(22), envisages that, in the absence of Gp2, continuous transcription from the strong host RNAP-dependent early gene promoters (T7 A1-A3) during the infection cycle, could create a ‘roadblock’ to transcription by the much faster transcribing T7 RNAP leading to undesired pausing of the T7 RNAP. The gene discussed is GP2; the disease is infection.