The clonal profile of anti-HIV-1 antibodies is established at the time of infection as part of a vigorous immune response against HIV-1, and remains stable during the infection process. This bias towards antibodies specific for the initially infecting clonal virus population, termed imprinting, is inappropriate for attempts of the infected host to control viral variants that subsequently emerge. Here, Heinz Köhler, Sybille Müller and Peter Nara argue that immunodominant epitopes on viral variants or recombinant proteins are selected that induce and maintain this deceptive state, and thereby remain unrecognized through a functional and cross-reactive hole in the B-cell repertoire.