Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression? (I am asking before I read the article)
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression?
From what I see, O’Brien and Goedert don’t report about this. However, Cohen’s Science article to which I linked above provides more details about the cases of infected lab workers, claiming that two of them didn’t receive any antivirals until the progress of AIDS was well underway: http://www.sciencemag.org/feature/data/cohen/266-5191-1647a.pdf
I have seen that, but I don’t take it as strong evidence of anything either way.
Clearly HIV antibodies are correlated with ill-health, poor immune function and low CD4 counts—that was established in the very beginning by Gallo et all and is the entire basis of their original claim.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong.
So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
This is very different than the intentional infection test you need to establish strong causation along a koch’s postulate principle. I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
Instead the theory is that HIV came from a chimp SIV and somehow became lethal and horizontally transmissable at the same time in humans. But from the studies of sexual transmission—it is only weakly blood transmissable. So overall, it’s alot to swallow. I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors. As Duesberg notes, the cocaine/meth craze boomed in the 80′s right as the AIDS epidemic started—they overlap perfectly.
Deusberg’s theory is that drugs specifically are a major cause of the immunosupression, which I think has some absolute validity, but we should also notice that there are other causes, and some people just have poor immune health, and this has been the case for long before HIV came on the scene.
I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
I think that, in general, viruses that jump species barriers are more lethal in their new hosts than their old ones. Selection pressure tends to make viruses that are transmitted from individual to individual less dangerous over time, not more, because a dead host can’t spread the virus. So the fact that chimps tolerate SIV better than humans tolerate HIV isn’t a strike against the “HIV is mutated SIV” theory.
Also, there exists a more direct counterexample: FIV, feline immunodeficiency virus, is an HIV-like virus that is commonly found in lions. It doesn’t harm lions very much, but it’s lethal to domestic cats, which haven’t co-evolved with the virus the way lions have. (Specifically, lions compensate for the loss of T-cells to the virus by producing them in much larger numbers than other animals do.)
Perhaps not all viruses that jump species barriers are more lethal, but we care most about the lethal ones for sure, and lethality or host damage is a side effect of high replication, so yes I agree with your analysis.
I also said:
I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors.
I’m reading the OBrien Goddert response now that cites some animal studis showing how some animal HIV analogs do fulfill koch’s postulate now. I am reading into the sources, but I wasn’t aware overall that they had found animal HIV analogs that caused AIDS like symptoms. I’ll have to update towards the ‘HIV is more pathogenic’ stance if this all checks out.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong. So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
According to O’Brien and Goedert, however, the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients. This looks like powerful evidence against the competing hypothesis. On the other hand, it seems like there have been disputes about the validity of these identification procedures, and Duesberg and other skeptics raised some specific objections to them back then. However, this gets into technical issues that I’m definitely not competent to judge on.
(I should add that I haven’t delved into the references provided by O’Brien and Goedert, which Robin has conveniently listed in his above comment, to see if their summary of the facts is accurate and complete.)
Also, while we are looking at evidence for one side or the other, I should present some of the recent evidence that supports the Deusberg hypothesis, namely that cocaine use can cause HIV progression and AIDS-defining illness. Heavy cocaine use and HIV+ status are extremely correlated, the question is one then of causation.
Just search for “cocaine cd4 counts”|
From a rat study linked here
We noted a 200- to 300-fold increase in HIV RNA copy numbers in the peripheral blood obtained from cocaine-treated, HIV-infected animals when compared with HIV-infected controlsExposure to cocaine alone did not affect the implantation of PBL, suggesting a specific interaction between cocaine and HIV. This report describes a model for evaluating HIV cofactors and supports cocaine’s role in the development and progression of AIDS.
Even more interesting—an abstract from a more recent study showing that crack cocaine can cause AIDS independently (in women at least)
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women.
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
If O’Brien and Goedert are right, it would depend on how many strains there are and what their prevalence is ahead of time—I think Bayes’ Theorem would apply, no? Also, I guess we just have to presume that no other sick people from the sample were not reported. And finally, the sample size of 1 or 2 raises some theoretical issues, but still it would be interesting.
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
No. There are two major HIV strains, HIV-1 and HIV-2, with the vast majority of infections in the US being HIV-1. However, there are many substrains of both. In general, since HIV has a high mutation rate, there are individual genetic markers for different people. No one who has HIV for more than a few weeks has a single form of HIV in them but already will have a population of slightly distinct forms. This is part of what makes HIV so pesky for the immune system, for developing vaccines, and for developing drugs to combat it. Note that this isn’t that rare. For example, influenza does something similar although my impression is that this is not nearly as extreme an example.
Frankly, this is a very basic aspect of HIV biology, which you could find on any primer on the subject. If one doesn’t know about this, this suggests major gaps in one’s knowledge base about HIV and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
Because he said “2 HIV strains” rather than “2 major HIV strains with many substrains”? He should be disqualified from participating in debate on a topic because he failed to use sufficiently precise language on a point not relevant to the current discussion?
I’m a non-partisan on this issue, having not researched it enough to have a firm opinion… but the consistent use of these kinds of dark side debate tactics by one side makes me seriously tempted to update in the opposite direction.
the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients.
It seemed pretty clear from context that Vlad was talking about substrains. If there’s anything that went wrong here, judging from Jacob’s followup remark, it was an illusion of transparency failure on my part in that Vlad’s meaning seemed clear to me, and I then made the (erroneous) conclusion that someone with a basic background would also get what Vlad was talking about.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with. Indeed, sometimes it is very necessary. See for example some of the discussion on cousin it’s recent post where it seemed that some individuals (well, primarily one individual) were making repeated subtle but highly relevant errors about certain ideas related to Godel’s theorems and Turing machines. After repeated attempts to explain, the mathematicians in the thread (including myself) started trying to explain that the errors in question were basic enough that further attempts to explain would likely be fruitless. That’s not a dark side tactic, sometimes that’s just true.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with
Yes, I absolutely agree. But that’s not the tactic I was referring to. The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
Hrrm? Imprecision if anything occurred on Vlad’s part, not Jacob’s. Again, see issue of illusion of transparency matter. See also Vlad’s remark below.
It seemed pretty clear from context that Vlad was talking about substrains.
Yes, of course. I’m not familiar with the finer points of terminology in this area, but the O’Brien-Goedert paper uses the term “strain” both for the two major strains and their sub-strains, and I’ve noticed the same in many other papers too. So I don’t think this was imprecise in any way.
Vlad originally used the word ‘strains’, not substrains, and I have only ever heard ‘strains’ used in reference to HIV1 and HIV2 as you say. But yes I am at least somewhat aware of sub-strains through protein coding variation in viruses in general, and how mutations lead to new epidemics.
I’m not sure what the proper ‘background’ is just to discuss an issue, but I probably don’t have it, regardless.
(I initially posted an excerpt from the paper in this comment, but in the meantime, I found an ungated version. The stuff about the accidental transmissions is on page 615.)
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
The article cited here? I downloaded a copy if anyone wants to PM me an email address.
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
If you want absolute certainty, you need to fulfill koch’s postulates, which is the medical disease variant of experimental physics, and is well grounded.
So yes, in questions of science, we do demand specific evidence for near-certain proof, but naturally when that is not possible for whatever reason, we can still update based on other evidence and reach well grounded conclusions.
First of all, you never have absolute certainty. Proof is for math and alcohol. You may also want to read the Sequences relevant to Bayesian reasoning especially about how 0 and 1 are not probabilities.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic. Even Koch was willing to treat the first postulate as a guideline rather than a hard and fast rule; he worked with multiple examples of microorganisms that showed up in some healthy people but didn’t cause disease In fact we know now that this very common. Many causes of minor infections, such as staph, are present on everyone. It then takes some problem, such a wound, or disruption of the immune system to cause the person to become unhealthy. For viral examples, look at asymptomatic herpes or HPV.
Frankly, referring to Koch’s postulates like this are one of the things that makes many people with medical knowledge not take the HIV-AIDS skeptics very seriously. As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be. This seems for example to occur frequently with creationists who use an oversimplified form of Mendelian genetics that seems to date prior to the work of Hardy, Weinberg, and Fisher. As a way of preventing this signal, referring to such things as Koch’s work can be done, but you need to be clear that you understand the limitations it has. Otherwise, it just sets off alarm bells.
As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic.
It is also difficult to empirically test elements of String Theory or evolutionary history. This difficulty isn’t taken to be evidence for against those theories. Lack of easy clear cut empirical tests is just that—lack of a simple theorem discriminator. I am not claiming that it is some magic pass required for any theory to be credible.
On the other hand, nor can one use lack of said simple theorem discriminator to get a free pass and somehow claim to have extra certainty—that most come from evidence regardless.
However, in this case I do think that the general idea of Koch’s postulate is highly relevant, it is not ‘cranky’ to invoke it, and in fact it is probably the single strongest piece of evidence for the mainstream position—as Vlad M pointed out to me.
I am currently reading:
”
HIV causes AIDS: Koch’s postulates fulfilled”
Guest editorial
Stephen .I O’Brien* and .lames ,i Goederff
It reviews SIV models where SIV can be prepared and injected into monkeys and in some cases does cause AIDS like disease progression (usually more quickly than HIV).
So I don’t think your associations between “referring to Koch’s postulates” and cranks, and your general heuristic are valid at all, not when the mainstream is listing this as a centerpiece of evidence.
I haven’t read the editorial yet, but I’m not sure where the notion that this was a centerpiece of evidence comes from. I was vaguely aware of this result but never have paid it much attention. I suspect that if one talked to active AIDS and HIV researchers they’d say that there was a very strong case even without this. But yes, conservation of expected evidence does come into play here, so you have a valid point. In any event, the upshot that Koch’s postulates are not seen as any sort of absolute is very much relevant.
S.J. O’Brien and J.J. Goedert (1996) (the paper cited by Vladimir_M) specifically references Koch’s postulates. The accidental infection of laboratory workers is only one of five items cited in reference to (I believe) #3, “The cultured microorganism should cause disease when introduced into a healthy organism.”
Yes, but were they treated with chemotherapy agents such as AZT which cause bone marrow and immune supression? (I am asking before I read the article)
For the controlled experiment example, it would have to be double blind the entire time. Nobody would ever know who got placebo and who didnt’, and no difference in treatment regimens either way—all on the same diet, same lifestyle, etc etc. I highly doubt the accidental cases fit that profile.
jacob_cannell:
From what I see, O’Brien and Goedert don’t report about this. However, Cohen’s Science article to which I linked above provides more details about the cases of infected lab workers, claiming that two of them didn’t receive any antivirals until the progress of AIDS was well underway:
http://www.sciencemag.org/feature/data/cohen/266-5191-1647a.pdf
I have seen that, but I don’t take it as strong evidence of anything either way.
Clearly HIV antibodies are correlated with ill-health, poor immune function and low CD4 counts—that was established in the very beginning by Gallo et all and is the entire basis of their original claim.
But the competing hypothesis is not the null hypothesis, the competing hypothesis is that the HIV presence is a marker of some severe immune function failure, and that HIV itself is a largely harmless vertically transmitted retrovirus—like all the others. If it does become active, it is because something is already seriously wrong.
So of course if you have a lab, and you are testing lab-workers deathly afraid of contracting HIV, in either theory some may come up HIV+, and in either theory those that test positive will be ill.
This is very different than the intentional infection test you need to establish strong causation along a koch’s postulate principle. I think one of the stronger flaws in current HIV theory is the chimpanzee models—they have many HIV similar retroviruses (SIV’s), they are common in wild chimps, are all vertically transmitted, and don’t appear to be problematic for chimps. If HIV killed chimps outright, the mainstream theory would have some more ammo.
Instead the theory is that HIV came from a chimp SIV and somehow became lethal and horizontally transmissable at the same time in humans. But from the studies of sexual transmission—it is only weakly blood transmissable. So overall, it’s alot to swallow. I think it is plausible that this happened and HIV causes novel problems in humans, but it certainly has not been well demonstrated, mainly because HIV doesn’t cause specific symptoms and it is extremely difficult to properly dissociate other causitive factors. As Duesberg notes, the cocaine/meth craze boomed in the 80′s right as the AIDS epidemic started—they overlap perfectly.
Deusberg’s theory is that drugs specifically are a major cause of the immunosupression, which I think has some absolute validity, but we should also notice that there are other causes, and some people just have poor immune health, and this has been the case for long before HIV came on the scene.
I think that, in general, viruses that jump species barriers are more lethal in their new hosts than their old ones. Selection pressure tends to make viruses that are transmitted from individual to individual less dangerous over time, not more, because a dead host can’t spread the virus. So the fact that chimps tolerate SIV better than humans tolerate HIV isn’t a strike against the “HIV is mutated SIV” theory.
Also, there exists a more direct counterexample: FIV, feline immunodeficiency virus, is an HIV-like virus that is commonly found in lions. It doesn’t harm lions very much, but it’s lethal to domestic cats, which haven’t co-evolved with the virus the way lions have. (Specifically, lions compensate for the loss of T-cells to the virus by producing them in much larger numbers than other animals do.)
Perhaps not all viruses that jump species barriers are more lethal, but we care most about the lethal ones for sure, and lethality or host damage is a side effect of high replication, so yes I agree with your analysis.
I also said:
I’m reading the OBrien Goddert response now that cites some animal studis showing how some animal HIV analogs do fulfill koch’s postulate now. I am reading into the sources, but I wasn’t aware overall that they had found animal HIV analogs that caused AIDS like symptoms. I’ll have to update towards the ‘HIV is more pathogenic’ stance if this all checks out.
jacob_cannell:
According to O’Brien and Goedert, however, the strains of HIV found in these accidentally infected individuals were effectively identical to those from the source of their accidental infection, showing much less difference than is usual for strains taken from two random patients. This looks like powerful evidence against the competing hypothesis. On the other hand, it seems like there have been disputes about the validity of these identification procedures, and Duesberg and other skeptics raised some specific objections to them back then. However, this gets into technical issues that I’m definitely not competent to judge on.
(I should add that I haven’t delved into the references provided by O’Brien and Goedert, which Robin has conveniently listed in his above comment, to see if their summary of the facts is accurate and complete.)
Also, while we are looking at evidence for one side or the other, I should present some of the recent evidence that supports the Deusberg hypothesis, namely that cocaine use can cause HIV progression and AIDS-defining illness. Heavy cocaine use and HIV+ status are extremely correlated, the question is one then of causation.
Just search for “cocaine cd4 counts”| From a rat study linked here
Even more interesting—an abstract from a more recent study showing that crack cocaine can cause AIDS independently (in women at least)
CONCLUSION: Use of crack cocaine independently predicts AIDS-related mortality, immunologic and virologic markers of HIV-1 disease progression, and development of AIDS-defining illnesses among women.
A blog discussion of this here
Perhaps the tide’s are turning in Deusberg’s favor?
I was under the impression that there was only 2 HIV strains, and only HIV-1 is of concern in the west, but I’m no expert on this.
Do you have the O’Brien/Goedert paper link or any of this discussion? Your earlier link was just an editorial summary. Sounds interesting, I’d like to read more into it. (i am going to search now, but if you have the link . . .)
If O’Brien and Goedert are right, it would depend on how many strains there are and what their prevalence is ahead of time—I think Bayes’ Theorem would apply, no? Also, I guess we just have to presume that no other sick people from the sample were not reported. And finally, the sample size of 1 or 2 raises some theoretical issues, but still it would be interesting.
No. There are two major HIV strains, HIV-1 and HIV-2, with the vast majority of infections in the US being HIV-1. However, there are many substrains of both. In general, since HIV has a high mutation rate, there are individual genetic markers for different people. No one who has HIV for more than a few weeks has a single form of HIV in them but already will have a population of slightly distinct forms. This is part of what makes HIV so pesky for the immune system, for developing vaccines, and for developing drugs to combat it. Note that this isn’t that rare. For example, influenza does something similar although my impression is that this is not nearly as extreme an example.
Frankly, this is a very basic aspect of HIV biology, which you could find on any primer on the subject. If one doesn’t know about this, this suggests major gaps in one’s knowledge base about HIV and I’m not at all sure that one who doesn’t know about this has enough background to discuss issues related to whether HIV causes AIDS.
Because he said “2 HIV strains” rather than “2 major HIV strains with many substrains”? He should be disqualified from participating in debate on a topic because he failed to use sufficiently precise language on a point not relevant to the current discussion?
I’m a non-partisan on this issue, having not researched it enough to have a firm opinion… but the consistent use of these kinds of dark side debate tactics by one side makes me seriously tempted to update in the opposite direction.
This isn’t a “dark side” tactic. Vlad wrote:
It seemed pretty clear from context that Vlad was talking about substrains. If there’s anything that went wrong here, judging from Jacob’s followup remark, it was an illusion of transparency failure on my part in that Vlad’s meaning seemed clear to me, and I then made the (erroneous) conclusion that someone with a basic background would also get what Vlad was talking about.
Note incidentally, that using heuristics about whether or not someone has enough background to understand or discuss something is not intrinsically a dark side issue to start with. Indeed, sometimes it is very necessary. See for example some of the discussion on cousin it’s recent post where it seemed that some individuals (well, primarily one individual) were making repeated subtle but highly relevant errors about certain ideas related to Godel’s theorems and Turing machines. After repeated attempts to explain, the mathematicians in the thread (including myself) started trying to explain that the errors in question were basic enough that further attempts to explain would likely be fruitless. That’s not a dark side tactic, sometimes that’s just true.
Yes, I absolutely agree. But that’s not the tactic I was referring to. The tactic in question consists of finding some nitpicky objection to something your opponent said, something not directly relevant to the issue at hand, and something which isn’t even wrong, just insufficiently precise, and discounting the substance of their argument on that basis.
Hrrm? Imprecision if anything occurred on Vlad’s part, not Jacob’s. Again, see issue of illusion of transparency matter. See also Vlad’s remark below.
JoshuaZ:
Yes, of course. I’m not familiar with the finer points of terminology in this area, but the O’Brien-Goedert paper uses the term “strain” both for the two major strains and their sub-strains, and I’ve noticed the same in many other papers too. So I don’t think this was imprecise in any way.
Vlad originally used the word ‘strains’, not substrains, and I have only ever heard ‘strains’ used in reference to HIV1 and HIV2 as you say. But yes I am at least somewhat aware of sub-strains through protein coding variation in viruses in general, and how mutations lead to new epidemics.
I’m not sure what the proper ‘background’ is just to discuss an issue, but I probably don’t have it, regardless.
Ok. Seems to be an error in communication more than anything else then.
FWIW, you seem to have a much better understanding of a lot of this material than most of the HIV-AIDS skeptics I’ve interacted with in the past.
(I initially posted an excerpt from the paper in this comment, but in the meantime, I found an ungated version. The stuff about the accidental transmissions is on page 615.)
The article cited here? I downloaded a copy if anyone wants to PM me an email address.
I’m not sure you are allowed to demand that specific piece of evidence.
If you want absolute certainty, you need to fulfill koch’s postulates, which is the medical disease variant of experimental physics, and is well grounded.
So yes, in questions of science, we do demand specific evidence for near-certain proof, but naturally when that is not possible for whatever reason, we can still update based on other evidence and reach well grounded conclusions.
First of all, you never have absolute certainty. Proof is for math and alcohol. You may also want to read the Sequences relevant to Bayesian reasoning especially about how 0 and 1 are not probabilities.
Note also that even outside a Bayesian context, Koch’s postulates are a rough framework. For example, sometimes there is great difficulty growing an organism in a culture (Koch’s second postulate requires this), and sometimes only a fraction of a population may be symptomatic. Even Koch was willing to treat the first postulate as a guideline rather than a hard and fast rule; he worked with multiple examples of microorganisms that showed up in some healthy people but didn’t cause disease In fact we know now that this very common. Many causes of minor infections, such as staph, are present on everyone. It then takes some problem, such a wound, or disruption of the immune system to cause the person to become unhealthy. For viral examples, look at asymptomatic herpes or HPV.
Frankly, referring to Koch’s postulates like this are one of the things that makes many people with medical knowledge not take the HIV-AIDS skeptics very seriously. As a general heuristic, cranks like to take old ideas and try to use them to argue against some modern result even when that idea isn’t used in the current form or isn’t as absolute as they make it out to be. This seems for example to occur frequently with creationists who use an oversimplified form of Mendelian genetics that seems to date prior to the work of Hardy, Weinberg, and Fisher. As a way of preventing this signal, referring to such things as Koch’s work can be done, but you need to be clear that you understand the limitations it has. Otherwise, it just sets off alarm bells.
This bears repeating.
It is also difficult to empirically test elements of String Theory or evolutionary history. This difficulty isn’t taken to be evidence for against those theories. Lack of easy clear cut empirical tests is just that—lack of a simple theorem discriminator. I am not claiming that it is some magic pass required for any theory to be credible.
On the other hand, nor can one use lack of said simple theorem discriminator to get a free pass and somehow claim to have extra certainty—that most come from evidence regardless.
However, in this case I do think that the general idea of Koch’s postulate is highly relevant, it is not ‘cranky’ to invoke it, and in fact it is probably the single strongest piece of evidence for the mainstream position—as Vlad M pointed out to me.
I am currently reading: ” HIV causes AIDS: Koch’s postulates fulfilled” Guest editorial Stephen .I O’Brien* and .lames ,i Goederff
It reviews SIV models where SIV can be prepared and injected into monkeys and in some cases does cause AIDS like disease progression (usually more quickly than HIV).
So I don’t think your associations between “referring to Koch’s postulates” and cranks, and your general heuristic are valid at all, not when the mainstream is listing this as a centerpiece of evidence.
I haven’t read the editorial yet, but I’m not sure where the notion that this was a centerpiece of evidence comes from. I was vaguely aware of this result but never have paid it much attention. I suspect that if one talked to active AIDS and HIV researchers they’d say that there was a very strong case even without this. But yes, conservation of expected evidence does come into play here, so you have a valid point. In any event, the upshot that Koch’s postulates are not seen as any sort of absolute is very much relevant.
S.J. O’Brien and J.J. Goedert (1996) (the paper cited by Vladimir_M) specifically references Koch’s postulates. The accidental infection of laboratory workers is only one of five items cited in reference to (I believe) #3, “The cultured microorganism should cause disease when introduced into a healthy organism.”