Table 1.

Major Mechanisms of Infection in HNoV and MNoV. Human and murine norovirus (HNoV and MNoV) infections exhibit distinct characteristics, such as symptomatology and known attachment factors/receptors, but share overlap in the carbohydrate nature of their attachment factors, in cellular tropism, as well as in harboring a potential for persistent viral shedding.

	Human norovirus	Murine norovirus
Symptoms	Abdominal pain, nausea, vomiting, and diarrhea [17,20,21]	Asymptomatic in wild-type mice; potential for lethality in immunocompromised mice (Table 2)
Duration of infection	Acute symptomatic phase (1–4 days), which may be followed by viral shedding for weeks to months [22–24]	Acute strains cleared in 7–10 days; persistent strains are shed for many months/lifetime of animal [24,30]
In vitro tropism	B cells and enterocytes [4,5]	Macrophages, dendritic cells, microglial cells, and B cells [4,8,44]
In vivo tropism	Intestinal epithelial cells, myeloid cells, and lymphoid cells in immunocompromised patients [40]	Intestinal epithelial cells, macrophages, dendritic cells, B cells, and Kupffer cells (stellate macrophages in the liver) in immunocompromised mice [4,41,42,72]
Known attachment factors and receptors	Histo-blood group antigens are attachment factors conferring susceptibility to most HNoV strains [51,52]. Some strains bind heparan sulfate, sialic acid, and β-galactosylceramide [81–83]. No proteinaceous receptors are known	Strain-dependent attachment factors include terminal sialic acid residues on gangliosides and glycoproteins, and glycans on N-linked proteins [79,80]; CD300LF and CD300LD are proteinaceous viral receptors [44,45]