I say so-called, because, as far as I know, his research is focused on SIV, the simian immunodeficiency virus, rather than HIV, the human immunodeficiency virus. In spite of this, and like essentially every scientist studying monkeys dying of this experimental infection, he still calls himself an HIV researcher. Check out his website: http://www.pathology.wisc.edu/Faculty/bio.aspx?name=doconnor
Anyway, here's the passage, cut and pasted:
Yet O'Connor argues non-human primate AIDS research has already saved lives. It wasn't that long ago when researchers felt they were on to something because a vaccine they'd tested was working. It wasn't until a wider test of younger and immunocompromised Macaques was done that it was discovered the attenuated vaccine actually transmitted HIV.Did you get that? Let me put it in terms that might be a little easier to understand.
“So it was the work that was done in non-human primates that prevented us from making a potentially catastrophic mistake in advancing these sorts of attenuated vaccines, which have been used against a wide variety of other diseases into people,” he said.
Experiments on monkeys misled scientists into believing that a vaccine they developed would protect monkeys from SIV. Further testing showed that the vaccine didn't work and actually caused the monkeys to get SAIDS (the monkey version of AIDS).
O'Connor claims that this line of research saved human lives because they discovered (in the nick of time?) that they had been wrong all along and then didn't test the vaccine in humans.
Let me put it in even simpler terms: I invent a bullet proof vest and announce it is absolute protection from bullets. Then I discover that it doesn't work. Then I announce that my research has saved lives because no one wore the faulty vest.
If this pretzel logic is typical of O'Connor's thinking, then he should be fired, because he is unlikely to be thinking clearly about the biology of retrovirus resistance.
O'Connor addressed the Dane County Board's Health and Human Needs Committee about Resolution 35: "Establishing an Advisory Panel to Study the Treatment of Monkeys Used in Experiments in Dane County and the Ethics of Experimenting on Monkeys." Unsurprisingly, he argued that the County should not sanction any critical look at the use of monkeys. (See: County committee pushes for citizen panel to examine monkey research. Capital Times. June 30, 2010.)
During that meeting, one of the committee members asked him if they had found a cure for SIV, the monkey virus. O'Connor beat around the bush, hemmed and hawed, and was then asked again. What he said is akin to his claim above, complete nonsense.
He said that experiments on monkeys had led directly to the use of antivirals as a treatment for accidental exposure to HIV in healthcare workers. He said that experiments with SIV in monkeys had shown that treatment with antivirals could stop the establishment of an infection if the medications were received within two or three hours of exposure.
My ears perked up when he said this, because the monkey vivisectors are embarrassed by the paucity of easily demonstrable benefits resulting from their use of monkeys, and whenever they make an overt claim, it gives one something concrete to investigate.
In this case, it took me about a minute to find what appears to be an authoritative refutation of his claim.
I looked at this paper because it is available in its entirety for free. I found it on PubMed. It's from 1996: "Prophylaxis for occupational exposure to HIV." Consider these passages:
Health care providers who are parenterally exposed to human immunodeficiency virus (HIV) are at risk for infection. The average risk attributed to needle punctures and similar percutaneous injuries involving HIV is approximately 0.32% (95% CI, 0.18% to 0.46%), or 21 infections after 6498 exposures. This risk estimate, which is based on data taken from 25 prospective studies of occupational exposure, does not account for factors that may change the probability of transmission during a specific exposure. The virus inoculum (the volume of material involved in an exposure and the titer of infectious virus in that material) is one important determinant of risk. New data suggest that antiretroviral treatment after exposure may also be an important factor affecting the outcome of occupational exposure to HIV.
In a case–control study, the Centers for Disease Control and Prevention (CDC) found that five factors were independently associated with the risk for HIV infection after percutaneous injury...
Use of zidovudine soon after exposure, the final factor that predicted infection in the CDC study, was associated with a 79% reduction in the odds of HIV transmission (odds ratio, 0.21 [CI, 0.10 to 0.60]). This observation is the first epidemiologic evidence for a benefit from antiretroviral treatment among health care providers exposed to HIV, and it has stimulated renewed interest in prophylaxis after exposure.
The efficacy of antiretroviral prophylaxis is biologically plausible. Local host defenses appear to be critical in deciding the outcome of transcutaneous exposure...The process of initial virus uptake, antigen processing, and presentation to immune effector cells is not instantaneous and may take several hours or even days. Thus, a window of opportunity for intervention before local virus propagation or dissemination almost certainly exists. Early antiviral treatment may favor the host by minimizing the effective viral inoculum...
The results of experiments done in animal models to evaluate the efficacy of antiretroviral treatment after exposure are inconclusive. Zidovudine treatment after exposure can prevent retroviral infection in mice and cats, but data from these models are difficult to generalize to humans. Most studies of prophylaxis with licensed antiretroviral drugs in primates have not shown efficacy, although treatment with zidovudine before exposure was effective in one study of infant macaques that were inoculated with a low titer of simian immunodeficiency virus. The titer of virus used in most experiments involving primates is substantially higher than the amount that would be encountered in occupational exposure. In addition, the animals used in these experiments are usually inoculated intravenously, a method that would bypass potentially important cutaneous host defenses. Hence, absence of efficacy of prophylaxis in a primate model cannot be generalized to predict the outcome of percutaneous occupational exposure. Adverse consequences of treatment on the natural history of infection and delays in seroconversion have not been seen in animal experiments.
So what was O'Connor talking about when he said that experiments on monkeys are responsible for the use of antivirals to treat accidental exposure to HIV? Not reality, apparently.
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