Human immunodeficiency virus development into AIDS

Research into the chemistry of template-dependent nucleic acid biosynthesis, combined with modern techniques of molecular biology, has elucidated the life cycle and structure of the human immunodeficiency virus, the retrovirus that causes AIDS. A few years after the isolation of HIV, this research resulted in the development of drugs capable of prolonging the lives of people infected by HIV. 

The history of combating the human immunodeficiency virus (HIV) can be viewed as a model of today s development of pharmaceuticals (Stone, 1995). Since the middle of the 1980s a total of 20 anti-AIDS pharmaceuticals based on 16 distinct chemical entities have been introduced into the market the first was AZT by Glaxo in 1987. A causal therapy, however, has not been developed yet. Most advantageous effects of today s actives are temporary because HIV is characterized by an extreme mutability and can cause resistance phenomena through rapid mutation within months or sometimes weeks against most approved preparations or those in clinical phases. The criterion for efficacy is the reduction of the number, or even total elimination, of viruses in the blood combined with an enhanced count of C D4-T-lymphocytes. 

Recently, it has been possible to grow cells of the human immune system in special mice. These mice carry a genetic defect called severe combined immunodeficiency (SCID), which leaves them with crippled immune systems, much like those in AIDS patients. Because SCID mice lack functional cellular immunity, it is possible to implant them with human cells without tissue rejection taking place. Researchers have recently developed techniques to implant human fetal tissues containing stem cells for the blood into SCID mice. It is then possible to reconstitute these mice with functional human immune system cells, including T lymphocytes and B lymphocytes. They have also found that if these SCID mice are infected by HIV, the virus will establish infection in the human tissue and destroy the T helper lymphocytes, just as it does in humans. Thus, it may be possible to study some of the mechanisms by which HIV attacks the immune system in these mice. In addition, they may be very useful for testing potential antiviral drugs. 

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