Thus, it would be unlikely that ST9a RNA would ever infect transgenic potatoes. In the unlikely event a satellite infected the transgenic plants and was amplified by the replicase transgene, the satellite would not be able to move systemically in the plant without other helper virus components. For example, in the absence of coat protein, the satellite RNAs could not be encapsidated and effectively transmitted in the field because both of these functions are provided by the helper virus. Although satellites can either attenuate or intensify symptoms, symptom development in the plant would be mainly of an agronomic problem not environmental impact. One of the quintessential characteristics of viral replicases is their specificity toward the RNA that they replicate.
All plants have an endogenous RNA-dependent RNA polymerase.
If the minus strand is produced, then the sequences that encode subgenomic promoter sequences would be produced. Allen Miller has suggested that these sequences have been important in recombinational events between subgroup I and II luteoviruses. Based on the studies of this plant enzyme and viral replicases, there is no evidence to support a hypothesis that the complementary minus strand of the transgene mRNA could be synthesized by the host plant RNA polymerase. Assume that replicase transgene is expressed in cells where the virus does not replicate. Compared to natural infections, the number of cells that contain replicase sequences has increased.