Identification and Genetic Evolution Analysis of One Strain of H3N2 Canine Influenza Virus Isolated from Nanjing, China
Dildar Hussain Kalhoro1,2,, Shan Liang1, Muhammad Saleem Kalhoro2, Shoaib Ahmed Pirzado2, Nasir Rajput2, Muhammad Naeem2, Fahmida Parveen2 andYongjie Liu1*
1College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China
2Faculty of Animal Husbandry and Veterinary Sciences, Sindh Agriculture University, Tandojam-70060, Pakistan
* Corresponding author: liuyongjie@njau.edu.cn
Fig. 1.
Reverse transcription PCR for the amplification of M gene. Lane M, DNA marker; Lanes 1 to 4, M gene; Lane 5, negative control.
Fig. 2.
Reverse transcription PCR for the amplification of HA and NA gene of influenza virus. Lane M, DNA marker; Lane 1, negative control; Lane 2, HA gene; Lane 3: NA gene.
Fig. 3.
Phylogenetic trees for the A/canine/Nanjing/ 01/2014 (H3N2) HA gene.
Fig. 4.
Phylogenetic tree for the A/canine/Nanjing/01/2014 (H3N2) NA gene and those of other influenza A viruses. The trees were generated with the MEGA program (version 5.0) by using neighbor-joining analysis.
Fig. 5.
Alignment of HA1 amino acid sequences of H3N2 influenza isolates and the most similar avian isolate. Boxed residues represent the antigenic sites A–E, and orange colored residues denote potential glycosylation sites, blue indicates receptor-binding sites and pink represent cleavage site.
Fig. 6.
Alignment of NA amino acid sequences of H3N2 influenza isolates and the most similar avian isolate. Black boxed residues represent antigenic sites A-E, and orange colored residues denote potential glycosylation sites, blue indicates receptor-binding sites.