关键词: COVID-19 Co-infection ILI/SARI case Influenza A (H1N1)pdm09 SARS-CoV-2

Mesh : Humans Influenza A Virus, H1N1 Subtype / genetics SARS-CoV-2 / genetics Influenza, Human / virology epidemiology COVID-19 / virology epidemiology Phylogeny Adult Middle Aged Male Female Adolescent Young Adult Genome, Viral / genetics Aged Coinfection / virology epidemiology Child Child, Preschool Severe Acute Respiratory Syndrome / virology epidemiology Mutation Infant

来  源:   DOI:10.1038/s41598-024-58993-w   PDF(Pubmed)

Abstract:
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.
摘要:
流感样疾病(ILI)和严重急性呼吸道感染(SARI)病例更容易发生流感和SARS-CoV-2感染。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进行了遗传鉴定。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和5例合并感染(0.78%)的H1N1pdm09和SARS-CoV-2。系统发育分析显示,H1N1pdm09与进化枝6B.1A.5a.2相似,与InfA/Perth/34/2020,InfA/Victoria/88/2020和InfA/Victoria/2570/2019遗传相关性。Pan24HA和26NA非同义突变和新型HA(G6D,Y7F,Y78H,P212L,G339R,观察到T508K和S523T)和NA(S229A)突变。S74R,N129D,N156K,S162N,K163Q和S164T改变HACb和Sa抗体识别位点。同样,M19T,V13T取代和跨膜和NA头部结构域中的多个突变驱动抗原漂移。SARS-CoV-2菌株的遗传特征为OmicronBA.2.75谱系,包含30种非同义尖峰突变,表现出增强的毒力和传播率。共感染虽然检测到非常少,在H1N1N1pdm09和SARS-CoV-2病毒感染个体的突变变化可以改变抗体受体结合位点,允许病毒逃避免疫反应,从而导致更好的适应性和传播。因此,需要持续的基因组监测来应对任何未来的爆发。
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