Whether or not one believes HIV is sexually transmitted, seroconversions occurred. What were their causes, if not HIV infection due to sexual transmission?
First of all, in the other theories, there is no transmission to explain—and it certainly doesn’t have to involve iv drug use.
Where does the HIV come from if not an external source?
I’m having difficulty squaring some of your comments on seropositivity and HIV testing with the high reported sensitivity & specificity of properly conducted HIV tests.
First off, before we get into anything else, we need to understand and agree on what seropositivity actually means. Seropositivity means a positive result on an antibody test such as western blot, to some combination of antigens identified by Gallo in 1985 in his large scale blood screening tests. He did a large number of tests on transformed (immortalized) cell lines derived from AIDS patients and found a combination of antigens that could screen blood—separating AIDS and pre-AIDS blood from regular blood.
The problem is he (like Motagnier) failed to isolate the ‘virus’, and most or all of the antibodies in the test react or cross-react with antigens to opportunistic microbes (candida namely) and cellular debris. The p24 protein in particular is essentially just a normal cellular wall or microvescile component—so the ‘HIV’ test is really just a general test of opportunistic infection and apoptosis or immune directed killing of CD4 cells (possibly due to widespread viral parasite burden). It is not a measure of ‘HIV’, it is a direct measure of declining CD4 cells and AIDS or pre-AIDS.
The antibody tests are not standardized geographically or temporarily, so it also makes it very difficult to compare across studies—“seropositivity” means different things in different places and times.
As just one random example—most dogs typically have a mix of ‘HIV’ antigens, and are HIV ‘seropositive’ in whole or in part:
reported that 72⁄144 (50%) of dog blood samples “obtained from the Veterinary Medical Teaching Hospital, University of California, Davis” tested in commercial Western blot assays, “reacted with one or more HIV recombinant proteins [gp120--21.5%, gp41--23%, p31--22%, p24-- 43%]”
You post a link to a paper which supposedly shows the ” high reported sensitivity & specificity” of HIV tests. This is not actually what that paper is about, but it references several other papers for this claim—the first I investigated being this. The important quote:
Thirty-fourwomentested HIV-1 positive
with both rapid test and EIA, and all
were confirmed by Western blot
(prevalence=7/1000).
So they are just using Western blot as ‘confirmation’. So they are just using one antibody test to confirm another antibody test—which of course is rather ridiculous.
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
But one can attempt to use the presumed viral DNA as a gold standard, and the result is extremely poor sensitivity and specificity:
Poor sensitivity is perhaps a gross understatement—the study actually shows that around 18-25% of the population at large test positive for ‘HIV DNA’, and this is only weakly correlated with seropositivity.
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
Seroconversion in the west is closely correlated with AIDS or pre-AIDS. This does not appear to be as true in Africa, so we are generally talking about two different worlds. Part of this may be genetic (black americans have amazingly higher seropositvity in general), the other part may relate simply to higher precedence of opportunistic infections and antigens that seropositivity measures. KS for example is vary rare in the west and along with systemic candidaisis was part of the original AIDS definition, but it is one of the most common cancers in Africa.
Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not),
I am arguing that.
Seropositivity does not strongly correlate with ‘HIV’ infection (by DNA test), which is why it is better to discuss AIDS itself as being sexually transmittable or not.
The Gallo blood test is tightly correlated with AIDS (at least in the west) - simply because that is what it was designed to do, so you can use that as data for AIDS transmission discussions.
Unless you are now arguing that seroconversion doesn’t actually indicate HIV infection (and I can’t tell whether you are or not),
I am arguing that.
OK. At this point, I’m going to have to disengage and walk away from this debate. I’m realizing that the inferential distance between us is far bigger than I originally thought, and trying to bridge it would need me to considerably ramp up the effort I’m already putting into this. (Even then I can imagine this going on indefinitely, which isn’t a very appealing prospect to me, nor to other Less Wrong posters, by the looks of it.)
I’d still like to respond briefly to one part of your comment, which comments on my own words rather than HIV/AIDS:
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
It’s wholly legitimate for me to respond to someone citing Mullis’s credentials (as if I didn’t know about them already) by explaining why I give them little weight, and my next paragraph was meant to summarize why I gave “your remarks about PCR” (that is, those you paraphrased from Mullis) short shrift. In other words, I acknowledged the argument by rejecting it.
I’m glad you can walk away, I have a harder time initiating that. I’m curious though about the direction of the inferential distance you see—do you have a biology background?
The dissidents point to a rather surprising pile of evidence that the serological HIV tests are based on rather general, cross-reactive antibodies, and this is essentially a fundamental flaw in HIV science which has never been corrected. Now it may be that the orthodoxy has a really good counter to this, but if they do I have yet to find it. The orthodox position on this, from papers linked to wikipedia, points to studies which measure the sensitivity of various HIV antibody tests by comparing them to . . other HIV antibody tests.
The few large double-blind meta-studies that compare the different antibody tests to PCR tests show terrible sensitivity and specificity between the two, and I haven’t seen the orthodox counter to this. So something is wrong with the antibody tests, the PCR tests, or the whole thing. I imagine it’s a little bit of both—the antibody tests are cross-reactive (hence many dogs test positive), and PCR tests are difficult and subject to experimenter bias.
Perhaps the orthodox counter is that there are a whole big host of HIV related viruses, and the antibody tests are cross-reactive across these related species. This seems to then just beg more questions than it answers, and doesn’t circumvent some of the specific non-viral cross-reactions the dissidents point to.
My paraphrase of Mullis’s argument may actually be a mix of other dissident positions. I just rechecked that part of his book and he covers the difficulty of PCR and the confirmation bias but largely in regards to the OJ trial. On HIV he mainly rehashes Deusberg’s argument.
I’m curious though about the direction of the inferential distance you see—do you have a biology background?
None at all. (I expect the inferential distance would be even greater if I did. If I had personal experience of working with retroviruses, for instance, I reckon my prior probabilities for claims like “HIV can not be isolated” or “HIV doesn’t exist” would be far, far less than they are. And they are already very low.)
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
When ‘HIV’ was first ‘discovered’ in the original papers by Gallo and Montagnier, they had difficulty isolating and didn’t publish pictures from what I understand—that didn’t happen until years later. Gallo’s great discovery for HTLVIII was based on running a lager number of antigen/antibody tests with an immortalized cell line to find an antibody test that could screen AIDS and pre-AIDS blood from regular blood. That is the basis of all the current HIV tests.
The first published pictures came more than a decade later, and they showed that “HIV isolate” really consists largely of cellular debris and microvesciles. In these EM photos, they do find some occasional particles of roughly the right size and label them as “HIV”, but they could also just be any of a number of other things, and for all intents and purposes, HIV ‘particles’ look like regular microvesciles.
The titles of the papers say it all:
“Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations”
“Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations”
I have lost the link, but there are better more recent pictures taken with ATM, and they show that for all intents and purposes, it’s impossible to distinguish ‘HIV’ from regular microvesicles that bud from the cell wall naturally. If HIV can be said to exist at all as a unique exogenous virus, it is only because of unique RNA content in the microvesicle, and in this sense is very much unlike all other known viruses.
Of course, the part of HIV’s genome which is supposed to code for the outer envelope is pretty much the same as the endogenous sequences that already exist in the human genome—the HERVs.
First off, before we get into anything else, we need to understand and agree on what seropositivity actually means. Seropositivity means a positive result on an antibody test such as western blot, to some combination of antigens identified by Gallo in 1985 in his large scale blood screening tests. He did a large number of tests on transformed (immortalized) cell lines derived from AIDS patients and found a combination of antigens that could screen blood—separating AIDS and pre-AIDS blood from regular blood.
The problem is he (like Motagnier) failed to isolate the ‘virus’, and most or all of the antibodies in the test react or cross-react with antigens to opportunistic microbes (candida namely) and cellular debris. The p24 protein in particular is essentially just a normal cellular wall or microvescile component—so the ‘HIV’ test is really just a general test of opportunistic infection and apoptosis or immune directed killing of CD4 cells (possibly due to widespread viral parasite burden). It is not a measure of ‘HIV’, it is a direct measure of declining CD4 cells and AIDS or pre-AIDS.
more on this
and a longer, more detailed analysis of cross-reactivity for the different ‘HIV’ proteins
The antibody tests are not standardized geographically or temporarily, so it also makes it very difficult to compare across studies—“seropositivity” means different things in different places and times.
As just one random example—most dogs typically have a mix of ‘HIV’ antigens, and are HIV ‘seropositive’ in whole or in part:
from this paper
You post a link to a paper which supposedly shows the ” high reported sensitivity & specificity” of HIV tests. This is not actually what that paper is about, but it references several other papers for this claim—the first I investigated being this. The important quote:
So they are just using Western blot as ‘confirmation’. So they are just using one antibody test to confirm another antibody test—which of course is rather ridiculous.
To actually compute the sensitivity and specificity for a “HIV” test, one needs a gold standard such as viral isolation or perhaps a DNA test. Unfortunately HIV can not be isolated, either because it doesn’t exit or it exists in only minute quantities.
But one can attempt to use the presumed viral DNA as a gold standard, and the result is extremely poor sensitivity and specificity:
Poor sensitivity, specificity, and reproducibility of detection of HIV-1 DNA in serum by polymerase chain reaction. The Transfusion Safety Study Group.
Poor sensitivity is perhaps a gross understatement—the study actually shows that around 18-25% of the population at large test positive for ‘HIV DNA’, and this is only weakly correlated with seropositivity.
You completely dismiss Mullis’s argument based solely on an ad hominem “not much impressed by Mullis’s nobel credentials” without seeming to acknowledge or understand the argument itself.
Seroconversion in the west is closely correlated with AIDS or pre-AIDS. This does not appear to be as true in Africa, so we are generally talking about two different worlds. Part of this may be genetic (black americans have amazingly higher seropositvity in general), the other part may relate simply to higher precedence of opportunistic infections and antigens that seropositivity measures. KS for example is vary rare in the west and along with systemic candidaisis was part of the original AIDS definition, but it is one of the most common cancers in Africa.
I am arguing that.
Seropositivity does not strongly correlate with ‘HIV’ infection (by DNA test), which is why it is better to discuss AIDS itself as being sexually transmittable or not.
The Gallo blood test is tightly correlated with AIDS (at least in the west) - simply because that is what it was designed to do, so you can use that as data for AIDS transmission discussions.
OK. At this point, I’m going to have to disengage and walk away from this debate. I’m realizing that the inferential distance between us is far bigger than I originally thought, and trying to bridge it would need me to considerably ramp up the effort I’m already putting into this. (Even then I can imagine this going on indefinitely, which isn’t a very appealing prospect to me, nor to other Less Wrong posters, by the looks of it.)
I’d still like to respond briefly to one part of your comment, which comments on my own words rather than HIV/AIDS:
It’s wholly legitimate for me to respond to someone citing Mullis’s credentials (as if I didn’t know about them already) by explaining why I give them little weight, and my next paragraph was meant to summarize why I gave “your remarks about PCR” (that is, those you paraphrased from Mullis) short shrift. In other words, I acknowledged the argument by rejecting it.
I’m glad you can walk away, I have a harder time initiating that. I’m curious though about the direction of the inferential distance you see—do you have a biology background?
The dissidents point to a rather surprising pile of evidence that the serological HIV tests are based on rather general, cross-reactive antibodies, and this is essentially a fundamental flaw in HIV science which has never been corrected. Now it may be that the orthodoxy has a really good counter to this, but if they do I have yet to find it. The orthodox position on this, from papers linked to wikipedia, points to studies which measure the sensitivity of various HIV antibody tests by comparing them to . . other HIV antibody tests.
The few large double-blind meta-studies that compare the different antibody tests to PCR tests show terrible sensitivity and specificity between the two, and I haven’t seen the orthodox counter to this. So something is wrong with the antibody tests, the PCR tests, or the whole thing. I imagine it’s a little bit of both—the antibody tests are cross-reactive (hence many dogs test positive), and PCR tests are difficult and subject to experimenter bias.
Perhaps the orthodox counter is that there are a whole big host of HIV related viruses, and the antibody tests are cross-reactive across these related species. This seems to then just beg more questions than it answers, and doesn’t circumvent some of the specific non-viral cross-reactions the dissidents point to.
My paraphrase of Mullis’s argument may actually be a mix of other dissident positions. I just rechecked that part of his book and he covers the difficulty of PCR and the confirmation bias but largely in regards to the OJ trial. On HIV he mainly rehashes Deusberg’s argument.
All right, enough.
None at all. (I expect the inferential distance would be even greater if I did. If I had personal experience of working with retroviruses, for instance, I reckon my prior probabilities for claims like “HIV can not be isolated” or “HIV doesn’t exist” would be far, far less than they are. And they are already very low.)
So those electron microscope pictures are fakes?
Which electron microscope pictures?
When ‘HIV’ was first ‘discovered’ in the original papers by Gallo and Montagnier, they had difficulty isolating and didn’t publish pictures from what I understand—that didn’t happen until years later. Gallo’s great discovery for HTLVIII was based on running a lager number of antigen/antibody tests with an immortalized cell line to find an antibody test that could screen AIDS and pre-AIDS blood from regular blood. That is the basis of all the current HIV tests.
The first published pictures came more than a decade later, and they showed that “HIV isolate” really consists largely of cellular debris and microvesciles. In these EM photos, they do find some occasional particles of roughly the right size and label them as “HIV”, but they could also just be any of a number of other things, and for all intents and purposes, HIV ‘particles’ look like regular microvesciles.
The titles of the papers say it all:
“Cell membrane vesicles are a major contaminant of gradient-enriched human immunodeficiency virus type-1 preparations”
“Microvesicles are a source of contaminating cellular proteins found in purified HIV-1 preparations”
more on HIV ‘pictures’
I have lost the link, but there are better more recent pictures taken with ATM, and they show that for all intents and purposes, it’s impossible to distinguish ‘HIV’ from regular microvesicles that bud from the cell wall naturally. If HIV can be said to exist at all as a unique exogenous virus, it is only because of unique RNA content in the microvesicle, and in this sense is very much unlike all other known viruses.
Of course, the part of HIV’s genome which is supposed to code for the outer envelope is pretty much the same as the endogenous sequences that already exist in the human genome—the HERVs.
Huh. While I still think that the HIV explanation is the most likely one for AIDS, I am slightly less convinced.