Coinfection with influenza A virus enhances SARS-CoV-2 infectivity

Bai, Lei; Zhao, Yongliang; Dong, Jiazhen; Liang, Simeng; Guo, Ming; Liu, Xinjin; Wang, Xin; Huang, Zhixiang; Sun, Xiaoyi; Zhang, Zhen; Dong, Lianghui; Liu, Qianyun; Zheng, Yucheng; Niu, Danping; Xiang, Min; Song, Kun; Ye, Jiajie; Zheng, Wenchao; Tang, Zhidong; Tang, Mingliang; Zhou, Yu; Shen, Chao; Dai, Ming; Zhou, Li; Chen, Yu; Yan, Huan; Lan, Ke; Xu, Ke

The upcoming flu season in the Northern Hemisphere merging with the current COVID-19 pandemic raises a potentially severe threat to public health. Through experimental coinfection with influenza A virus (IAV) and either pseudotyped or live SARS-CoV-2 virus, we found that IAV preinfection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, in vivo, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice coinfected with IAV. Moreover, such enhancement of SARS-CoV-2 infectivity was not observed with several other respiratory viruses, likely due to a unique feature of IAV to elevate ACE2 expression. This study illustrates that IAV has a unique ability to aggravate SARS-CoV-2 infection, and thus, prevention of IAV infection is of great significance during the COVID-19 pandemic.