AIDS Denialism: Deadly Ignorance Part II: Koch’s Postulates, AIDS and more Wackaloonery

(Click for Part I and Part III of this series)
In my previous post, I wrote about some of the faces of AIDS denialism, and the arguments (and I use that word loosely) that these "skeptics" present. What their arguments revolve around - and indeed the arguments put forth by virtually all members of the AIDS denialism community - is that there is no evidence that AIDS is caused by HIV. Certainly, by all accounts, the medical and scientific communities have demonstrated otherwise. But how do we know that HIV is the causal agent behind AIDS? How do we know what the causal agent is behind any disease? Do we have a standard method of determining causality, and is the HIV/AIDS connection supported by this method? The answer is yes.

In 1884, a Prussian physician by the name of Robert Koch, along with is colleague, the bacteriologist Friedrich Loeffler formulated a set of criteria that they used to establish a causal relationship between an illness and a causative agent. These criteria were published in 1890 by Koch and have since been known as Koch's Postulates. Koch used this set of postulates to determine the etiology of both tuberculosis and anthrax¹, and in the 120 years since their first publication, the causes of many other diseases have been determined by successful application of Koch's Postulates. The four tenants of Koch's Postulates are as follows:

1. The causative agent must be found in all organisms exhibiting the disease, and not in healthy individuals.
   
2. The causative agent must be isolated from a diseased individual and grown in culture.
   
3. The causative agent, when introduced to a healthy individual, should cause the original disease.
   
4. The causative agent must be reisolated from the inoculated, diseased host and shown to be identical to the original agent.
   

Note that the first postulate is not universally required, as many diseases exhibit asymptomatic carriers (as is the case for HIV). The third postulate is unique in that it states "should" rather than "must" – this is because infection rates are never 100%. The fourth postulate was originally required by Koch, but fulfilling the first three postulates is generally considered to be sufficient to indicate causation. If all four postulates are fulfilled by a particular causative agent, then it can be said that the agent is the likely cause of the disease.


So, when these four postulates are applied to HIV/AIDS, does the result support the claim that HIV causes AIDS? The answer is a resounding "yes". Let's take the postulates one at a time.


The causative agent must be found in all organisms exhibiting the disease, and not in healthy individuals.

As noted above, this first postulate is not universally required, as asymptomatic carriers of HIV appear as healthy individuals. Nevertheless, those with HIV-1 and no symptoms at time of diagnosis, eventually progress to AIDS. And in 95% of cases, individuals suspected to have AIDS test positive for HIV virions, HIV antibodies or positive for HIV viral loads². This association between HIV and AIDS is supported by a wealth of evidence from countless studies, and cannot be dismissed.

The AIDS denialists, however, will insist that this first postulate has not been fulfilled. They will point out that there are cases of individuals exhibiting AIDS-defining characteristics who have not tested positive for HIV antibodies. This, they are quick to claim, is in violation of the first postulate, since these cases show the disease without the putative causative agent. There is a very straightforward answer to this, though: immune deficiencies can develop in more ways than just being induced by HIV infection. There is a virtual plethora of ways immune deficiencies can arise, and these will exhibit symptoms similar to AIDS – bacteria, genetic conditions, environmental factors, and immune suppressing drugs can all cause symptoms associated with AIDS. In such cases, it is not surprising that patients test HIV negative! But in cases where individuals present all or most of the AIDS-defining characteristics – particularly a depletion of CD4+ lymphocytes – the HIV virus is found³. Koch's first postulate remains fulfilled.


The causative agent must be isolated from a diseased individual and grown in culture.
Culturing the proposed pathogen is not only the second postulate but also, perhaps, the most important step in identifying the suspected pathogen. Viruses can be more difficult to grow in culture than bacterial strains, but this has not prevented HIV from being cultured from samples taken from AIDS patients. Over the years, it has been cultured in T-cells, macrophages as well as in HeLa cells. Furthermore, isolated and cultured strains of HIV have had their genomes sequenced and cloned, with literally thousands of unique sequences added to sequence data bases. Isolation of HIV from samples is not an issue, and there have been multiple^4,5 protocols established and published on how to accomplish this. There are even commercially available kits which allow HIV to be isolated from infected samples. Culturing HIV has become a routine practice in HIV research to the point where it is more or less a triviality. Postulate 2 has been fulfilled and continues to be filled on a daily basis.

The causative agent, when introduced to a healthy individual, should cause the original disease.
The third postulate is perhaps the most controversial of the postulates. For one, it cannot be fulfilled solely on the basis of epidemiological data but must rather rely on experimental evidence. When looking at diseases in animals or when using animal models, the third postulate is easy to demonstrate experimentally. When it comes to the transmission of diseases in human subjects, however, the third postulate is tougher to demonstrate. No ethics board would ever allow researchers to experimentally infect healthy people with cultured HIV to see if they progress to AIDS. Nevertheless, this postulate has been fulfilled due to the unfortunate accidental transmission to humans who were doing research on HIV⁶.

In this case, three lab workers were working with HIV-1, and all became accidentally infected with the virus. None of these workers belonged to any of the high-risk groups; they were not drug users, had not had blood transfusions, and did not engage in homosexual behaviour. All three of the workers exhibited depleted CD4+ cell counts (two of which were low enough to warrant an AIDS diagnosis) and one progressing to pneumonia⁷. AIDS "skeptics" who insist that HIV does not cause AIDS and that AIDS is caused by drug use are at a loss when it comes to explaining this case study. How else could the infected workers, who were not part of any risk groups, have developed AIDS unless it was due to HIV infection? How do they explain the onset of symptoms in these workers if HIV is, as they claim, pathologically asymptomatic?

Evidence from animal studies has also given support to the third postulate. Studies in which baboons have been infected with HIV-2 have shown these animals to develop AIDS-like symptoms including depletion of CD4+ lymphocytes⁸ (and I highly doubt these baboons were drug users!). Mouse strains used to model SCID which have been given human peripheral blood lymphocytes (hPBLs)⁹ also develop severe immunodeficiencies when infected with HIV¹⁰. These mice also show depleted CD4+ cell counts.

Studies like this show experimentally that cultured HIV, introduced into healthy individuals, result in the hosts progressing to AIDS. This is sufficient to fulfill the third postulate.

The causative agent must be reisolated from the inoculated, diseased host and shown to be identical to the original agent.
This fourth postulate, as noted above, is now often considered extraneous to suggesting causation by a suspected pathogen. Nevertheless, the example of the infected lab workers cited above is a good case of this postulate also being demonstrated. The virus was reisolated from the infected lab workers, and sequenced¹¹. The divergence between the sequences from the strains isolated from the workers was very small – about the same as the divergence in sequence between HIV-infected infants and their mothers. In other words, it was the same strain that they had been working with. Consider Postulate 4 demonstrated.
 
So it is plainly obvious that all of Koch's postulates are fulfilled, and HIV can be said to be the likely causative agent behind AIDS. Koch's postulates demonstrate reasonable criteria for determining causation, and provide reasonable evidence that the AIDS "skeptics" are wrong.

I will continue in Part III, where I examine the fuzzy math used by AIDS "skeptics" to distort reality and push their dangerous nonsense.

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1. The infectious agents behind these diseases, Mycobacterium tuberculosis and Bacillus anthracis, respectively, were discovered and first isolated by Koch himself.
   
2. See the references in Part I for more on this.
   
3. There is an exception to this. A rare condition exists called hypogammaglobulinemia where individuals are unable to mount an immune response to invading pathogens. People with this disorder who are infected with HIV will not show HIV antibodies present when tested.
   
4. See http://www.miltenyibiotec.com/download/protocols_macsmolecular_en/516/SP_Iso_HIV1.pdf
   
5. See http://www.currentprotocols.com/protocol/im1202
   
6. Weiss SH, Goedert J J, Gartner S, Popovic M, Waters D, Markham P, Veronese FD, Gall MH, Barkley WE, Gibbons Jet et al: Risk of human immunodeflciency virus (HIV-1) infection among laboratory workers. Science 1988, 239:68-71.
   
7. I have been unable to find any information on these three workers more recent than the above referenced article. If anyone has updated information, I would be interested in hearing it!
   
8. Barnett SW, Murthy KK, Herndier BG, Levy JA: An AIDS-like condition induced in baboons by HIV-2. Science 1994,266:642-646.
   
9. SCID-model mice are unable to produce B and T lymphocytes. Transplanting hPBLs into these mice reconstitutes a functioning immune system.
   
10. Mosier DE, Bulizia R J, Baird SM, Wilson DB, Specter DH, Spector SA: Human immunodeficiency virus infection of human PBLSCID mice. Science 1991,251:791-794.
    
11. Reitz MS Jr, Hall L, Robert-Gurofl M, Lautenberger .I, Hahn BH,Shaw GM, Kong LI, Weiss SH, Waters D, Gallo RC,Blattner W: Viral variability and serum antibody response in a laboratory worker infected with HIV-1 (HTLV-IIIB). AIDS Res Hum Retroviruses 1994, 10:1143-1155.