Enhanced BMV RNA replication upon repression of an essential gene suggests that, when present, the host factor contributes to an inhibitory response in a cellular process/pathway that competes with the virus. For example, of the 19 genes whose repression stimulated BMV RNA replication, 9 genes (DHR2, ECM16, NOP7, PWP1, RIO2, RPA43, UTP4, UTP18, YGR251W) are functionally associated with ribosome biosynthesis ( Table 4 ). All of these genes perform or participate in ATP-dependent processes and depleting products of the implicated genes may result in an increased pool of energy and/or nucleotides available to the virus (Fig. 2, Tables 3 and 4) . Alternatively, depleting these genes may alter the competition between viral and cellular translation. UTP4 and UTP18 function in rRNA processing, a cellular pathway that enhances TBSV replication (as shown by the effects of UTP9 and UTP15) [38] , but has the opposite effect on BMV RNA replication. Depleting genes involved in processing cellular mRNA 39 ends (RNA15), regulating transcription (SPT6), modulating cellular gene expression (SWD2), and controlling nucleocytoplasmic trafficking (NUP57) may increase the availability of ribosomes and/or alter the levels of specific proteins, preferentially stimulating BMV RNA replication (Fig. 2, Tables 3 and 4 ) by disrupting cellular pathways that would compete with BMV RNA translation or replication under wild type conditions. Thus, experimental depletion of these genes is in some ways analogous to the global shutoff of host mRNA pathways, employed by many mammalian viruses through diverse mechanisms [42, 43, 44] . Additional studies are necessary to define the role of these mRNA metabolism genes in BMV RNA replication.