shown, but resistance to two classes was
common, at one case in seven.
As for the nucleoside class, resistance was 25 per cent in 1996, only
six per cent in 1999, but had increased to 20 per cent in 2001. The 1996
resistance was thought largely to be due to single or dual therapy with
AZT, whereas the 'new' resistance in 2001 was more often due to 3TC resistance
mutations.
The good news: a similar survey of 52 newly-infected patients in Spain
found that, on the contrary, overall transmission of resistant virus declined
from 27 per cent in 1997-99 to six per cent in 2000-1. And an Australian
study found an even bigger decline; resistance in new infections to the
nucleoside drugs fell in a group of 135 patients from 44 per cent pre-1995
(ie pre-triple combo therapy) to 19 per cent after this time.
Even in the US, not all cities followed the San Francisco pattern. In
923 newly-infected patients from 10 US cities studied by a team in Atlanta,
Georgia, overall drug resistance peaked at 10 per cent in 1999, before
declining slightly in 2000. Resistance to more than one class stayed very
low, at 1.2 per cent in 2000.
How to explain these figures? The pattern observed in San Francisco and
Australia seems to indicate that transmitted resistance is driven not
so much by good or bad adherence, or the prevalence of unprotected sex,
but simply by which drugs are used. Resistance rises either when regimes
that do not suppress HIV completely are mainly used (as pre-1996), or
drugs with a low 'resistance threshold' such as 3TC.
In the UK, so far, resistance in new infections has followed the European
rather than Californian pattern. But Professor Brian Gazzard of London's
Kobler Clinic has
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speculated that because the non-nucleoside drugs, to which HIV easily
