but are not yet approved: nelfinavir and VX-748 (Sternberg, 1996).
Sternberg (1996) explains that AZT (zidovudine), 3TC (Epivir) and something called ddC (HIVID) are, like the inhibitors of protease (an enzyme), also attackers of a viral enzyme; they just "cripple" a different one. A cousin of AZT called simply 1592 so far, was also reported at Vancouver, as were still other PIs (Tanouye, 1996). Altogether, then, the two types of drugs, in combinations as large as three named ones in each group (6 total per cocktail) and up to 20 pills per day, addle, baffle, cripple, and generally assail HIV until the bug-chemical that is a virus cannot successfully replicate and eventually reaches "undetectable amounts" in the patient's blood (Sternberg, 1996).
In what may be a quite different sort of development, but a contemporaneous one, Beim (1996) reports in the July/August issue of American Health that the National Institute of Allergy and Infectious Diseases has identified a particular protein on the surface of white blood cells in certain patients which allows HIV to pass through the cell wall and destroy the cell internally. It seems that drugs or vaccines, to use Beim's (1996) term, could be found to block HIV from entering by rendering the protein itself absent or ineffectual. If this requires a protease inhibitor, so be it, but this appears to be a quite separate finding. According to Beim (1996), absence of the protein on the outside of white cells may explain why some patients do not become HIV-infected, despite repeated exposures.
Still further, and perhaps related in yet a third way, Beim (1996) reports a new drug for Kaposi's sarcoma, reputedly the most common cancer affecting men who have AIDS; the drug is called DaunoXome. The FDA has said this drug is comparable to a "current three-drug regimen (adriamycin, bleomycin, and vincristine)" (Beim, 1996, p. 15). This sounds like a retreat from, or an improvement upon, an ...