Genomic Analysis of Circulating Influenza Virus from 2016 in Nepal

Abstract

Background Influenza constitutes a contagious viral infection primarily attributed to influenza viruses A or B, predominantly affecting the upper respiratory system. The rapid evolution of influenza viruses results in substantial variability. Type A encompasses 16 highly variable hemagglutinins (H1 to H16) and 9 distinct NAs (N1 to N9). Conversely, influenza type B lacks subtypes owing to fixed, albeit small, antigenic variabilities. Given the swift evolution and diversification, comprehendinggenomic epidemiology becomes imperative for discerning emerging strains and trackingtransmission. Objectives This study delves into the genomic analysis of various sequences of H1N1 and Influenza type B, isolated from Nepal and deposited in the Global Initiative on Sharing Avian Influenza Data (GISAID). Methods The viral genomic material, after extraction, were sent to National Institute of Infectious Disease, Japan for whole genome sequencing in 2016. The sequences were subsequently submitted to GISAID. The H1N1 virus genomes (n=18) in this study were investigated against the reference genome A/California/07/2009 (GenBank: CY121680). Similarly, Influenza Type B virus genomes (n=27) were examined against reference genome B/Brisbane/60/2008 (GenBank: KX058884) and B/Wisconsin/01/2010 (GenBank: JN993010). Mutational analyses were performed using Nextclade, followed by an investigation into the mutations present in the sequences. Finally, phylogenetic analysis was conducted using the Nextclade and CLUSTAL Omega. Results Out of the 18 HA genome segments of H1N1, all (n=12) except 6 isolates belonged to clade 6B, while the remainder were of clade 6B.1. For Influenza Type B, all 27 HA genome segments were classified under clade V1A when compared to B/Brisbane/60/2008. Similarly, in comparison to the reference genome B/Wisconsin/01/2010 (genbank: JN993010), all (n=23) except 4 isolates were of clade Y3, while the rest were of clade Y2. Conclusion The analysis of the HA1 (sub-segment of HA) proves valuable for strain identification based on mutations. The HA segment in influenza type A exhibits the fastest mutation rate, influencing virulence, while mutations in NA are associated with drug resistance. Given the heightened risk of influenza outbreaks due to emerging mutations, assortments, and drug resistance, vigilance in monitoring mutations in these segments are crucial.