Influenza Like Illness (ILI) and Severe Acute Respiratory Infection (SARI) cases are more prone to Influenza and SARS-CoV-2 infection. Accordingly, we genetically characterized Influenza and SARS-CoV-2 in 633 ILI and SARI cases by rRT-PCR and WGS. ILI and SARI cases showed H1N1pdm09 prevalence of 20.9% and 23.2% respectively. 135 (21.3%) H1N1pdm09 and 23 (3.6%) H3N2 and 5 coinfection (0.78%) of H1N1pdm09 and SARS-CoV-2 were detected. Phylogenetic analysis revealed H1N1pdm09 resemblance to clade 6B.1A.5a.2 and their genetic relatedness to InfA/Perth/34/2020, InfA/Victoria/88/2020 and InfA/Victoria/2570/2019. Pan 24 HA and 26 NA nonsynonymous mutations and novel HA (G6D, Y7F, Y78H, P212L, G339R, T508K and S523T) and NA (S229A) mutations were observed. S74R, N129D, N156K, S162N, K163Q and S164T alter HA Cb and Sa antibody recognizing site. Similarly, M19T, V13T substitution and multiple mutations in transmembrane and NA head domain drive antigenic drift. SARS-CoV-2 strains genetically characterized to Omicron BA.2.75 lineage containing thirty nonsynonymous spike mutations exhibited enhanced virulence and transmission rates. Coinfection although detected very minimal, the mutational changes in H1N1pdm09 and SARS-CoV-2 virus infected individuals could alter antibody receptor binding sites, allowing the viruses to escape immune response resulting in better adaptability and transmission. Thus continuous genomic surveillance is required to tackle any future outbreak.

流感样疾病 (ILI) 和严重急性呼吸道感染 (SARI) 病例更容易感染流感和 SARS-CoV-2。因此，我们通过 rRT-PCR 和 WGS 对 633 例 ILI 和 SARI 病例中的流感和 SARS-CoV-2 进行了遗传学表征。 ILI 和 SARI 病例显示 H1N1pdm09 患病率分别为 20.9% 和 23.2%。检测到 135 例 (21.3%) H1N1pdm09 和 23 例 (3.6%) H3N2，以及 5 例 (0.78%) H1N1pdm09 和 SARS-CoV-2 混合感染。系统发育分析显示，H1N1pdm09 与进化枝 6B.1A.5a.2 相似，且与 InfA/Perth/34/2020、InfA/Victoria/88/2020 和 InfA/Victoria/2570/2019 具有遗传相关性。观察到 Pan 24 HA 和 26 NA 非同义突变以及新的 HA（G6D、Y7F、Y78H、P212L、G339R、T508K 和 S523T）和 NA（S229A）突变。 S74R、N129D、N156K、S162N、K163Q 和 S164T 改变 HA Cb 和 Sa 抗体识别位点。同样，M19T、V13T 取代以及跨膜和 NA 头域的多重突变也会导致抗原漂移。 SARS-CoV-2 毒株的遗传特征为 Omicron BA.2.75 谱系，含有 30 个非同义刺突突变，表现出增强的毒力和传播率。尽管检测到的混合感染非常少，但 H1N1pdm09 和 SARS-CoV-2 病毒感染者的突变可能会改变抗体受体结合位点，使病毒逃避免疫反应，从而获得更好的适应性和传播能力。因此，需要持续的基因组监测来应对未来的任何爆发。