Based on the available data, it seems that TBSV (+)RNA synthesis is not only affected by the p33/p92 replication proteins, but by GAPDH and Ded1p host proteins as well. Since the viral replication proteins were shown to bind to TBSV (2)RNA nonspecifically [57] , we propose that the above host proteins, which bind strongly to the TBSV (2)repRNA, are involved in facilitating the proper and efficient recruitment of the p92 RdRp protein to the (2)RNA template (or alternatively to the dsRNA intermediate) within the VRC as shown in Figure 9 . For example, Ded1p might unwind either local secondary structure in (2)repRNA or dsRNA region and that, in turn, could favor binding of GAPDH or p92 to the (2)RNA template. This is followed by binding of GAPDH to an AU-rich internal site and proper positioning of the p92 RdRp (bound to GAPDH, [50] ) over the (+)-strand initiation promoter, leading to (+)RNA synthesis.