HOPES that women may soon be offered a “chemical condom” to protect them
from HIV infection have faded.

AIDS researchers believed that women might protect themselves from HIV by
using a common spermicide, nonoxynol-9 (N-9) (This Week, 6 January 1996, p 8).
But American researchers studying 940 Cameroonian prostitutes have found that
women applying a film containing N-9 were just as likely to contract HIV as
those given placebo films without the chemical.

In the 1980s, scientists discovered that N-9 kills HIV in laboratory tests.
It soon became the leading contender as a “vaginal viricide” to join condoms,
which are still unpopular in many cultures, in the battle against HIV
infection.

Early trials in Kenya used high doses of N-9, but had to be stopped because
many women in the trial developed vaginal ulcers. The Cameroonian study used
only a fourteenth of the dose given in Kenya because the researchers wanted to
find out whether smaller quantities of N-9 could ward off HIV without irritating
the vagina. But the trial failed on both counts: 42.2 per cent of the women who
used the N-9 film reported genital sores, compared with 33.5 per cent in the
placebo group.

“It would have been nice to have something that worked right off the bat,”
says Rodney Hoff of the US National Institute of Allergy and Infectious Diseases
near Washington DC, who coordinated the Cameroonian study. However, he notes
that other formulations of N-9, such as gels, might work better.

Other researchers argue that research to develop alternatives to N-9 should
also be a priority. “Amazingly, little development has occurred,” says Kevin De
Cock of the London School of Hygiene and Tropical Medicine.

The Environmental Genome Project, launched by the US National Institute of
Environmental Health Sciences (NIEHS) in Research Triangle Park, North Carolina,
will cost some $60 million. The project aims to take blood samples from
about 20 000 Americans from 10 different population groups of different ages,
sexes and ethnic backgrounds.

“There are very few diseases that are the absolute consequence of a single
event—either a genetic change or an environmental event,” says NIEHS
director Kenneth Olden. Only a small percentage of all cancer cases, for
instance, can be attributed to a defective gene. “This will revolutionise how we
think of gene-environment interactions.”

The effort will focus on genes controlling the distribution and metabolism of
toxic substances. One is the GST gene, which codes for the enzyme
glutathione S-transferase. This helps the body dispose of carcinogens known to
be involved in cancers of the lung and brain. Genes involved in DNA repair
pathways and the regulation of cell division and growth will also be
included.

Eventually, NIEHS officials hope to expand the project to other populations
worldwide. “This will help us understand how we get disease and determine who is
at increased risk,” says Karl Kelsey, a molecular geneticist at Harvard
University.