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This is an archive article published on May 15, 2002

Stopping the experiments was the right step

We would like to comment on the article, ‘Maneka’s experiments with research: Animal ‘‘distress’’ (IE, May 12)...

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We would like to comment on the article, ‘Maneka’s experiments with research: Animal ‘‘distress’’ (IE, May 12) leads to a govt ban on testing at top AIDS vaccine centre’, by Sreelatha Menon.

Perhaps, overlooked in the article is the fact that Maneka Gandhi acted in the interest of human welfare as well as animal welfare. By stopping experiments on animals, she may have done more to advance AIDS research in India than any animal experimenter has.

The quest for a vaccine or cure for AIDS has been singularly unsuccessful in monkeys, chimpanzees and other animals. There are many reasons for this. SIV infects monkeys, not humans, and is a very different virus from HIV. The differences between HIV and SIV are very important in vaccine or medication development. White blood cells called cytotoxic T lymphocytes, that are specific for HIV, do not even recognise SIV-infected cells.

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SIV use the CCR5 coreceptor for virus uptake into cells, but HIV-infected humans, shift from CCR5 to CXCR4 as they progress to AIDS. This shift has not been seen in SIV-infected monkeys.

With few exceptions, HIV-1 infection of chimpanzees is universally mild with no notable decline in CD4+ T-cell levels, immunosuppression or other signs of an AIDS-like illness. Rather, HIV-1 infection of chimpanzees results in detectable plasma HIV that decreases within 2-3 months of infection and becomes low to undetectable within a few years. The ability to detect or culture HIV after this initial time period is variable.

The virus used to infect Jerom (the only chimpanzee to come down with an AIDS-like illness) was different from the type that usually infects humans. After Jerom was infected his blood was given to other chimpanzees that then dropped their CD4 counts but, in contrast to Jerom, they did not exhibit signs of illness. When HIV infects humans for the first time it binds to the CCR-5 receptor, then it develops a preference for the CXCR4 receptor. The virus used to infect Jerom relied on the CXCR4 receptor from the outset. These differences are significant. Because AIDS is a complicated human disease, a vaccine that works in monkeys or chimpanzees may not work in humans. There is a very good reason why chimpanzees and other animals make poor models for vaccine development: chimpanzees have evolved to be chimpanzees and mice to be mice; not humans. Yes, all species have an immune system but each species uses its immune system to combat different viruses in different ways. A virus lethal to humans may be totally harmless to animals and vice-versa.

Researchers who use animals are operating under the paradigm that says humans and animals are more similar than different. Modern evolutionary biology reveals that the differences are today far more important than the similarities with regard to how the organism operates at the cellular level, the level where disease occurs. The paradigm that predicts animals would be valuable to learn about diseases affecting humans appeared viable in the 19th century when we knew so little. On the gross level, humans and animals were similar: chimpanzees had hearts, so did humans. But today we are studying things on the very level that defines the species’ as being different — the molecular level. It is unreasonable to assume that at this level what we learn about one species will apply to another.

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The writer is science advisor, National Anti-Vivisection Society and president, Americans For Medical Advancement. He has just co-authored ‘Specious Science: How Genetics and Evolution Reveal Why Medical Research on Animals Harms Humans’

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