The authors suggested loss of attachment efficiency by viral particles and capsid disintegration due to the alkaline nature of the PSS as the mechanism of antiviral property.57 Sato are significantly shorter (and are significantly longer (and but has been shown to have and activity against norovirus, rotavirus, and adenovirus.70 The specific mechanism of action against norovirus is thought to involve interference of protein synthesis and the activation of host cellular antiviral response pathways.71 The efficacy of nitazoxanide for the treatment of norovirus gastroenteritis in adults has been evaluated in YM155 (Sepantronium Bromide) only one randomized controlled double-blinded trial. virus-like particle known as Norwalk virus or small round-structured virus (SRSV) was later visualized YM155 (Sepantronium Bromide) in stool specimens using immune electron microscopy.5,6 Later, the genus YM155 (Sepantronium Bromide) of the virus was formally named Norovirus after the place of the original outbreak.7 is the only species within the genus as per the International Committee on Taxonomy of Viruses classification.8 The genus is a group of non-enveloped, single-stranded positive-sense ribonucleic acid (RNA) viruses belonging to the family. The human norovirus genome contains three open reading frames (ORFs) that encode eight viral proteins (VPs). The variable amino acid sequence of the major capsid protein (VP1) within ORF-2 determines the genogroup. There are 10 known genogroups (GICGX),2,9,10 of which only genogroups GI, GII, and GIV cause human disease.11 Initially emerging in 2012, the GII.4 strain has become the most prevalent genotype and is implicated in approximately 80% of norovirus outbreaks.10,12 Herein, we review norovirus epidemiology, describe its pathogenesis and immunity, and discuss norovirus transmission and its consequences for outbreaks and infection prevention and control efforts. We review clinical symptoms of norovirus infection, therapies and associated uncertainties, and vaccine development. Epidemiology Norovirus is the most commonly recognized foodborne gastroenteritis pathogen globally and is responsible for approximately 20% of all foodborne illnesses reported by the World Health Organization. Norovirus accounted for nearly 125?million cases of a total of 600?million cases of foodborne illnesses and 34,929 deaths globally in 2010 2010.13 In the United States alone, norovirus is estimated to be responsible for 19C21?million total illnesses resulting in 1.7C1.9?million outpatient visits, 400,000 emergency room visits, 56,000C71,000 hospitalizations, and 570C800 deaths per year.14 These numbers likely underestimate the true incidence of norovirus gastroenteritis as not all individuals afflicted may seek or require medical care.2 There are several patterns of norovirus infections that are of importance. Although norovirus infections are detected year-round, norovirus infection rates are highest during the winter months peaking in February and March in the northern hemisphere.15 Norovirus afflicts across age groups, but young children and elderly adults are more vulnerable to severe disease and associated morbidity and mortality. For instance, there is a notable bimodal age-related tendency of hospitalization from norovirus infection; young children and elderly populations are more susceptible to hospitalization compared to the other age groups (Table 1).16 Furthermore, norovirus has been reported as the etiological YM155 (Sepantronium Bromide) agent of gastroenteritis outbreaks in crowded, semi-closed environments, and healthcare-associated settings, such as long-term care facilities, hospitals, cruise ships, correctional facilities, restaurants, schools, child care centers, and parties.17 Hospitals and long-term care facilities bear the most outbreak burden with?>?50% of Norovirus outbreaks occurring in these settings.18 Its propensity to cause outbreaks is due to its environmental stability, low inoculum required for infection, and the potential high volume and long period of viral shedding.19 Hospitalizations and mortality rates due to norovirus gastroenteritis are higher during outbreaks than during non-outbreaks. In a comparison of hospitalization between norovirus outbreak identified in 1969. However, some of the other strains, including GII.4, PDGFB infect non-secretors and demonstrate immune evasion by means of high antigenic variation, antibody-binding epitope blockade, and potentially binding to non-HBGA ligands.12,28C30 Knowledge of host immune responses to norovirus infections is primarily derived from challenge studies due to the historic lack of an cell culture model.27 Early challenge studies suggested norovirus.