Co-infection of influenza A virus enhances SARS-CoV-2 infectivity

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

doi: https://doi.org/10.1101/2020.10.14.335893

This article is a preprint and has not been certified by peer review [what does this mean?].

PDF: https://www.biorxiv.org/content/10.1101/2020.10.14.335893v1.full.pdf

Abstract

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 co-infection of IAV with either pseudotyped or SARS-CoV-2 live virus, we found that IAV pre-infection significantly promoted the infectivity of SARS-CoV-2 in a broad range of cell types. Remarkably, increased SARS-CoV-2 viral load and more severe lung damage were observed in mice co-infected with IAV in vivo. Moreover, such enhancement of SARS-CoV-2 infectivity was not seen with several other viruses probably due to a unique IAV segment as an inducer to elevate ACE2 expression. This study illustrates that IAV has a special nature to aggravate SARS-CoV-2 infection, and prevention of IAV is of great significance during the COVID-19 pandemic.

Competing Interest Statement

The authors have declared no competing interest.

https://www.biorxiv.org/content/10.1101/2020.10.14.335893v1