Animal Rights

Similar Is Not Close Enough

| by Dr Ray Greek

A press release from the Helmholtz Association of German Research Centres discusses a new approach to studying Hepatitis C virus (HCV). It contain two statements that I find interesting:           

At TWINCORE researchers are now adapting the HCV to mice, thus enabling immunologists and vaccine researchers to take the next steps against this illness in the future. Because the immune system of mice is very similar to that of humans and it is only when vaccines are successful and safe in animal experiments that researchers can take the risk of transferring them to humans. (Emphasis added.)

To say the immune system of mice is very similar to the immune system of humans is meaningless. Similarity implies intent and the intent as stated is to develop a vaccine for humans. As evidenced by research on the polio vaccine and more recently with HIV, the notion that similar is sufficient is simply untrue. Very small differences between complex systems (in this case mice and humans) can result in opposite outcomes to vaccines and other pertubations to the system.

This is closely tied to the second issue I have with the press release, namely that vaccines must be proven safe and effective in animals before going to human trials. As there is no predictive value of animal models for drug development in general, to require a vaccine to pass these tests is unscientific; it is more like magic. How many vaccines have we lost because they were unsafe in mice or did not work on monkeys? We have certainly lost drugs. Sankar in The Scientist 2005:

Rats and humans are 90% identical at the genetic level, notes Howard Jacob, cofounder of Wauwatosa, Wisconsin-based PhysioGenix. However, the majority of the drugs shown to be safe in animals end up failing in clinical trials. "There is only 10% predictive power, since 90% of drugs fail in the human trials" in the traditional toxicology tests involving rats, says Jacob. Conversely, some lead compounds may be eliminated due to their toxicity in rats or dogs, but might actually have an acceptable risk profile in humans. (1)

An editorial in Nature Reviews Drug Discovery 2003:

In Tamoxifen’s case, a drug first developed as a potential contraceptive languished for many years before its present application was found. Furthermore, its propensity to cause liver tumours in rats, a toxicity problem that thankfully does not carry over into humans, was not detected until after the drug had been on the market for many years. If it had been found in preclinical testing, the drug would almost certainly have been withdrawn from the pipeline. With the COX2 inhibitors, Rod Flower notes that the transgenic animal models used to test the hypothesis that COX2 would make an anti-inflammatory target gave results that, if relied upon, might have killed the project. Both stories emphasize the role of the dogged researchers who kept their eyes focused on the prize while navigating around obstacles and exploiting any opportunity that came along. It might sound a bit trite, but at the very least we can say that one of the best strategies for drug discovery is to start with a group of people who really want to discover drugs. (2)

The National Cancer Institute believes society may have lost cures for cancers because the drugs failed animal tests (3).

Allow me, at this point to anticipate the hysteria from the vested interest groups: “Would you want your child to take a drug or vaccine that had not been tested on animals? Are you that cruel? Why do you hate children?” This combination ad hominem and argumentum ad misericordiam (appeal to pity) makes the major false assumption that testing on animals will predict whether a drug or vaccine will be safe in humans. Testing drugs and vaccines on a different species does not predict response for humans. (See Animal Models in Light of Evolution for more.) A child about to consume a new drug is no safer after the animal testing than before.

Byers et al 2009:

Vaccines that have shown promise in these animal models often fail to produce an efficacious immune response in human Phase III clinical trials [(4, 5)]. Results such as these represent a significant loss of time and money and question the predictive value of these models. In vitro models using animal PBMC cells have shown promise in the evaluation of vaccine immunogenicity (6) . . . (7)

It should also be noted that because of differences in genes, like single nucleotide polymorphisms (SNPs), not all children may be protected by the same vaccine (8, 9). But in the future such children may be able to receive a personalized shot. It is estimated that “between 5 and 20 per cent of people vaccinated against hepatitis B, and between 2 and 10 per cent of those vaccinated against measles, will not be protected if they ever encounter these viruses” (9).

(Since the topic here is vaccine testing I should include the fact that animals can be used to test for impurities in vaccines like the polio vaccine. There are nonanimal testing methods that also allow this but animals can be used for this purpose. This is an example of using animals as bioreactors and, as I have said many times, such uses are scientifically tenable (see page 30 of Animal Models in Light of Evolution). This does not negate the fact that animals cannot predict human response to drugs and disease vis-à-vis efficacy, toxicity and so forth. Testing for impurities in the vaccine occurs during production while the tests we are addressing occur during development. Animal testing as a predictive modality is sold to society on the basis of predicting human response during development.)


1. U. Sankar, The Scientist 19, 32 (August 1, 2005).

2. Editorial, Nat Rev Drug Discov 2, 167 (Mar, 2003).

3. T. Gura, Science 278, 1041 (Nov 7, 1997).

4. K. Uberla, Med Microbiol Immunol 194, 201 (Aug, 2005).

5. D. I. Watkins, D. R. Burton, E. G. Kallas, J. P. Moore, W. C. Koff, Nat Med 14, 617 (Jun, 2008).

6. S. J. Piersma et al., Vaccine 24, 3076 (Apr 12, 2006).

7. A. M. Byers, T. M. Tapia, E. R. Sassano, V. Wittman, Biologicals 37, 148 (Jun, 2009).

8. B. Yucesoy et al., Vaccine 27, 6991 (Nov 23, 2009).

9. C. King, New Scientist, 11 (December 5, 2009).