Molecular Characterization And Plaque Phenotype Differences Of Mya98Lineage FMDY Type O

In2010, several outbreaks of foot-and-mouth disease （FMD） serotype O occurred in China, affectingmany animals, including pigs, cattle and sheep. Molecular characteristic analysis and plaque phenotypecomparison of4foot-and-mouth disease viruses （FMDV） isolated from various hosts revealed that thevirus strain O/CHN/Mya98/2010S2owned22specific amino acid substitutions （AASs） sites differentform bovine strains within the range of the open reading frame （ORF）, but the virus strainO/CHN/Mya98/2010S1shared a number of similar amino acid sites with bovine virus strains. All of thevirus strains performed small plaque phenotypes, but the virus strain O/CHN/Mya98/2010S2manifestedas a mixture of small and large plaques in the plaque assay, suggesting that the variable sites of thisvirus strain were of significance to the change in virus plaque phenotype.In addition, a persistent infection virus （PIV） strain, O/CHN/Mya98/33-P （BF11, one of the4isolates）,was passaged through pig and cattle. Results of the10animal-passaged virus strains’ molecularcharacteristics revealed that the deletion of the28th amino acid, L^pro, of the PIV strain formed stablemolecular characteristics, and there were7different conserved amino acid sites in structural andnon-structural proteins than in the previously reported reference strains of Mya98lineage. Additionally,the analyses of the molecular characterization and plaque phenotype of the5cell-adapted virus strainsrevealed that the deletion of the28thamino acid of the L^proand7conserved amino acid sites were stillexists, but they performed mixed plaque phenotype. With the evidence of the molecular characterizationand plaque phenotype, we concluded that the deletion of the28thamino acid, L^proand7conservedamino acid sites were the significant molecular characteristics of PIV strain O/CHN/Mya98/33-P andthe2AASs of the structural protein VP1T101A and H59Q or P may play a decisive role in theformation of large plaque phenotype. The cell-adapted virus strains PF2B, PF3B, PF4-TB, CF3B wereall performed mixed plaque on BHK-21cell, and their some amino acid variable sites were adjoined tothe variable sites of O/CHN/Mya98/2010S2. Hence, we speculated that these amino acid sites may playa decisive role in the alteration of the FMDV plaque phenotype. From the phylogenetic relationship, theanimal-passaged virus, PF1, had the farthest genetic distance from the parental virus, but PF6had theclosest genetic distance. The PF6performed a tendency of atavism, and some AASs were back to theoriginal characterizations. Thus, we speculated that when FMDV affected different hosts, the viruscould adapt to new environments through random mutation of several amino acid sites.In this study, we are going to detect the association between the molecular characterization and plaquephenotype of FMDV of Mya98lineage which were isolated from different hosts to confirm somesignificant AASs which can alter the plaque phenotype, and we also can build contagious FMDV cloneswith specific site mutations through genetic engineering, and use them to verify the role of these keysite mutations on molecular pathogenesis. At the same time, we passaged a PIV strain of FMDVthrough different host animals to further study the molecular characterizations and plaque phenotypes ofMya98lineage.