Enteric viruses encounter a vast microbial community in the mammalian digestive tract. We found that gut microbes are required for replication and pathogenesis of two unrelated enteric viruses, poliovirus and reovirus. Similarly, other groups have demonstrated that mouse mammary tumor virus and norovirus also rely on intestinal microbiota for replication. A common theme has emerged: Enteric viruses bind bacterial surface polysaccharides. We found that exposure to bacteria or bacterial surface polysaccharides, including lipopolysaccharide and peptidoglycan, enhanced poliovirus stability and cell attachment/viral receptor binding, providing one mechanism by which intestinal microbiota promote enteric picornavirus infection. Virion stabilization by bacteria may be important for transmission, since a mutant poliovirus with reduced binding to bacteria had a fecal-oral transmission defect due to virion instability in feces. We visualized virion-bacteria interactions using electron microscopy and found that each bacterium binds several poliovirus or reovirus virions. These results raise the possibility that bacteria may deliver virions to host cells to initiate the first viral replication cycle in the gut and that virion-bound bacteria may be the infectious unit for inter-host transmission. We found that bacteria can facilitate delivery of more than one virus to a mammalian cell, which can enhance viral fitness through genetic recombination. Our results suggest that bacteria may promote viral evolution by facilitating synchronous co-infection. In more recent work, we found that bacterial metabolites can alter the host to enhance coxsackievirus replication. Our ongoing work is examining mechanisms and consequences of microbiota-mediated enteric virus replication.