Foreword to


by Peter Duesberg


The DNA chain terminator AZT was designed over twenty years ago for the treatment of leukemia. Its antileukemic mechanism of action is to kill growing Iymphocytes by termination of DNA synthesis. However, since AZT failed to prolong the lives of leukemic animals, it was not accepted for cancer chemotherapy. In 1987 it was approved to treat symptomatic and asymptomatic carriers of HIV to cure or prevent AIDS, based on the hypothesis that HIV causes AIDS. One year later, in 1988, the designers of AZT received a Nobel prize for medicine, although there was no evidence that AZT would cure or prevent AIDS.

The rationale of AZT therapy is simple, if not naïve the retrovirus HIV depends on DNA synthesis for multiplication, and AZT terminates DNA synthesis. Thus AZT should stop AIDS, if AIDS were caused by HIV, and if HIV were multiplying during AIDS. Yet there is still no proof for the now six year-old hypothesis that HIV causes AIDS. Moreover, many studies show that no more than one in 1,000 Iymphocytes are ever infected by HIV even in people dying from AIDS. Since AZT cannot distinguish between an infected and an uninfected cell, 999 uninfected cells must be killed to kill just one HlV-infected cell. This means that AZT, as a treatment for AIDS, has a very high toxicity index. In view of this, there is no rational explanation of how AZT couid be beneficial to AIDS patients, even if HIV were proven to cause AIDS.

There is always a small chance for an unpredictable effect, a miracle, even in science. If AZT were to prevent or cure AIDS despite the facts that the virusAIDS hypothesis is ungrounded and that HIV does not make DNA during AIDS, it would be such a miracle. Unfortunately there is very little room for a miracle with AZT, because its mechanism of action is so embarrassingly clear, namely totally nonspecific termination of DNA synthesis. One could be lucky with miracle-anti-AIDS functions of drugs whose mechanism of action is poorly understood, such as aspirin, or even chicken soup but hardly with a substance that is a chain terminator of Iymphocyte DNA synthesis in a person already deficient in Iymphocytes.

It is conceivable that AZT may provide short-term benefits against AIDS to a person with acute microbial infections like tuberculosis, pneumonia, candidiasis or herpes, since these diseases are called AIDS if HIV antibody is present, by killing these microbes together with host cells. However, such infections could be controlled much better with confirmed, specific therapeutics than with the randomly toxic AZT.

The ultimate judge of a hypothesis like the virus AIDS hypothesis is its usefulness in terms of therapeutic benefits and prevention. The virus-AIDS hypothesis has not stopped the spread of AIDS, it has not saved a single AIDS patient, and it is about to create 50,000 new ones the number of people currently being treated with AZT. Whatever slight claims AZT once had in being useful against AIDS - have been 'AZTed' by John Lauritsen's "Poison by Prescription: The AZT Story".

Peter Duesberg Professor of Molecular Biology University of California, Berkeley April 1990