Interestingly, in systemic infections (see Figure 3—figure supplement 1), AGO4 silencing mildly increased viral accumulation of the wild-type TYLCV (1.33-fold), but dramatically improved performance of the V2 null mutant virus (3.23-fold), suggesting that one of the main roles of V2 during the viral infection is the suppression of AGO4 function (Figure 3F). The gene discussed is AGO4; the disease is viral infectious disease.