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A mysterious sexually transmitted agent might be the root cause of Kaposi’s
sarcoma, the skin cancer that first led doctors to diagnose AIDS. This is
one view in a debate that has erupted over the causes of the illness in
people with HIV.

HIV weakens the immune system, opening the door to a range of opportunistic
infections and illnesses. But does the virus itself cause any of the illnesses?
Robert Gallo and his team at the National Institutes of Health (NIH) in
the US believe that in the case of Kaposi’s sarcoma it does. They argue
that HIV promotes the growth of skin tumours.

Others think an elusive sexually transmissible agent is to blame. As
evidence, they point to studies reporting a much higher incidence of Kaposi’s
sarcoma among gay and bisexual men with HIV than among intravenous drug
users. Gallo concedes that a second agent might be involved, but he remains
unimpressed with the evidence. ‘We’ve spent seven years looking and we haven’t
found any virus or microbe.’ According to Gallo, HIV-infected cells are
the real problem. Subverted by the virus, the cells release proteins, called
cytokines, that speed the growth of nearby tumour cells. The chief culprit
within the virus, says Gallo, is a protein called Tat. Tat has a split personality,
he argues: it helps HIV to replicate and encourages the growth of Kaposi’s
sarcoma cells. Gallo’s main evidence comes from experiments on mice. When
his team implanted a gene encoding Tat into mice, the mice developed Kaposi’s
sarcoma. But others say they have been unable to repeat the mouse experiments.

The geographical spread of Kaposi’s sarcoma argues overwhelmingly for
the cancer-causing agent being something other than HIV, says Martin Schechter,
an epidemiologist at the University of British Columbia in Canada. In North
America, he says, Kaposi’s sarcoma has been largely confined to people who
contracted HIV between 1987 and 1982 in three cities: San Francisco, Los
Angeles and New York. Many people with AIDS who developed Kaposi’s sarcoma
in Britain and France during the 1980s, also contracted HIV in these US
cities, he adds.

Harold Jaffe and his colleagues at the Centers for Disease Control in
Atlanta found that women who had contracted HIV from a bisexual partner
were much more likely to develop Kaposi’s sarcoma than women who had contracted
HIV from haemophiliacs.

‘If you put all this together, you have an additional agent that is
transmitted largely by anal intercourse,’ says Schechter. As sexual behaviour
has changed in the gay community, he argues, transmission of the agent has
slowed. But if such an agent does exist most researchers doubt it could
be a conventional virus.