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The presentation of these early results at the First Conference on Retroviruses and Related Infections was met with caution. HIV had proven itself a wily foe, and its defense mechanism was resistance.
So far in the battle against HIV, several treatments had shown impressive initial impact against the virus but were soon overwhelmed by HIV’s ability to mutate around and rebound against these drugs. Not only did this render the drug being taken ineffective, but sometimes HIV that had developed resistance to one drug turned out to have cross-resistance to other similar drugs, making further treatment difficult.
By early 1994, the exciting results of the trial showed the first signs of diminishing. Some of the patients seemed to be developing resistance to CRIXIVAN as early as one month after starting treatment. However, there was still one patient, who would come to be known as Patient 142, who had seen the level of HIV virus in his blood drop to below detectable levels. Encouraged by his results, and by the fact that even patients who were experiencing an HIV rebound while on CRIXIVAN were still seeing increased levels of CD4 cells (which generally eroded upon HIV rebound with previous drugs), the Merck scientists decided to modify the dosage of CRIXIVAN. The researchers hoped the new dose would deliver a blow from which the virus would be unable to recover.