No it isn’t, surprisingly enough, as any pharmacologist will tell you. Think of table salt - sodium chloride - a compound of dramatically unstable metal and poisonous gas. Combined they make food delicious. But not apart. So you wouldn’t sprinkle sodium flakes on your mash, any more than you’d chase a hit of tequila with a lick of pool chlorine. Sodium is no good at all in the saltshaker unless combined with chlorine. As useless as AZT before three phosphate groups have been lumped on to it inside our cells to create the active form of the drug, AZT triphosphate: AZTTP.

According to GlaxoSmithKline, AZT prevents HIV replication by a process called DNA chain termination. The idea is that after we swallow it, AZT will be converted inside our cells into AZTTP. In this form it looks like thymidine, one of the building blocks of DNA, which enables it to fake its way into a growing viral DNA chain. But the resemblance is as between an ox and a bull, because the difference between triphosphorylated AZT and thymidine is that the former is sterile. It lacks the biochemical link that enables further DNA building blocks to join the party. So once AZTTP gets into a DNA chain, it will end it.

Now obviously there must be enough AZTTP about for it to do this. To illustrate, let’s go back to the pool. A bucket of chlorine daily is far too much for safe swimming. But a teaspoon a week won’t do either. The guys who make pool chlorine know just how much you need to keep algae in check. They’ve performed experiments to determine the minimum effective dose. This sufficient quantity of chlorine necessary to keep your pool clear is known as an “inhibition concentration.” Use less and you’ll soon be splashing about in pea soup.

Before AZT was rushed to the market as an AIDS drug in 1987, the inhibition concentration (“IC50”) of AZTTP was investigated by a research team that included scientists from the manufacturer’s own laboratories. The study, reported in November 1986 by Furman et al in a very smart scientific journal, Proceedings of the National Academy of Sciences of the United States of America, found that the minimum concentration of the activated drug necessary to reduce HIV replication (“retrotranscription”) inside our cells by half is 0.7 micromolar, or 0.7 picomoles of the active drug per million cells. In other words they determined the low-water mark for drug efficacy according to the conventions of their business, the minimum level of AZTTP necessary for it to have a significant effect. The experiments were done in test tubes in entirely artificial conditions, quite unlike what goes on in our bodies, where, for reasons too many and complex to recount here, very much more AZTTP than that would be necessary. But to date, no one has repeated the study in vitro, let alone determined the IC50 value for AZTTP in vivo, so 0.7mM remains the only figure we have to go on. Bear in mind though that it is unrealistically low, and by a long shot too.

Well here’s the amazing part. Not until 1991 did it enter anybody’s bright head to find out the extent to which AZT is triphosphorylated inside our cells - in vivo as opposed to in petri dishes. Apart from the first botched study, every one of sixteen that followed consistently returned findings revealing that AZT is not triphosphorylated to levels anywhere near the activated drug’s IC50 level - with the best-designed and executed studies of the lot reporting intracellular AZTTP concentrations of ten- even 100-fold below it. And even more amazing, although the dismally low level to which AZT is triphosphorylated in the body has often drawn comment, not until a couple of years ago did anyone think to compare all these AZTTP in vivo data with the drug’s IC50 value.

In September 1999 an Australian biophysicist, Eleni Papadopulos-Eleopulos, and several co-authors published a monumental review of the literature on the pharmacology of AZT in another posh journal, Current Medical Research and Opinion (1). Analysing the manufacturer’s claims for AZT, they pointed out that taken as a medicine it cannot possibly be antiretroviral because it’s metabolised in the body into its active form to miniscule levels only, way below the minimum concentration necessary for it to act as a viral DNA chain terminator. Which sounds improbable to be sure, since nearly everybody knows that AZT zaps HIV. Why, if it sold almost a billion dollars worth in 2000 alone, it must do. Ready for your next surprise? It doesn’t.

According to AIDS experts, HIV infection levels can be monitored directly over time by measuring levels of viral DNA (viral burden) and viral RNA (viral load). There are a couple of other pointers too, but these are the main ones. Papadopulos-Eleopulos et al noted that every single study (and more have since come in) investigating the effect of AZT administration on viral DNA has found that it has none. Which means that AZT does not terminate it. Similarly, weighed by the criteria for efficacy set by leading American and English AIDS clinicians, AZT has no effect on viral load worth mentioning. And none on any other index of HIV infection levels. From which they drew the astounding yet long obvious conclusion: “A critical analysis of the presently available data…shows there is neither theoretical nor experimental evidence which proves that AZT, used either alone or in combination with other drugs, has any [anti-HIV] effect.” In fact GlaxoSmithKline make the equally stunning admission in their current PRODUCT INFORMATION advisory on AZT: “The relationship between in vitro susceptibility of HIV to [AZT] and the inhibition of HIV replication in humans or clinical response to therapy has not been established.” Yes indeed.

However, like arsenic, once universally prescribed by English doctors for scurvy, AZT is extremely poisonous to all cells it reaches (2). As the skull and crossbones label on bottles of AZT supplied to animal research labs tells: "Toxic by inhalation, in contact with skin, and if swallowed. Target organ(s): Blood Bone marrow. If you feel unwell seek medical advice (show the label where possible). Wear suitable protective clothing." So it’s all risk and no benefit you might say.

It’s in relation to these matters that GlaxoSmithKline is going to have to please explain, when a damages claim comes up for trial in a few months time, brought by the widow and fatherless child of an attorney who died horribly following treatment with AZT. Hayman v GlaxoSmithKline, launched out of the Natal Provincial Division of the High Court of South Africa, (and imminently out of an American court too) will be the first internationally in which the integrity of the manufacturer’s claims for the drug will be judicially tested. Fireworks guaranteed.

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FOOTNOTES

(1.) www.librapharm.co.uk/cmro/vol_15/supplement/main.htm
(2.) Debating AZT: Mbeki and the AIDS drug controversy by Anthony Brink; paperback.
Posted online at: http://debatingazt.aidsmyth.com

For further information about Hayman v GlaxoSmithKline,
Case No: 1894/2001, contact
Attorney Richard Stretch, Lister and Lister, Pietermaritzburg;
phone 033 3454530 or 082 7761481; rs45@pixie.co.za
or Advocate Brink; phone 083 6260945; arbrink@iafrica.com
IN EUROPE: Fintan Dunne & Kathy McMahon, www.aidsmyth.com
mail@aidsmyth.com +353-87-948-9817 or +353-87-937-3637