of study, was because the infected partners –even upon entry of the study — had relatively “later-stage” infections.

I don’t want to put words in your mouth, but is that the gist of your comment?

Problem: How does this square with the 10-year latency period between infection and symptoms?

You’re saying early infection = highest risk of transmision. Sounds plausible. But, why wouldn’t early infection also = most acute manifestation of symptoms?

Your view:

On Day 1 of infection, the patient is: (a) highly contagious, but (b) symptom free.

On Day 1000 of infection, the patient is: (a) not-contagious, yet (b) deathly ill from AIDS.

It seems to me, you can’t have it both ways.

Barnes, Hank
#55 JP
February 21, 2006

Darin Brown–

1. I quote myself: “clearly, the geometric distribution isn’t the best way to model HIV transmission”. I just brought it up because you brought is up, because dale brought is up, because Dr. Smith has two new nephews.

2. You’re right, I didn’t read the full paper from Chris Noble. But this whole debate piqued my interest, and I ended up stumbling across this:

“Incidence of HIV Infection in Stable Sexual Partnerships: A Retrospective Cohort Study of 1802 Couples in Mwanza Region, Tanzania” (Hugonnet et al. 2002 JAIDS 30(1)73-80).

In the text (which I read this time), they show that, of the 42 discordant couples, there are 6 seroconversions in 2 years.

For comparison, there are 1742 couples where both partners are HIV- at the outset. After 2 years, there were 21 seroconversions. The difference between the two groups is significant.

I don’t think you have a strong argument that HIV isn’t sexually transmitted, no matter how you frame it.
#56 Dale
February 21, 2006

Darin, your mathematical sleight of hand not withstanding, the majority of HIV is not acquired perinatally. This can be concluded based on empirical observation because many individuals born to HIV positive mothers have been followed from birth to seroconversion. What is known is that viral infection precedes seroconversion but that if a child is seronegative past ~ 18 months of age, the child is almost certainly HIV negative. Then there are all those adults who are seronegative for years until suddenly they seroconvert (and rarely serorevert). The probability of seroconversion can be correlated with certain high risk activities involving an HIV positive individual and in some cases, the viral DNA acquired has been shown genetically to be linked to the viral DNA from the HIV positive contact. Perinatal transmission can’t explain seroconversion in adults.

And Hank, Chris isn’t saying late as in end stage AIDS, but late as in during that relatively symptom free ten year period. Early refers to early after infection, including prior to seroconversion. Don’t forget the 70 partners of HIV positive individuals who had seroconverted before being recruited into the study.
#57 JP
February 21, 2006

Hank Barnes–

Don’t know about HIV, but I’m pretty sure that the flu (to take another virus) is contagious before you have symptoms, and stops being contagious a few days after the symptoms start. That’s what I’d always heard, at least.
#58 Darin Brown
February 21, 2006

JP said,

>Darin Brown–

>1. I quote myself: “clearly, the geometric distribution isn’t the best way to model HIV transmission”. I just brought it up because you brought is up, because dale brought is up, because Dr. Smith has two new nephews.

Is that paragraph supposed to mean something?

>2. You’re right, I didn’t read the full paper from Chris Noble. But this whole debate piqued my interest, and I ended up stumbling across this:

>”Incidence of HIV Infection in Stable Sexual Partnerships: A Retrospective Cohort Study of 1802 Couples in Mwanza Region, Tanzania” (Hugonnet et al. 2002 JAIDS 30(1)73-80).

>In the text (which I read this time), they show that, of the 42 discordant couples, there are 6 seroconversions in 2 years.

I think you mean “transmissions”, not “seroconversions”? At any rate, congratulations on joining the insurgency. Taking 100 coital acts/year, times 2 years, times 42 couples = 8400 coital acts. 6 transmissions out of 8400 coital acts is a transmission rate of 1 in 1400. Unless you’re misrepresenting the data.

>I don’t think you have a strong argument that HIV isn’t sexually transmitted, no matter how you frame it.

Nah, you’re right. There’s Padian, with zero transmissions over 3000 couple-months. There’s Rakai, with 1 in 856 transmission rate over 6700 couple-months. By your own admission, there’s another study with 1 in 1400 in just over 1000 couple-months. It’s clearly sexually transmitted, though, I follow your reasoning.
#59 Darin Brown
February 21, 2006

Dale –

I never said that perinatal transmission “explained seroconversion in adults”. Don’t put words in my mouth. I was answering Chris’s question of how HIV could maintain a constant prevalence rate while having a 50% perinatal transmission rate. That’s all.

And it wasn’t “mathematical sleight of hand”. Just some numbers from CDC and CIA.
#60 Darin Brown
February 21, 2006

Okay, reading scientific papers is obviously too much for you people. So, why don’t we try something even more basic…a simple experiment. (That way, you should be able to see the data directly at the moment it’s tabulated, so you won’t have to be bothered to stumble through details when it’s written up.)

The experiment is simple:

Take 1,000,000 elementary school children, (say, 10-12 years of age). Test them for HIV seroprevalence.

PREDICTIONS:
===========

1. The HIV seroprevalence rate should be about 1 in 3000.
2. The HIV seroprevalence rate should be equal between the sexes.

In other words, we expect to see exactly the same thing that we saw in the 1990 Army recruit study, except this time, since we have children aged 10-12, we have almost completely eliminated any possible risk behaviours which would account for HIV transmission.

If the predictions are true, then HIV cannot cause AIDS, because a perinatally transmitted virus that has equal distribution between the sexes cannot possibly be the cause of a sexually transmitted disease that overwhelming afflicts males in the US population. It’s as simple as that.

Simple, clean, ethical, and not even very expensive. (And I’m not really interested in concerns of “ethics of privacy” from people who gave AZT monotherapy to tens of thousands of patients in the past.)

So, what do you have to lose? (That’s a rhetorical question.)
#61 Hank Barnes
February 21, 2006

Regarding Padian, Dale earlier wrote:

No seroconversions in 3000 couple months means less than 1 per 250 couple years. Less than 1, not zero, because neither you nor Hank nor Dr. Padian can possibly know what might have happened in month 3001

True, we don’t what might have happened in month 3001.

But, then you write:

Don’t forget the 70 partners of HIV positive individuals who had seroconverted before being recruited into the study.

So, lemme unnerstand:

The month after this 10-year study is an unknown, but the months before the study tells us something scientific?
#62 Hank Barnes
February 21, 2006

JP,

Don’t know about HIV, but I’m pretty sure that the flu (to take another virus) is contagious before you have symptoms, and stops being contagious a few days after the symptoms start. That’s what I’d always heard, at least.

Does the flu have a 10-year latency period between infection and first symptom?

I had the flu last week — did someone cough on me during the Clinton administration?

I love making a complete comparison between the flu and HIV:)
#63 Harvey Bialy
February 21, 2006

I have recently discovered, I think, the reason for the acute discrepancy between the HIV+ frequency in African populations when determined for epidemiological surveillance purposes, and when determined in the two “scientific” studies quoted above.

I believe the reason is to be found in this document :

Report of the Pilot Study to Validate HIV ELISA Testing in South Africa, June 2003 (and Appendices)

located here:

http://www.rethinkaids.info/documents/Africa

At least one of the HIV antibody tests routinely performed in South Africa for example is almost completely unreliable in terms of meeting its manufacturer’s performance specifications when used in the clinical laboratory settings in South Africa.

Read it, please. Even if you don’t think my explanation is correct, the study reported there is quite exact in its methodology and results.
#64 George Kaplan
February 21, 2006

The above-mentioned Report of the Pilot Study to Validate HIV ELISA Testing in South Africa, June 2003 (and Appendices)

can be found here:

http://www.rethinkaids.info/body.cfm?id=61

Please disregard the dead link above. Thanks
#65 Dale
February 21, 2006

Darin, re your experiment. This is an experiment which as described by you would not lead to the conclusion you suggest. Putting aside the problems with doing this experiment in the USA (where current perinatal transmission rates are extremely low due to ART therapy administered to HIV positive mothers and putting aside all the legal problems with getting permission to test) – putting aside those problems lets assume you do your experiment and seroprevallence is equal between the sexes. That would certainly suggest that HIV seroprevallence in adults is not due to perinatal transmission but it would say nothing about a causal relationship between HIV and AIDS. The orthodox scientific position is that it is lateral viral transmission (through needle sharing, MSM and heterosexual sex) that is largely responsible for seroprevallence in adults.

To disprove the orthodox position you would have to take your 1 million school children and perform HIV tests at some interval (yearly? every five years?) well into adulthood. You would have to show that in that population seroprevallence remained similar between the sexes while AIDS was still predominantly a problem in MSM and IVD. You would have to show that seroprevallence was similar amongst MSM and heterosexuals, IVD users and non IVD users and that in all these groups seroprevallence was essentially unchanged from what you measured at your initial HIV testing. Then you could claim support for your hypothesis that HIV has nothing to do with AIDS.
#66 Darin Brown
February 21, 2006

Dale,

I think you have a misunderstanding of the purpose of the experiment. The hypothesis that we would be testing, is whether HIV is a perinatally transmitted passenger virus, like all other retroviruses. The experiment really has little to do with the exact seroprevalence of HIV in the children, as compared to the general population. The experiment is simple: *IF* there are healthy HIV-positive 10-12 year-old children, randomly distributed in the population, then HIV is perinatally transmitted, and there is no way a perinatally transmitted virus can be pathogenic. It’s as simple and as complicated as that.

I was going to try a more elaborate explanation, but then I found this previously written one, which I don’t dare attempt to improve upon:

“Since perinatal transmission of HIV is at least 50% efficient (18, 20, 34, 62), and sexual transmission is less than 0.2% efficient, it appears that HIV, like other retroviruses, depends on perinatal transmission for survival. Therefore, it cannot be fatally pathogenic in most infections within 2-10 years, as postulated by the virus-AIDS hypothesis. This provides the only plausible explanation for the random distribution of HIV in even as few as 0.03% of 17- to 19-year-old healthy Americans (53) and in about 10% of Africans of all ages (31, 34, 49, 51).” (Duesberg, AIDS epidemiology: Inconsistencies with human immunodeficiency virus and with infectious disease, PNAS Vol. 88, pp. 1575-1579, February 1991 Medical Sciences)

The paper (and references) are available at

http://www.virusmyth.net/aids/data/pdpnas91.htm

With regard to the reference (53), this is the Army recruit study (Burke et al, 1990) to which I previously referred. Here, it would neither be legal nor ethical to attempt an epidemiological retrospective analysis of the mothers of the recruits. But such problems would not arise from the proposed experiment. Indeed, such an experiment was discussed in South Africa several years ago, just for this very reason.
#67 Dale
February 21, 2006

Darin writes “The hypothesis that we would be testing, is whether HIV is a perinatally transmitted passenger virus, like all other retroviruses. The experiment really has little to do with the exact seroprevalence of HIV in the children, as compared to the general population. The experiment is simple: *IF* there are healthy HIV-positive 10-12 year-old children, randomly distributed in the population, then HIV is perinatally transmitted,”

Of course HIV is perinatally transmitted and a fraction of the individuals to whom it is transmitted are still healthy at 10-12 years of age, although many have already acquired AIDS. That’s empirical observation, not mathematical modeling. Studies looking at HIV positive versus HIV negative children of HIV positive mothers say the former have a 5 fold or greater mortality rate within their first couple of years than the latter. Doesn’t sound like a passenger virus to me.
#68 Harvey Bialy
February 21, 2006

I would like to add a few personal remarks to the “retrospective, tracing” studies that Pres. Mbeki’s panel agreed upon in South Africa in July 2000.

The announcement of the agreement to carry out these studies was greeted with genuine pleasure by the South Africa media because not only was it a substantial point of “experimental accord” between the two otherwise irreconcilable panel positions regarding HIV and its causal role in AIDS, but it also provided an occasion for Helen Galye of the CDC (now the AIDS director of the Gates Fdn.) and Peter Duesberg to be photographed together, almost cuddly.

When I returned to Mexico, Helen and I and some of her colleagues at the CDC had two telephone exchanges regarding the organizational aspects of these studies.

Not surprisingly, it turned out to be “too difficult, because the original records are anonymous and trying to collect all the necessary documents would be impossible.”

However, and I have this on digital mini-discs, Helene was quite forthcoming in admitting that the study was excellent in principle, and would most probably give a result that strongly supported, if not, proved the hypothesis that HIV in the US was a passenger virus, but that of course said nothing about HIV’s behavior in Africa.
#69 Dean Esmay
February 22, 2006

I am very much enjoying this recent discussion, and particularly delighted to see Chris Noble again. Hi Chris! Much love to you my brother!

Chris had ample opportunity a year ago to ask any questions about those “magic graphs” (his phrasing), because I provided him that opportunity. Now he’s got new questions, which I find interesting.

Last year, although I had never spoken to Duesberg, I got into a phone conversation with Harvey after emailing him a few questions about HIV. That’s when he asked me to look at those graphs. As I contemplated them I thought they said something important, so agreed to publish them if they (Harvey, Duesberg, Rasnick, etc.) would agree to answer any questions I or my readers had. I thought this was a terrific opportunity for them to either make their case before a wider audience, OR, for them to be destroyed in the eyes of that same audience. Win-win either way as I saw it. I like debunking psuedoscientists–I do it a lot–so I figured this was promising. Dean�s World is by no means a peer-reviewed journal, but we have a wide readership (about 6 million page views last month), with lots of working scientists, public policy makers, working journalists, and educated laymen. Harvey had me convinced that they had something important here, BUT, if I were wrong I would be more than happy to be proven wrong, and to have the experience of helping to show how Duesberg & Co. were dishonest, stupid, or just plain wrong.

Notably, at the time I published those graphs, I also made an open offer: if any credentialed epidemiologist would care to directly address the graphs, the data they were based on, and the inferences drawn from same, I would immediately publish that response. Completely unedited, and in full. The only requirement: that he or she put their name and credentials on the response. No other requirements. I would�and will�publish such a response in full, or link to it if it�s published elsewhere.

To date, there has been no such response. None that I’m aware of anyway. It remains an open offer.

As I recall, out friend Chris Noble (who had never appeared on my blog before, and whom I initially confused with a friend with the same name) spent most of his time attacking the intellect and character of Duesberg, Harvey, myself, and anyone who dared bring these questions up. Chris behaved very much in the style of Orac-The-Surgeon-Who-Knows-All. The crowning moment was when he and some of his buddies attacked me when I noted that my wife and I were busy having a baby that very week, by c-section, and that I was badly pressed for time. This was used to accuse me of avoiding questions, even though I repeatedly said I was struggling for time, couldn’t possibly keep up with the (VERY lengthy) discussion at the moment, but would immediately forward on any serious questions to Duesberg.

As I recall, when Noble attacked the graphs originally, it was for not being sufficiently referenced (although how he thought it would get through peer review at a prestigious journal like J. Biosci without evidence I didn�t know). Still, I immediately asked for references from Duesberg, and he immediately forwarded me to his co-author Rasnick. Rasnick rounded references up for me and emailed them along. (This by the way is quite typical of my experience; email Duesberg, Rasnick, or some of the other HIV skeptics with direct requests, and you get polite responses with data and references within a reasonably short time period. If the people who sling around hateful words like “denialist” were equally forthcoming, I probably would have long ago lost interest in this subject. For whatever that�s worth.)

Anyway, now I see that Chris has a new challenge to the graphs that he has not previously brought to my attention. I find myself wondering why it wasn’t raised before, and why he wouldn�t simply email Duesberg about it? Perhaps Chris was too busy calling people names and accusing them of being idiots and “denialists” to bother? I don�t know.

But this new challenge from Dr. Noble brings to mind the same question I’ve had before: this stuff has been published previously in a quite respectable peer-reviewed journal. If you’re a credentialed scientist, and you don�t want to publish a detailed response on my blog, you�re also free to challenge it in the pages of J. Biosci. If your debunking is any good at all, they�ll probably publish it, and if they don’t a competitor certainly would. So why don�t you? Duesberg’s last paper on HIV was only in 2003, and J. Biosci is a world-class and fully respectable journal.

Indeed, getting away from the subject of these graphs, a much larger question presents itself: Duesberg makes many very specific claims about what is found in the literature on HIV, and provides copious references in all his papers. These papers make it through peer review in some of the most respected journals on the planet, including Genetica, The Lancet, PNAS, and more. If Duesberg could be shown, in the pages of any of these journals, to be distorting or twisting the data, he would effectively be demolished.

As Gerald Pollack, professor of bioengineering at the University of Washington recently wrote in his review of Harvey’s biography of Duesberg, “If the papers that Duesberg cites are not misrepresented – and it is difficult to see how hundreds of papers could be misrepresented without the AIDS establishment coming down mercilessly on his misrepresentations – then his points are indeed compelling.” (see http://www.deanesmay.com/posts/1136852361.shtml )

By “coming down mercilessly,” Pollack doesn’t mean on Usenet discussions or blog postings, nor in the pages of the New York Times. He means in the peer-reviewed journals. As he told me in private correspondence–and remember, Professor Pollack has NEVER been an HIV dissident, has NEVER written on the issue until reading Harvey’s book recently–if Duesberg could be shown to be distorting or abusing the literature, he would be finished, destroyed. Not just on this issue, but on anything else he tried to publish. Like Woo Suk Hwang, if he were exposed as a scientific fraud, he would no longer be published in any respectable journal, on ANY subject. He�d either disappear completely in shame, or be stuck laboring in obscurity and publishing in obscure semi-journals like “Alternative Medicine Magazine,” or “Medical Hypotheses” at best.

So for Chris, and Tara, and all the rest: here�s your big chance now. You want to make your name, and reduce the “denialist” beast to the same level as crystal healing and vitamin pushers and such? Publish a blow-by-blow takedown of Duesberg’s 2003 paper and submit it to J. Biosci or a competing journal. You�ll make your scientific bones, no question. International acclaim will be yours. You’ll be the one who finally slew Duesberg before the eyes of the scientific establishment.

Good luck. From what I�ve seen int he last year, you’ll need it.

(I cheerfully look forward to responses which mock my character, my motives, and my intelligence. It comes with the territory. It used to hurt my feelings, but increasingly it just amuses me.)
#70 Dean Esmay
February 22, 2006

Oh, and if, as has been suggested earlier in this thread, there HAVE been rebuttals published to Duesberg’s papers, could you please cite them? Specifically I would like to see any rebuttals that appeared in the peer-reviewed literature to the following papers:

Duesberg, P., Koehnlein, C. and Rasnick, D. (2003) The Chemical Bases of the Various AIDS Epidemics: Recreational Drugs, Anti-viral Chemotherapy and Malnutrition. (J. Biosci. 28: 383-412)

Duesberg, P.H. (1995) Foreign-protein-mediated immunodeficiency in hemophiliacs with and without HIV
(Genetica 95: 51-70)

Duesberg, P. H. (1993) The HIV gap in national AIDS statistics (Biotechnology 11: 955-956)

Duesberg, P. H. (1993) The Enigma of Slow Viruses (The Lancet 342: 720)

Duesberg, P. H. and Schwartz, J. R. (1992) Latent viruses and mutated oncogenes: no evidence for pathogenicity
(Prog Nucleic Acid Res Mol Biol 43: 135-204)

Duesberg, P. H. (1992) AIDS acquired by drug consumption and other noncontagious risk factors (Pharmac. Ther. 55: 201-277), and a searchable textfile.

Duesberg, P. H. (1991) AIDS epidemiology: inconsistencies with human immunodeficiency virus and with infectious disease (Proc Natl Acad Sci USA 88: 1575-1579)

Duesberg, P. H. (1989) Human immunodeficiency virus and acquired immunodeficiency syndrome: Correlation but not causation (Proc Natl Acad Sci USA 86: 755-764)

Those papers are available right here and strike me, in my position as a humble spectator, as the most important ones published since the “debate” that John Maddox limited by restricting participants to a few hundred words and abolishing the right of response.

So, there have been rebuttals to these papers that appeared in these important journals? If so, can someone cite them for me? If I had to restrict to only two of the above, I’d like to see any detailed rebuttal to the 1992 paper in Pharmacology & Therepeutics, or to the 2003 paper in J. Biosci. I’d also be particularly interested in any rebuttals to the piece from the Lancet on slow viruses, and the piece in Genetica that addresses the hemophiliac question.

Not detailed rebuttals here please. Show me the detailed rebuttals that appeared in the peer-reviewed literature. Thanks in advance, I will do whatever I can to get ahold of them if they are available.
#71 JP
February 22, 2006

Darin Brown–

“6 transmissions out of 8400 coital acts is a transmission rate of 1 in 1400. Unless you’re misrepresenting the data.”

Sure. Here’s a comparison:

The transmission rate per sexual act for herpes simplex 2: 1/1200 (from “Effect of Condoms on Reducing the Transmission of Herpes Simplex Virus Type 2 From Men to Women JAMA 2001 285(3100-3106)”)

Herpes is considered to be sexually transmitted. Why not HIV?
#72 Orac
February 22, 2006

I cheerfully look forward to responses which mock my character, my motives, and my intelligence. It comes with the territory. It used to hurt my feelings, but increasingly it just amuses me.)

Pot. Kettle. Black. After all, you have impugned my honesty on more than one occasion, Dean.
#73 Dale
February 22, 2006

Dean

Duesberg’s AIDS arguments were dismissed by the scientific community a decade ago in Nature and Science. Unlike Hwang and stem cells, Duesberg has never published any original data on AIDS or HIV; what he has done is to reinterprete existing data. Scientists in the field can read the existing data and Duesberg’s interpretations for themselves; they don’t need anyone to write endless rebuttals regarding the relative merits of the interpretations.