Of all of the viruses were Gln and Gly, respectively, implying

Of all of the viruses were Gln and Gly, respectively, implying that these viruses may retain the characteristic of preferentially binding to avian-like a2, 3-NeuAcGal linkages [21,22].The NA genes of the 15 strains sequenced and DK/VN/ 208/05 mainly Naringin web formed three groups (Figure 1B). Homology among the genes within these groups was over 97 , but the percent identity of the genes was less than 97 among the different groups. Group 1 contained four viruses, DK/VN/208/ 05, CK/VN/44/07, CK/VN/45/07, and DK/VN/31/07. Seven of the 15 strains sequenced formed group 2, six of which were isolated in Southern Vietnam. However, DK/VN/ 43/07, which was isolated in Northern Vietnam, also belonged to group 2. The NA genes of the other five viruses were in group 3. Analysis of the deduced amino acid sequences of the NA genes demonstrated that all 15 viruses had a 20-amino acid deletion (residues 49?8) in the stalk of their NA proteins. Mutations in NA associated with oseltamivir or zanamivir resistance were not detected [23,24]. The PA genes of the 15 sequenced strains mainly formed two groups (Figure 1C). Group 1 contained six viruses isolated from Northern Vietnam and DK/VN/31/07 from the South. Group 2 contained seven viruses isolated from Southern Vietnam and DK/VN/43/07 from the North. Homology among the genes within these groups was over 97 , but the homology of the genes between the two groups was less than 95 .Evolution of H5N1 Influenza Viruses in VietnamThe PB2 and PB1 genes of the 15 strains also formed two groups, similar to those of the PA genes; however, the PB2 and PB1 genes of MDK/VN/22/07 were included in group 1. Similarly, the same trends were seen in the phylogenetic tree for the NS genes of the viruses. The NP and M genes of all of these viruses shared over 97 homology and were considered to belong to one lineage. Mutations at certain positions in the M2 protein, including I26, A27, and N31, were associated with the amantadine resistance of influenza viruses [25,26]. The I26 and N31 mutations were detected in the M2 protein of all six of the clade 1 viruses and in one clade 2.3.4 virus (Table 1); the N31 mutation was also detected in the M2 protein of two clade 2.3.4 viruses (Table 1). It is interesting to note that, in addition to the I26 and N31 mutations in the M2 protein, the DK/VN/43/07, a clade 2.3.4 virus, also contained the A27 mutation. The deduced NS amino acid sequences of the 15 strains had a 15-nucleotide deletion that resulted in a 5-amino acid deletion in the NS protein (amino acid positions 80?4) [11]. On the basis of genomic diversity, the 15 strains sequenced in this study were divided into five genotypes (Fig. 2). Genotype A contained six clade 1 viruses. Genotype B contained the three clade 2.3.4 viruses analyzed in this study and DK/VN/208/05, which was reported previously by others [27]. Genotype C contained four viruses, which were reassortants of genotype B viruses that contributed new NA genes. Genotype D contained one virus, 1379592 which was a reassortant virus of a genotype C virus that derived its PA and NS genes from a genotype A (clade 1)virus. Genotype E contained one virus that had the HA gene of a clade 2.3.4 virus and its remaining seven genes from a genotype A (clade 1) virus. These results indicated that reassortment between clade 1 and calde 2.3.4 viruses actively occurred in Vietnam.Studies with MiceTo determine the ability of H5N1 avian influenza viruses to 60940-34-3 site replicate and be pathogenic in mammals, we.Of all of the viruses were Gln and Gly, respectively, implying that these viruses may retain the characteristic of preferentially binding to avian-like a2, 3-NeuAcGal linkages [21,22].The NA genes of the 15 strains sequenced and DK/VN/ 208/05 mainly formed three groups (Figure 1B). Homology among the genes within these groups was over 97 , but the percent identity of the genes was less than 97 among the different groups. Group 1 contained four viruses, DK/VN/208/ 05, CK/VN/44/07, CK/VN/45/07, and DK/VN/31/07. Seven of the 15 strains sequenced formed group 2, six of which were isolated in Southern Vietnam. However, DK/VN/ 43/07, which was isolated in Northern Vietnam, also belonged to group 2. The NA genes of the other five viruses were in group 3. Analysis of the deduced amino acid sequences of the NA genes demonstrated that all 15 viruses had a 20-amino acid deletion (residues 49?8) in the stalk of their NA proteins. Mutations in NA associated with oseltamivir or zanamivir resistance were not detected [23,24]. The PA genes of the 15 sequenced strains mainly formed two groups (Figure 1C). Group 1 contained six viruses isolated from Northern Vietnam and DK/VN/31/07 from the South. Group 2 contained seven viruses isolated from Southern Vietnam and DK/VN/43/07 from the North. Homology among the genes within these groups was over 97 , but the homology of the genes between the two groups was less than 95 .Evolution of H5N1 Influenza Viruses in VietnamThe PB2 and PB1 genes of the 15 strains also formed two groups, similar to those of the PA genes; however, the PB2 and PB1 genes of MDK/VN/22/07 were included in group 1. Similarly, the same trends were seen in the phylogenetic tree for the NS genes of the viruses. The NP and M genes of all of these viruses shared over 97 homology and were considered to belong to one lineage. Mutations at certain positions in the M2 protein, including I26, A27, and N31, were associated with the amantadine resistance of influenza viruses [25,26]. The I26 and N31 mutations were detected in the M2 protein of all six of the clade 1 viruses and in one clade 2.3.4 virus (Table 1); the N31 mutation was also detected in the M2 protein of two clade 2.3.4 viruses (Table 1). It is interesting to note that, in addition to the I26 and N31 mutations in the M2 protein, the DK/VN/43/07, a clade 2.3.4 virus, also contained the A27 mutation. The deduced NS amino acid sequences of the 15 strains had a 15-nucleotide deletion that resulted in a 5-amino acid deletion in the NS protein (amino acid positions 80?4) [11]. On the basis of genomic diversity, the 15 strains sequenced in this study were divided into five genotypes (Fig. 2). Genotype A contained six clade 1 viruses. Genotype B contained the three clade 2.3.4 viruses analyzed in this study and DK/VN/208/05, which was reported previously by others [27]. Genotype C contained four viruses, which were reassortants of genotype B viruses that contributed new NA genes. Genotype D contained one virus, 1379592 which was a reassortant virus of a genotype C virus that derived its PA and NS genes from a genotype A (clade 1)virus. Genotype E contained one virus that had the HA gene of a clade 2.3.4 virus and its remaining seven genes from a genotype A (clade 1) virus. These results indicated that reassortment between clade 1 and calde 2.3.4 viruses actively occurred in Vietnam.Studies with MiceTo determine the ability of H5N1 avian influenza viruses to replicate and be pathogenic in mammals, we.