The molecular mechanisms by which human MxA inhibits cytoplasmically replicating RNA viruses such as VSV is primarily by inhibition of early viral transcription (within 45 min of the start of the infection) [15,16,17,18]; soluble (dispersed) MxA inhibits VSV-virion-driven transcription in cell-free assays [17], and it has been suggested that it is the free dispersed MxA in the cell cytoplasm that is antivirally active [18]. This evidence concerns the gene MX1 and infection.