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a Isolates were subjected to AluI digestion followed by amplified ribosomal DNA restriction analysis (ARDRA) revealed 4 genotypic groups.
The assay correctly and specifically detected and subtyped 11 different influenza A isolates from human, avian, and swine species representing the 5 subtypes.
Of 40 isolates subtyped during period one, 92.5% were subtype A. Further, 27 (83.3%) of 30 subtype A isolates genotyped during period 1 clustered with GA2.
Within this species, serotype A isolates have been found to cause the majority of infections [2].
In contrast, HCNCp is not variable, as it was expressed in all the Assemblage A isolates and subclones we tested.
Of the total 212,636 influenza A isolates recorded across all study countries, 49% were not further subtyped.
This finding suggested that NE-causing strains may possess other virulence gene(s) not present in commensal type A isolates.
Those analyses revealed the presence of an identical ssp4 ORF in all eight surveyed non-type A isolates.
In type A isolates, the gene (cpe) encoding CPE can be either chromosomal or plasmid-borne [5], [6].
Similar(2)
Very recently, Mizuta et al. demonstrated that HRV-A isolates showed wide genetic diversity, and some viruses belonging to specific clusters of the phylogenetic tree of HRV-A isolates might be associated with bronchiolitis [ 17].
The genetic homogeneity of ospC-A isolates was confirmed by sequences at 6 additional chromosomal housekeeping loci (gap, alr, glpA, xylB, ackA, and tgt).
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