Department of Laboratory Medicine, Yale School of Medicine, New Haven, Connecticut, USA.
Department of Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA.
J Infect Dis. 2024 May 15;229(5):1430-1434. doi: 10.1093/infdis/jiad402.
To gain insight into interactions among respiratory viruses, we modeled influenza A virus (IAV)-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) coinfections using differentiated human airway epithelial cultures. Replicating IAV induced a more robust interferon response than SARS-CoV-2 and suppressed SARS-CoV-2 replication in both sequential and simultaneous infections, whereas SARS-CoV-2 did not enhance host cell defense during influenza infection or suppress IAV replication. Oseltamivir, an antiviral targeting influenza, reduced IAV replication during coinfection but also reduced the host antiviral response and restored SARS-CoV-2 replication. These results demonstrate how perturbations in one viral infection can impact its effect on a coinfecting virus.
为了深入了解呼吸道病毒之间的相互作用，我们使用分化的人呼吸道上皮细胞培养物来模拟甲型流感病毒（IAV）-严重急性呼吸综合征冠状病毒 2（SARS-CoV-2）的合并感染。复制的 IAV 引起的干扰素反应比 SARS-CoV-2 更强烈，并且在先后和同时感染中均抑制了 SARS-CoV-2 的复制，而 SARS-CoV-2 在流感感染期间并没有增强宿主细胞防御或抑制 IAV 的复制。奥司他韦是一种针对流感的抗病毒药物，它在合并感染期间减少了 IAV 的复制，但也降低了宿主的抗病毒反应并恢复了 SARS-CoV-2 的复制。这些结果表明，一种病毒感染的干扰如何影响其对合并感染病毒的影响。
