A remarkably rapid emergence and accumulation of rZH501-M847-A-type virus occurred in the mice inoculated with rZH501-M847-G (Figs. 7 and 8 ). In the past, an experimental infection using swine influenza virus resulted in a similarly rapid emergence of a variant virus in infected hosts during single infections [30] . There are other examples of this type of quasispecies emergence and fixation in vivo [31, 32, 33] . Although rZH501-M847-G was rescued from cDNAs and direct sequencing of the M segment of rZH501-M847-G did not show the presence of rZH501-M847-Atype in the inoculum (data not shown), rZH501-M847-A-type viruses might have been generated during T7 polymerasemediated primary transcription from the plasmid or during M segment RNA replication and existed as one of a minor virus population of ZH501-M847-G quasispecies in the inoculum. Alternatively, rZH501-M847-A-type virus was generated by a point mutation at M847 of the M segment in the rZH501-M847-G-infected mice and became a major virus population as early as 2 days p.i. As discussed above, we speculate that rZH501-M847-A may bind to GAGs less efficiently than does rZH501-M847-G. This putative phenotype of rZH501-M847-A-type virus might have prevented the efficient elimination of the virus from reticuloendothelial systems, and facilitated continuous replication and systemic infection.