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Porcine reproductive and respiratory syndrome (PRRS) is an economically important infectious disease infected with PRRS virus (PRRSV) for the pig industry worldwide.Especially,the highly pathogenic PRRSV (HP-PRRSV) was emerged in China in 2006,which caused atypical PRRS or "High Fever" disease.Since then,PRRSV evolutionary mechanism,especially the question that PRRSV evolved from low pathogenesis to high pathogenesis was never failed to fascinate us.In this study,we compared the genomic sequences of six PRRS attenuated live vaccine strains with the sequences of their parental strains (CH-la/CH-1R,HuN4/HuN4-F112,JXA1/JXA1-R,VR2332/respPRRS MLV and JA142/Ingelvac ATP),respectively by DNAStar program 7.0.Interestingly,the results indicated that the whole genome of the six PRRSV parental strains experienced some types of prone hypermutation in the process of successive passages on Marc-145 cells.Among mutations of all six PRRSV attenuated strains,substitutes of A→G/G→A and C→,U/U→C were significantly higher than the other types of substitution,especially the pair of VR-2332/respPRRS MLV.In addition,we compared PRRSV classic strain CH-la with 10 isolated epidemic HP-PRRSV strains (HuN4,JXA1,NM1,SY0909,JXwn06,CWZ-1-F3,GS09-16,GS09-29,GS09-32 and HEB),respectively.What amazed us was that significant hypermutation was similar to observed in vitro attenuation.Furthermore,we monitored the evolution of PRRSV in vivo.Four piglets (＃51,＃53,＃55 and ＃56) were infected with HP-PRRSV HuN4 strain.Circulating viruses were collected at 3,7 and 14 days post infection (DPI).Sequence analysis of the viral structure gene GP5 and non-structure gene NSP2 demonstrated that a prevalent A--～G/G--～A and C→U/U→C substitutions were observed in viruses isolated from all the four animals and at all the time points examined.In addition,NSP2 were more prone to be hypermutated.The aforementioned results implicated that the PRRSV evolved in vitro and vivo under certain strong pressure(s) of host factors.