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.

Cell division is fundamental to all cellular life. Most of the archaea employ one of two alternative division machineries, one centered around the prokaryotic tubulin homolog FtsZ and the other around the endosomal sorting complex required for transport (ESCRT). However, neither of these mechanisms has been thoroughly characterized in archaea. Here, we show that three of the four PRC (Photosynthetic Reaction Center) barrel domain proteins of Haloferax volcanii (renamed Cell division proteins B1/2/3 (CdpB1/2/3)), play important roles in division. CdpB1 interacts directly with the FtsZ membrane anchor SepF and is essential for division, whereas deletion of cdpB2 and cdpB3 causes a major and a minor division defect, respectively. Orthologs of CdpB proteins are also involved in cell division in other haloarchaea. Phylogenetic analysis shows that PRC barrel proteins are widely distributed among archaea, including the highly conserved CdvA protein of the crenarchaeal ESCRT-based division system. Thus, diverse PRC barrel proteins appear to be central to cell division in most if not all archaea. Further study of these proteins is expected to elucidate the division mechanisms in archaea and their evolution.

The upcoming flu season in the northern hemisphere merging with the current COVID-19 pandemic may raise a potentially severe threat to public health. However, little is known about the consequences of the co-infection of influenza A virus (IAV) and SARS-CoV-2. 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. Intriguingly, such enhancement of SARS-CoV-2 infectivity was only seen under co-infection with IAV but not with several other viruses including Sendai virus, human rhinovirus, human parainfluenza virus, human respiratory syncytial virus, or human enterovirus 71. IAV infection rather than interferon signaling induced elevated expression of ACE2 essential for such enhancement of SARS-CoV-2 infectivity. Remarkably, we further confirmed that the pre-infection of IAV indeed resulted in an increased SARS-CoV-2 viral load and more severe lung damage in hACE2-transgenic mice. This study illustrates that the co-infection of IAV aggravates SARS-CoV-2 infection and disease severity, which in turn suggests that preventing the convergence of flu season and COVID-19 pandemic would be of great significance.