Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe disease.
Secondary infection with Streptococcus pneumoniae decreases influenza virus replication and is linked to severe disease.
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DOI：
10.1093/femsmc/xtac007
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Lakdawala SS
中科院分区：
文献类型：
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作者：
Mueller Brown K;Le Sage V;French AJ;Jones JE;Padovani GH;Avery AJ;Schultz-Cherry S;Rosch JW;Hiller NL;Lakdawala SS
继发性细菌感染是严重流感病毒感染的常见并发症。在2009年H1N1流感大流行期间，由于继发性细菌性肺炎，在健康的年轻人中观察到死亡率增加，其中最常见的细菌物种之一是肺炎链球菌（Spn）。先前在小鼠和雪貂中的研究表明，Spn和流感病毒之间存在协同关系。在这项研究中，雪貂模型被用来检查是否继发Spn感染（菌株BHN 97和D39）影响复制和空气传播的2009年大流行H1N1病毒（H1N1pdm09）。H1N1pdm09感染后Spn的继发感染一致地导致雪貂鼻洗液中病毒滴度的显著降低。虽然继发性Spn感染似乎对流感病毒复制产生负面影响，但用Spn预定殖的动物同样易受H1N1pdm09空气传播的影响。与先前的工作一致，与单独感染H1N1pdm09或Spn的动物相比，先前感染H1N1pdm09和继发性Spn感染的雪貂具有增加的细菌负荷和更严重的临床症状。有趣的是，表现出最严重临床症状的供体动物减少了H1N1pdm09的空气传播。基于这些数据，我们提出了这两种病原体之间的不对称关系，而不是协同作用，因为继发性细菌感染增强了SPN定植和发病机制，但降低了病毒滴度。意义：呼吸道病毒的复制和空气传播受许多宿主和环境参数的影响。细菌和病毒合并感染对呼吸道病毒传播的复杂相互作用尚未得到充分研究。在我们的研究中，我们研究了Spn如何影响流感病毒的复制和传播。我们的数据支持先前的工作，证明流感病毒感染有利于细菌生长和传播。出乎意料的是，我们观察到继发性细菌感染对鼻腔中的病毒复制产生负面影响。这些发现为进一步研究细菌如何对流感病毒产生负面影响以及这种不对称关系对流感病毒流行病学的影响奠定了基础。
Secondary bacterial infection is a common complication in severe influenza virus infections. During the H1N1 pandemic of 2009, increased mortality was observed among healthy young adults due to secondary bacterial pneumonia, one of the most frequent bacterial species being Streptococcus pneumoniae (Spn). Previous studies in mice and ferrets have suggested a synergistic relationship between Spn and influenza viruses. In this study, the ferret model was used to examine whether secondary Spn infection (strains BHN97 and D39) influence replication and airborne transmission of the 2009 pandemic H1N1 virus (H1N1pdm09). Secondary infection with Spn after H1N1pdm09 infection consistently resulted in a significant decrease in viral titers in the ferret nasal washes. While secondary Spn infection appeared to negatively impact influenza virus replication, animals precolonized with Spn were equally susceptible to H1N1pdm09 airborne transmission. In line with previous work, ferrets with preceding H1N1pdm09 and secondary Spn infection had increased bacterial loads and more severe clinical symptoms as compared to animals infected with H1N1pdm09 or Spn alone. Interestingly, the donor animals that displayed the most severe clinical symptoms had reduced airborne transmission of H1N1pdm09. Based on these data, we propose an asymmetrical relationship between these two pathogens, rather than a synergistic one, since secondary bacterial infection enhances Spn colonization and pathogenesis but decreases viral titers. Significance: replication and airborne transmission of respiratory viruses is influenced by many host and environmental parameters. The complex interplay between bacterial and viral coinfections on transmission of respiratory viruses has been understudied. In our study, we examined how Spn influences the replication and transmission of influenza virus. Our data support previous work demonstrating that infection with influenza virus benefits bacterial growth and transmission. Unexpectedly, we observed that secondary bacterial infection negatively impacts viral replication in the nasal cavity. These findings set the stage for further studies to understand how bacteria may negatively influence influenza viruses, and the impact of this asymmetrical relationship on the epidemiology of influenza viruses.