There is experimental data that indirectly support this model: (i) disruption of the first 3 bp of Stem 1, which would displace the ribosome's pause site to a point 3 0 of the slippery site, has been shown to eliminate frameshifting (14) ; (ii) destabilizing Stem 2, which would allow it to be unwound more readily, has been shown to result in decreased frameshifting efficiency (15) (16) (17) ; (iii) replacing bulges in Stem 1 with base pairs would increase the energy required to unwind the first three bases, and a longer ribosomal pause over the slippery site would follow, yielding increased efficiencies in À1 frameshifting (15, 18) ; (iv) destabilizing the base of Stem 1 by replacing G:C base pairs with A:U pairs decreases À1 frameshifting efficiencies (19, 20) ; (v) the model eliminates the need for a 'pseudoknot recognizing factor', the evidence of which has not been forthcoming in either competition assays in in vitro translation systems (21) or by gel retardation assays (J. D. Dinman, unpublished data); and (vi) elimination of a potential torsion-restraining Stem 2, but not of a non-torsion-restraining Stem 2 in HIV-1, resulted in decreased À1 PRF efficiencies (22) .