Ok, so I have finished reading O’Brien and JJ Goedert. I think the accidental lab worker cases probably have low utility in distinguishing between pathologic HIV and passenger HIV theories, but the animal SIV studies potentially fulfill the ideal experiment design. If animals injected with pure close SIV analogs to HIV develop AIDS-like illness, that is about as good as evidence as one could hope for.
For the lab worker infections, they say that the genomes are close to the clonal strain used in the lab, but they don’t have a good probalistic model for this:
The sequence divergence
between LW virus envelope genes and clonal HTLV-IIIB
is <3%, which is the same genetic distance from LAV-LAI
to HTLV-IIIB, viral strains now agreed by all to have
been derived from a single patient [54,55]. This low
level of sequence divergence is equivalent to the variation
observed between HIV-infected infants and their mothers,
and threefold less than the extent of variation of HIV
between unconnected patients [56].
threefold more or less variation doesn’t sound like much to me, and regardless even assuming they did all get infected via the lab, it doesn’t mention treatment, so we don’t know if they were treated with AZT or what.
I think the animal models are more interesting—as all the drug cofounding variables are eliminated and everything is controlled.
The authors discuss 3 animal models—baboons, some wierd knockout mice with human t-cell graphs, and finally SIV injected into rhesus monkeys. They spend the most time discussing the latter paper so I looked into it.
“Induction of AIDS in Rhesus Monkeys by Molecularly Cloned Simian Immunodeficiency”.
In short, all 5 of the monkeys injected later become seropositive, and 50% of them progress to AIDs-like illnesses and die. Presumably some are naturally resistant.
There is a potential issue to this otherwise smoking gun, which is that it appears they had to inject whole culture of T-cells, as the virus can not be isolated directly into plasmid vectors:
We, and others, have experienced considerable considerable difficulty in subcloning the full-length proviral DNA into plasmid vectors.
SIV mac239-cloned DNA was transfected into primary macaque PBLs and into Hut 78 cells (a human CD4+ T cell line) by a DEAE-dexxtran procedure, and stock virus was frozen for subsequent animal inoculations
But if all they had then was provirus integrated into PBL ( peripheral blood lymphocytes ), then one must wonder about the risk of graft versus host disease, and transfusion reaction in general. Basically, the foreign T-cell line can actively invade and cause all kinds of havoc. Perhaps they have controlled for that and I’m completely off, but I don’t see where they mention it.
OBrien and Goodart conclude:
Control macaques inoculated with
saline, with inactivated SIVMAcA239 or with SIVMACA239
carrying mutations/deletions in the nef gene failed to
induce AIDS in the same macaque species [80,83,84].
Because SIV strains cause AIDS in monkeys and because
they are the closest phylogenetic relatives of HIV, they
provide an animal model fulfillment of Koch’s transmission
I haven’t seen mention of ‘inactivated’ sivmaca239 yet in 80, but maybe it is in 83 or 84. However, if they are forced to infect live T-cells because they can’t produce viable clonal plasmid, this seems to have a major confounding factor in graft vs host disease. I’d like to find a knowledge skeptic take on this—perhaps Duesberg confronts it, not sure yet.
If he doesn’t confront it, then that doesn’t look so good for his position.
It appears to me that you are noting different weaknesses, different alternative explanations of the results, in each experimental protocol. I imagine that could appear to happen if there were a strong publication bias for results in favor of the hypothesis (e.g. with medicinal prayer studies), but that has not been demonstrated.
From what I understand, there is strong reason to suspect such bias in the animal models, as many other animal tests were conducted previously attempting to show SIV causing AIDS, and they uniformly failed. From what I have read, the SIV injections failed to do anything in chimps. We don’t know how many other rhesus monkeys were injected, but I find it highly unlikely that the five in this study (3 out of 5 of which developed immune defeciency) were the first.
That bias is interesting and it would be useful to have a metastudy covering all the animals that have been injected, but of course most naturally occuring strains of species specific virus should be expected to be harmless. So the ‘bias’ doesn’t really tell you much and is expected either way.
I’ll look to see if there is any skeptic review of the SIV injections which did succeed, because in my mind that is fairly strong evidence. If HIV analogs cause AIDS-like illness in primates when they hop species or traditional barriers, this is a good experiemental model for HIV crossing over into humans and causing illness, and is far stronger in my mind than the murky epidimelogical data with all of it’s drug cofactor issues.
The lab monkeys are in a controlled environment—we know they weren’t using drugs, weren’t fed AZT, etc etc.
Ok, so I have finished reading O’Brien and JJ Goedert. I think the accidental lab worker cases probably have low utility in distinguishing between pathologic HIV and passenger HIV theories, but the animal SIV studies potentially fulfill the ideal experiment design. If animals injected with pure close SIV analogs to HIV develop AIDS-like illness, that is about as good as evidence as one could hope for.
For the lab worker infections, they say that the genomes are close to the clonal strain used in the lab, but they don’t have a good probalistic model for this:
threefold more or less variation doesn’t sound like much to me, and regardless even assuming they did all get infected via the lab, it doesn’t mention treatment, so we don’t know if they were treated with AZT or what.
I think the animal models are more interesting—as all the drug cofounding variables are eliminated and everything is controlled.
The authors discuss 3 animal models—baboons, some wierd knockout mice with human t-cell graphs, and finally SIV injected into rhesus monkeys. They spend the most time discussing the latter paper so I looked into it.
“Induction of AIDS in Rhesus Monkeys by Molecularly Cloned Simian Immunodeficiency”.
In short, all 5 of the monkeys injected later become seropositive, and 50% of them progress to AIDs-like illnesses and die. Presumably some are naturally resistant.
There is a potential issue to this otherwise smoking gun, which is that it appears they had to inject whole culture of T-cells, as the virus can not be isolated directly into plasmid vectors:
But if all they had then was provirus integrated into PBL ( peripheral blood lymphocytes ), then one must wonder about the risk of graft versus host disease, and transfusion reaction in general. Basically, the foreign T-cell line can actively invade and cause all kinds of havoc. Perhaps they have controlled for that and I’m completely off, but I don’t see where they mention it.
OBrien and Goodart conclude:
I haven’t seen mention of ‘inactivated’ sivmaca239 yet in 80, but maybe it is in 83 or 84. However, if they are forced to infect live T-cells because they can’t produce viable clonal plasmid, this seems to have a major confounding factor in graft vs host disease. I’d like to find a knowledge skeptic take on this—perhaps Duesberg confronts it, not sure yet.
If he doesn’t confront it, then that doesn’t look so good for his position.
It appears to me that you are noting different weaknesses, different alternative explanations of the results, in each experimental protocol. I imagine that could appear to happen if there were a strong publication bias for results in favor of the hypothesis (e.g. with medicinal prayer studies), but that has not been demonstrated.
From what I understand, there is strong reason to suspect such bias in the animal models, as many other animal tests were conducted previously attempting to show SIV causing AIDS, and they uniformly failed. From what I have read, the SIV injections failed to do anything in chimps. We don’t know how many other rhesus monkeys were injected, but I find it highly unlikely that the five in this study (3 out of 5 of which developed immune defeciency) were the first.
That bias is interesting and it would be useful to have a metastudy covering all the animals that have been injected, but of course most naturally occuring strains of species specific virus should be expected to be harmless. So the ‘bias’ doesn’t really tell you much and is expected either way.
I’ll look to see if there is any skeptic review of the SIV injections which did succeed, because in my mind that is fairly strong evidence. If HIV analogs cause AIDS-like illness in primates when they hop species or traditional barriers, this is a good experiemental model for HIV crossing over into humans and causing illness, and is far stronger in my mind than the murky epidimelogical data with all of it’s drug cofactor issues.
The lab monkeys are in a controlled environment—we know they weren’t using drugs, weren’t fed AZT, etc etc.