In A, cellular peptide binding assays of the wild-type p11C peptide and the mutant peptide (p11C*) for the MHC class i molecule Mamu-a*01 show reduced recognition for the mutant. The p11B peptide serves as an irrelevant control. In B, functional interferon g assays done on cell lines from monkeys 893, 833, and 798 show reduced response to peptide p11C in monkey 798 52 weeks after challenge.
Clinical research by nature begets clichés: ups and downs, one step forward, one step back. So it goes for a pair of back-to-back papers from 2002. This issue's first Hot Paper reports early success of an HIV-vaccine approach based on a cytotoxic T lymphocyte (CTL) response to viral gag protein.1 The second describes one of eight immunized monkeys that succumbed to AIDS-like illness after a breakthrough mutation enabled a challenge virus to evade protection from a similar vaccine.2
With early vaccine efforts to elicit ...
