HIV: Search for a cure now in its second decade: Scientific rivalry overshadowed French team's discovery in 1983
Steve Connor is the Science Editor of The Independent. He has won many awards for his journalism, including five-times winner of the prestigious British science writers’ award; the David Perlman Award of the American Geophysical Union; twice commended as specialist journalist of the year in the UK Press Awards; UK health journalist of the year and a special merit award of the European School of Oncology for his investigative journalism. He has a degree in zoology from the University of Oxford and has a special interest in genetics and medical science, human evolution and origins, climate change and the environment.
Thursday 04 August 1994
Scientists have broken down the genetic structure of HIV. They understand how it passes from one person to another and how it infects cells.
Despite this, however, the virus has proven a formidable opponent for the drugs and potential vaccines being developed to fight it. A cure is a distant prospect.
It was a team of French researchers, led by Luc Montagnier at the Pasteur Institute in Paris, who first identified the virus in 1983. But the discovery was overshadowed by work from a rival team of American researchers, led by Robert Gallo of the US National Cancer Institute near Washington DC.
Dr Gallo believed that the French were wrong and proposed that Aids was caused by a class of viruses known to be implicated in cancer. A year later, in April 1984, he announced his own discovery of a virus he called HTLV-3, which he wrongly claimed was similar to a leukaemia virus that he believed caused Aids.
A genetic analysis in the following year, however, revealed that the HTLV-3 virus was identical to the virus discovered by Montagnier's group. Both viruses were eventually renamed HIV - human immunodeficiency virus - and years later Gallo had to admit that HTLV-3 was a laboratory contamination. The French virus had somehow found its way into the American test-tubes.
Once scientists had identified what caused Aids, it was a relatively simple, yet vital, step to develop a blood test to identify infected people and protect blood supplies for transfusion patients and haemophiliacs. Britain introduced a test for screening blood donations in October 1985.
Identifying the virus also meant scientists could learn about its genetic structure. What genes it had and what they did? How might drugs be developed to block its life-support systems? Could vaccines help the body's immune defences to mount an effective attack on HIV's life cycle?
Unfortunately there were no simple answers to those questions.
Scientists quickly realised they were dealing with a formidable foe which possessed the ability to mutate faster than the flu virus, making it a constantly moving target for vaccines which work by stimulating the body's natural defences to attack an invading virus.
HIV also possesssed the attribute of integrating its genes into the genetic material of the people it infects. No drug or vaccine has been developed that can winkle out such rogue viruses.
A further difficulty is that HIV also infects the very cells that are supposed to prevent microbes invading the body - cells designed to engulf viruses and rip them apart with enzymes.
But instead of being destroyed at the point of entry, HIV takes up residence within the cell which acts as a Trojan Horse, carrying the virus deeper into the body's more vulnerable regions, such as the lymph glands.
And there is the long latency period between infection and the onset of Aids. It is not clear why it takes so long for the virus to trigger a collapse of the immune defences and scientists can only speculate on why some people are better survivors than others. Good nutrition and early medical intervention seem to lengthen the incubation period.
But one thing they are sure of: the long period of latency, when infected people can unwittingly pass on the virus before they develop symptoms, has turned out to be the most potent mechanism for the spread of HIV.
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