Commensal bacteria are known to have an important role in keeping the host healthy, but the role of eukaryotic viruses has been unknown; now, persistent infection in mice with various strains of enteric norovirus is shown to provide similar host protection. It is widely accepted that commensal bacteria in the human intestine have important physiological and health effects. This paper focuses on the much less studied relationship between eukaryotic viruses and mammalian hosts, and suggests that viral members of the gut microbiota can enter symbiotic relationships providing a beneficial effect similar to that provided by the bacteria colonizing our intestines. Ken Cadwell et al. demonstrate that persistent infection of mice with various strains of enteric murine norovirus (MNV) can reverse abnormalities in intestinal morphology and lymphoid cells. Additionally, MNV infection overcomes the deleterious effects of antibiotic treatment in models of infectious or chemical intestinal injury. Intestinal microbial communities have profound effects on host physiology1. Whereas the symbiotic contribution of commensal bacteria is well established, the role of eukaryotic viruses that are present in the gastrointestinal tract under homeostatic conditions is undefined2,3. Here we demonstrate that a common enteric RNA virus can replace the beneficial function of commensal bacteria in the intestine. Murine norovirus (MNV) infection of germ-free or antibiotic-treated mice restored intestinal morphology and lymphocyte function without inducing overt inflammation and disease. The presence of MNV also suppressed an expansion of group 2 innate lymphoid cells observed in the absence of bacteria, and induced transcriptional changes in the intestine associated with immune development and type I interferon (IFN) signalling. Consistent with this observation, the IFN-α receptor was essential for the ability of MNV to compensate for bacterial depletion. Importantly, MNV infection offset the deleterious effect of treatment with antibiotics in models of intestinal injury and pathogenic bacterial infection. These data indicate that eukaryotic viruses have the capacity to support intestinal homeostasis and shape mucosal immunity, similarly to commensal bacteria.

Parasitic worms affect gut microbes: Improved hygiene practices in high-income countries may come with an increased risk of developing inflammatory bowel disease (IBD) or other similar disorders. Ramanan et al. show that intestinal helminth infection, caused by parasitic worms, protects IBD-susceptible mice from developing the disease. The infection increases specific protective species and limits other inflammatory members of the microbiota. People from helminth-endemic regions harbored a similar protective microbiota, and their deworming led to an increase in inflammatory Bacteroidales species, similar to what the authors observed in the mice. Thus, a changing microbial environment may shape susceptibility to inflammatory disease. Science , this issue p. 608