Better Science Science Without Vivisection Karin Zupko, Ph.D. (1998)—Vivisectors use the public's fear of AIDS to promote their agenda by telling us that progress in the fight against AIDS requires experimenting on animals. But countless breakthroughs in AIDS research have been made through studying humans with the disease, including isolation and identification of the HIV virus, which is believed to cause AIDS; the mechanism of AIDS transmission; tests for the presence of HIV in blood; and the therapeutic effect of AZT. Advances in AIDS treatment and prevention will continue to come from studying humans, because it is a uniquely human disease. For example, some people are repeatedly exposed to the HIV virus, yet never become infected. In the research described below, scientists studied these people and gained insight on how to treat AIDS. Their work is an example of science without vivisection, which NEAVS supports. Researchers have identified two men who have been exposed to the virus many times, yet have not become infected. Their white blood cells, the target of the HIV virus, are highly resistant to infection by HIV in vitro (in the test tube). One group of researchers found that these men have a mutation in a part of their genetic material, a gene called CCR-5 (Cell, Vol. 86, August 9, 1996, pp. 367-377). The mutated gene makes a protein that is defective: it fails to migrate to the surface of the white blood cell, where it normally helps HIV attach to and infect the cell. The gene appears to be nonessential, as the men are healthy and apparently suffer no ill effects as the result of the mutation. People inherit their genetic material from their parents. They have two copies of most genes, one from their mother and one from their father. The scientists looked at the genetic material of 44 people of Western European descent and estimated that about 1 in 100 have two copies of the mutated gene (a copy from each parent), while 1 in 5 have one copy of the defective gene and one copy of the normal gene. In contrast, genetic material of a sample of people of Venezuelan descent did not contain the mutation. The scientists exposed white blood cells to HIV virus in vitro. They found that cells from the men who are resistant to HIV infection did not produce HIV virus; cells from people who have two normal copies of the gene produced normal amounts of virus, and cells from people who have one normal and one mutated gene made from 10-25% of the normal amount of virus. Two copies of the mutated gene protected the cells against infection, while one copy provided intermediate protection. Independent substantiation of results is essential in science, and a second group of researchers corroborated the findings of the first (Nature, Vol. 382, August 22, 1996, pp. 722-725). They studied 700 individuals of Western European descent who are not HIV-infected and found that two copies of the mutated gene are present in about 1 in 100 people, and about 1 in 5 have one copy of the defective gene. When they examined the genetic material of 124 Western and Central Africans and 248 Japanese, they detected no mutated genes. They also studied the genetic material of 723 Caucasians from Belgium and Paris who are HIV-infected. None had two copies of the mutated gene, and fewer HIV-infected people had one copy of the mutated gene than did the general population. Both results are consistent with the hypothesis that the mutated gene protects against infection. This combination of epidemiological (population studies) and in vitro research shows that the product of the mutated gene CCR-5, the protein that helps the HIV virus infect cells, is biologically important and suggests that drugs that interfere with the interaction of HIV and the CCR-5 protein may halt or delay the spread of infection.J Further studies of the mutation may also contribute to understanding basic concepts in biology. For example, analyzing the incidence of mutated genes in different parts of the world and how they change in heavily infected populations can elucidate complex genetic interactions between virus and host. In contrast to relevant clinical studies, animal experiments have caused immense suffering and wasted billions of dollars. Animals who are infected in the lab do not mimic human disease: physiology differs among species, and animal "models" are incapable of elucidating the complex nature of disease in humans. As is the case for other illnesses, animal experimentation has provided little, if anything in the understanding and treatment of AIDS. The solutions to AIDS and other human health problems lie in directly applicable human studies--science without vivisection--science NEAVS supports. Supporters of vivisection often accuse those who work to stop vivisection of being anti-science and anti-research. In a recent newsletter, the pro-vivisection group Americans for Medical Progress referred to NEAVS as "the anti-research New England Anti-Vivisection Society." We are not "anti-research." NEAVS advocates humane, responsible scientific research--studies that advance our understanding of disease without harming animals. What you can do Many publicly supported health charities fund vivisection. If you are interested in donating to AIDS charities, two that do not fund vivisection are listed below: Designer Institute Foundation for AIDS 150 West 26th Street, Suite 602 New York, NY 10001 Elton John AIDS Foundation Box 52066 Atlanta, GA 30355 Also, check out local AIDS support groups that provide services to AIDS patients in your area. They usually offer much assistance, but are often underfunded. For a complete list of health charities that fund or do not fund vivisection, look here.

Other NEAVS Fact Sheets: Benefits of Non-Animal Tests | Xenotransplants | Animal Welfare Act | Limitations of Animal Tests | Non-Animal Product Safety Test Alternatives << Back to Better Science  | Home