Virus interactions with bacteria: Partners in the infectious dance

The outcome of viral infection depends on the interplay between host factors and the environment.Host factors, like the expression of viral receptors, convey permissiveness to infection, define tropism, regulate antiviral immune responses, determine viral clearance, and spread.The host microbiota, the constellation of microbes inhabiting an organism, also plays a key role in the outcome of infection.Microbes and microbial products can directly interact with viral particles.Our understanding of how the microbiota impacts virus infection is largely limited to the bacterial component of the microbiota.Although bacteria do not support eukaryotic virus infection, they can promote viral fitness by enhancing virion stability, promoting infection of eukaryotic cells, and increasing coinfection rates.Virus binding of bacteria can also impact bacterial biology, including bacterial adherence to eukaryotic cells.These interactions can also indirectly affect the host response to viral infection.In this Pearl, we focus on how direct and indirect interactions between viruses and bacteria impact viral biology and touch on recent findings that illustrate how bacterial biology can also be impacted by interactions with eukaryotic viruses (Fig 1). Direct interactions between mammalian viruses and the microbiotaThe bacterial component of the microbiota can directly or indirectly impact the outcome of infection by a range of different viruses.Direct interactions have been observed between bacteria and influenza A virus (IAV) [1,2] as well as several enteric viruses: picornaviruses (including poliovirus [3, 4]); coxsackieviruses A21, B2, B3, Echovirus 30, Mengo, and Aichi viruses [5,6]; human noroviruses (HNoV) [7,8]; and mammalian orthoreovirus (reovirus) [9].Although bacteria can directly impact the outcome of infection by several viruses, the viral factors involved in the interaction between bacteria and viruses are largely undefined.In many cases, binding of viruses to bacteria is mediated through bacterial envelope components lipopolysaccharide (LPS), the main component of the gram-negative bacterial envelope, and peptidoglycan (PG), the main component of the gram-positive bacterial envelope.Poliovirus binds to LPS and PG from several bacterial species [3][4][5]10].Although the bacterial binding epitopes for poliovirus are unknown, the virus may bind LPS, PG, and chitin through the monosaccharide N-acetyl-glucosamine (GlcNAc) [4].HNoVs use histo-blood group antigens (HBGAs) to attach to eukaryotic cells [11] and can bind bacterial HBGAs [12].Reovirus thermostability is enhanced by LPS and PG independent of serotype, but lipoteichoic acid, a major component of the gram-positive bacterial envelope, elevates the thermostability of only one reovirus serotype [9].As different viral strains and serotypes differ in their interactions with bacterial envelope components, specific genetic determinants of norovirus, poliovirus, and reovirus, likely determine the use of specific bacterial components.