It has been shown that serial passage using chicken embryos enforces the selection of adapted viruses and inevitably alters the genetic codes of the primary viral isolates, especially for genes involved in cell adsorption and viral replication [8, 9] . The environment of the viral replication may also selectively modify the original cell tropism and pathogenesis of the isolated virus [15, 25] . It has been shown that a serially embryo-passaged of infectious bronchitis viruses (IBV) M41 strain exhibited significantly attenuated pathogenesis within the oviduct compared to the parental strain [7] . In addition, egg-mediated epitope alterations in amplified isolates might attenuate the protective efficiency of these viruses when used to vaccinate against the challenge of a wild-type virulent strain [16, 24] . For instance, after egg adaption, human influenza A virus, originally showing a2-6 sialic acid tropism only, exhibits increased hemagglutinin (HA) binding affinity to a2-3 sialic acid-containing gangliosides due to amino acid substitutions in the vicinity of the receptor binding site of the HA protein [8, 15] . For primary viral isolates, providing natural host cells for replication might eliminate the selection pressure of an exotic growth environment and avert the alteration of cell tropism and consequent genomic mutations.