IN THE WORKS

A Deadly Disease May Be Evolving In The Veins Of Junkies

INTRAVENOUS drug abusers are harbouring a virus that is evolving 300 times
faster than usual and could turn nasty, scientists warn. Several drug users
infected with the normally harmless virus have already developed a
devastating neurological disorder, although a firm link between the virus
and the disease is yet to be confirmed.

Marco Salemi and Anne-Mieke Vandamme at the Rega Institute for Medical
Research in Leuven, Belgium, and William Hall at University College Dublin
in Ireland, say needle sharing has made the virus epidemic among drug
users. And they believe it is this dramatic increase in transmission rate
that has suddenly kickstarted the virus's evolution. "We have to keep
monitoring this," says Salemi. "It could evolve into something more
pathogenic, we just don't know."

The virus is called HTLV-II. It is a retrovirus, which incorporates viral
DNA into the genome of infected cells. Its relative HTLV-I can cause
leukaemia and neurological disorders.

HTLV-II. however, is normally relatively benign. It is thought to have
jumped from monkeys to humans 15 000 to 30 000 years ago in the Americas.
For up to 2000 generations, the virus has been most common in Pygmy and
American Indian tribes, transmitted from mother to child via breast-feeding.

In the past 30 years, however, the virus has spread into a wider population
through contaminated blood in shared needles. The virus has been picked up
in drug users in the US, Asia and Europe, where between 5 and 10 per cent
of users are infected.

To find out more, Salemi's team took blood samples from drug users in Italy
and Ireland, and compared similar samples in databases from the US, Spain,
Sweden and Vietnam. They looked at how much the virus had evolved within
drug users compared to people in American Indian tribes.

They found that the genetic sequence of HTLV-11 changes at a rate of 1 per
cent every 100,000 years or so in the American tribes, the slowest for any
known virus. In drug users, however, this rate is 300 times faster.

This is probably because HTVL-II normally lies dormant. It only replicates
and mutates during a brief infectious period when trying to integrate
itself into a new host's cells. Because the virus is usually passed from
mother to child, this happens infrequently. However, a single drug user can
pass the virus on to hundreds of others within a few months. And each new
infection gives the virus a new chance to mutate and evolve.

Severe neurological disease has already cropped up in several drug users
infected by HTLV-II. although it is still unclear whether this is linked
instead to their known infection with HIV. Hall now hopes to test whether
HTLV-11 is becoming more pathogenic by studying drug abusers serving long
prison sentences in Brazil.

Martine Peeters at the Institute for Research and Development's Retrovirus
Laboratory in Montpellier, France, agrees that the study throws up
important questions. "We need more clinical follow-up," she says.

Matt Walker