Human norovirus is the leading cause of viral gastroenteritis worldwide resulting in an estimated 200,000 deaths annually. Since the mid 1990’s human noroviruses have been implicated in frequent global pandemics highlighting this virus as a major public health concern. Enteropathogenic E. coli (EPEC) is also an enteric pathogen of significant concern to public health. In many developing countries EPEC infections are the leading cause of death in children with diarrhea.
The gut mucosa is a key interface between the environment and the body and is the first point of exposure for many pathogens including EPEC and noroviruses. Furthermore, these pathogens are routinely circulating in the same environment and thus interactions are predicted to be likely. While the specific interactions between noroviruses and EPEC have not been investigated, previous studies have implicated bacterial cofactors as important for the establishment of norovirus infection.
Additionally, both EPEC, through its effector proteins delivered by a type III secretion system, and noroviruses, through the function of their nonstructural proteins, have been shown to modulate host cell functioning and immune sensing. In order to determine if this pathogenic coinfection results in a synergistic or antagonistic symbiosis, coinfections of bone marrow derived macrophages with murine norovirus (MNV) and EPEC were performed and viral replication assessed. Findings suggest a role for EPEC in modulating MNV replication early during infection and promotion of cell survival in the presence of an established MNV infection.