Human norovirus (HuNoV) is the primary cause of acute gastroenteritis globally and the leading cause of foodborne illness in the United States [1,3]. Despite the ubiquity of HuNoV, preventative therapeutics have not yet been developed against it.

Noroviruses infect the intestinal tract, where commensal gut bacteria reside. Previous research has shown that both human and murine noroviruses (MNV) directly engage with these commensal bacteria, leading to changes in bacterial gene expression [2]. A study by the Jones Laboratory has indicated that an increased production of small bacterial outer membrane vesicles (OMVs) was observed as a result of the alterations in gene expression in two Gram-negative bacterial species—Enterobacter cloacae and Bacteroides thetaiotaomicron—that commonly populate the human gut [2]. Previous studies have also shown that OMVs produced by E. cloacae and B. thetaiotaomicron can prompt an anti-viral immune response in murine-derived macrophages [1]. The specific component within the OMVs that contributes to the immune response is unknown, however.