Contextual influence of mammalian macro-autophagy in virus-bacteria coinfected cell phenotypes

It is widely recognized that viral infections can substantially impact host resistance to secondary bacterial infections.For example, pulmonary influenza infection can be associated with subsequent infection with bacteria such as Streptococcus pneumoniae, Streptococcus pyogenes, or Haemophilus influenzae leading to increased susceptibility to severe pneumonia [1,2].More recently, some patients with Coronavirus Disease 2019 (COVID-19) were found susceptible to natural coinfection with Streptococcus aureus, S. pneumoniae, or H. influenzae, or to various nosocomial bacterial infections in the context of prolonged hospitalization [3].While great advances are being made in understanding the conditions and consequences related to virusbacteria coinfection at the level of tissues and organisms (cell damages, immune cell infiltration, proinflammatory cytokine production, dysbiosis) [2,4], our knowledge of the mechanistic changes that can take place at the cellular level remains very limited.Autophagy is a degradative pathway important for cell homeostasis but also an important cell autonomous defense mechanism against intracellular pathogens.Here, we focus on the few available studies that address the question of the influence of virus infection-associated changes in the autophagic status of host cells on the outcome of secondary bacterial infections at the cell level.This is an emerging field of study that, in the future, may contribute to our understanding of the biology of virus/bacteria coinfections at large.