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Norovirus

Norovirus is a highly contagious, non-enveloped, single-stranded RNA virus belonging to the family Caliciviridae that causes acute gastroenteritis, commonly known as the "stomach flu" or "stomach bug," characterized by sudden onset of vomiting, diarrhea, nausea, and abdominal cramps.^[1] It is the leading cause of viral gastroenteritis outbreaks worldwide, accounting for over 90% of epidemic cases and responsible for approximately 50% of all gastroenteritis outbreaks globally.^[1] In the United States alone, norovirus leads to an estimated 19–21 million cases of acute gastroenteritis annually, resulting in about 103,000 hospitalizations and 900 deaths, primarily among adults over 65 years old.^[1]^[2] Norovirus infection affects people of all ages but poses a higher risk to young children under 5, older adults, and immunocompromised individuals, with symptoms typically appearing 12–48 hours after exposure and lasting 1–3 days.^[2]^[1] Globally, it contributes significantly to the burden of diarrhoeal diseases, which cause nearly 1.7 billion cases in children each year and result in over 443,000 deaths among those under 5, often exacerbating malnutrition and stunted growth in low-income settings. Norovirus alone causes an estimated 685 million cases annually worldwide, including 200 million in children under 5 years old and approximately 50,000 deaths in this age group.^[3]^[4] The virus spreads primarily through the fecal-oral route via contaminated food or water (especially raw shellfish), direct contact with infected individuals, or touching contaminated surfaces, and it remains infectious for at least two weeks after symptoms resolve, with as few as 18–1,000 viral particles sufficient to cause infection.^[2]^[1] Its environmental stability, including resistance to alcohol-based disinfectants like ethanol, though it can be inactivated by bleach-based solutions at appropriate concentrations, facilitates outbreaks in settings such as schools, cruise ships, nursing homes, and restaurants.^[1]^[5] Diagnosis is usually clinical based on symptoms and epidemiology, as routine viral testing is not performed; however, stool samples can confirm norovirus via PCR or antigen detection if needed to rule out other pathogens.^[1] There is no specific antiviral treatment or vaccine available, so management focuses on supportive care, particularly oral or intravenous rehydration to prevent dehydration, with antiemetics used symptomatically in severe cases.^[2]^[1] Prevention relies on rigorous hand hygiene with soap and water, thorough cooking of potentially contaminated foods, immediate disinfection of surfaces with bleach-based solutions, and isolating infected individuals for at least 48 hours after symptoms subside.^[2]^[3] Ongoing research into norovirus vaccines shows promise, particularly for high-risk populations, but none are currently approved.^[1]

Clinical manifestations

Signs and symptoms

Norovirus infection typically presents with an acute onset of gastrointestinal symptoms, including nausea, vomiting, watery non-bloody diarrhea, and abdominal cramps.^[2] Vomiting is often projectile, particularly in children, while diarrhea tends to predominate in adults.^[6] Additional symptoms may include low-grade fever, headache, myalgia, and chills, contributing to overall malaise.^[7] The incubation period ranges from 12 to 48 hours after exposure, with symptoms generally lasting 1 to 3 days in healthy individuals, making the illness self-limiting in most cases.^[8] However, dehydration from fluid loss due to vomiting and diarrhea is the primary complication and can be severe, often necessitating hospitalization, especially among vulnerable populations such as young children, the elderly, and immunocompromised individuals.^[8]^[9] Severity varies by age, with children under 2 years experiencing more frequent vomiting—sometimes without accompanying diarrhea—while adults report more pronounced diarrhea.^[9] In rare instances, particularly in young children, extraintestinal manifestations such as benign seizures or convulsions may occur, often linked to dehydration or electrolyte imbalances during the infection.^[10]

Pathophysiology

Norovirus primarily infects the small intestine by binding to histo-blood group antigens (HBGAs) on the surface of enterocytes via interactions with the viral capsid protein VP1, which facilitates attachment and entry into host cells.^[11] This binding is strain-specific and influenced by host secretor status, determined by the FUT2 gene, with non-secretors showing resistance to certain genotypes.^[12] Once attached, the virus may enter through M cells overlying Peyer's patches or directly invade enterocytes, leading to replication in epithelial cells and possibly immune cells such as macrophages and dendritic cells.^[7] Infection induces structural changes in the gastrointestinal mucosa, including villous blunting, crypt hyperplasia, and mild inflammation in the lamina propria, which impair nutrient absorption and promote secretory diarrhea through disrupted electrolyte transport.^[13] Viral nonstructural proteins, such as NS1/2 and VP4, contribute to pathogenesis by disrupting tight junctions between epithelial cells, increasing intestinal permeability, and inducing apoptosis via downregulation of anti-apoptotic factors like survivin, resulting in significant fluid loss and barrier dysfunction. These cellular alterations manifest clinically as acute vomiting and diarrhea, typically resolving within 1-3 days in immunocompetent individuals.^[7] The host immune response plays a critical role in controlling infection, with innate immunity—mediated by type I and III interferons—rapidly limiting viral spread by inhibiting replication in infected cells. However, the adaptive immune response, involving secretory IgA and CD8+ T-cells, develops more slowly, allowing high-titer viral shedding for weeks post-infection despite symptom resolution.^[14] The bacterial microbiota modulates disease severity; certain commensals like Lactobacillus and Bacillus species enhance interferon production to restrict infection, while others provide bacterial HBGAs that norovirus exploits for initial attachment and to create a permissive environment by altering IgA responses.^[15] Disruptions in microbiota composition post-infection can prolong susceptibility. Pathogenesis varies by genogroup, with GII strains—particularly GII.4 variants—historically exhibiting greater virulence due to enhanced HBGA binding and mechanisms of immune evasion, such as antigenic drift that allows escape from prior immunity, accounting for the majority of outbreaks since the early 2000s, though GII.17 strains supplanted GII.4 as the predominant genotype during the 2024-2025 season (as of April 2025), accounting for approximately 75% of U.S. outbreaks and contributing to an earlier seasonal onset.^[16]^[17] In contrast, GI strains tend to cause milder disease with less efficient evasion.^[18]

Virology

Classification and evolution

Noroviruses belong to the genus Norovirus within the family Caliciviridae, a group of non-enveloped, positive-sense single-stranded RNA viruses. They are taxonomically divided into ten genogroups (GI–GX) based on phylogenetic clustering of the complete VP1 capsid protein sequences, with GI, GII, and rarely GIV infecting humans; among these, GII is dominant and accounts for the vast majority of human cases.^[19] Over 48 genotypes have been identified across these genogroups, with nomenclature assigned according to the genogroup and genotype number (e.g., GII.4); GII.4 remains the most common pandemic strain, driving successive global waves of gastroenteritis outbreaks.^[20] Noroviruses evolve rapidly due to their RNA genome, with substitution rates in the VP1 capsid region estimated at approximately 5.56 × 10^{-3} substitutions per site per year, attributed to the error-prone nature of the viral RNA-dependent RNA polymerase lacking proofreading activity.^[21] High frequencies of recombination, particularly at the ORF1/ORF2 junction, further enhance genetic diversity by shuffling non-structural and structural genes. Antigenic drift through point mutations and occasional shifts via recombination in the capsid protein enable the periodic emergence of novel variants every 2–4 years, allowing evasion of population-level immunity; a prominent example is the GII.4 Sydney_2012 variant, which replaced prior strains and caused widespread outbreaks.^[22] Phylogenetic reconstructions demonstrate substantial intra-genogroup diversity, with multiple lineages co-circulating within GI and especially GII, reflecting ongoing diversification. Genogroups GIII (primarily bovine) and GIV (primarily canine and feline) exhibit zoonotic potential, as evidenced by genetic similarities between animal and human strains and rare detections of GIV in human samples, suggesting possible interspecies transmission pathways.^[23] In recent developments from 2024 to 2025, GII.17 variants have surged in prevalence, particularly in Asia, overtaking GII.4 as the leading cause of outbreaks and prompting enhanced surveillance by the World Health Organization.^[17]

Structure and genome

Norovirus possesses a non-enveloped icosahedral capsid measuring 27–40 nm in diameter.^[24] The capsid is primarily composed of 180 copies of the major capsid protein VP1, arranged in T=3 icosahedral symmetry.^[25] Each VP1 subunit features a shell (S) domain that forms the inner core and a protruding (P) domain that extends outward from the surface, with the P domain subdivided into P1 and P2 subdomains.^[26] The minor structural protein VP2, present in a small number of copies (estimates vary from 1 to 12) per virion, functions as an internal scaffolding protein that enhances capsid stability and genome packaging.^[25]^[27] The norovirus genome is a positive-sense, single-stranded RNA molecule approximately 7.5–7.7 kb in length, featuring a polyadenylated tail at the 3′ end and a structured 3′ untranslated region (UTR) that includes stem-loop elements.^[26] This genome is organized into three main open reading frames (ORFs). ORF1, which spans roughly 5 kb, encodes a polyprotein precursor that is cleaved by the viral protease into seven non-structural proteins designated NS1–NS7, including the RNA-dependent RNA polymerase (NS5).^[28] ORF2 encodes the major capsid protein VP1, while ORF3 encodes the minor capsid protein VP2.^[26] High-resolution cryo-electron microscopy (cryo-EM) structures of norovirus capsids, achieved at resolutions of 2.6–4.1 Å, have elucidated the atomic-level organization and revealed histo-blood group antigen (HBGA) binding sites on the P2 subdomain of VP1, which mediate host cell attachment.^[25] Due to challenges in propagating norovirus in cell culture, no crystal structures of the intact virion exist, limiting insights to cryo-EM and virus-like particle-based analyses.^[24] The VP1 protein contains hypervariable regions, particularly within the P2 subdomain, which contribute to antigenic diversity and immune evasion.^[26]

Replication cycle

The replication cycle of norovirus begins with viral attachment to host cells, primarily enterocytes in the gastrointestinal tract, mediated by the interaction of the major capsid protein VP1 with histo-blood group antigens (HBGAs) or other glycans such as fucosylated glycans on the cell surface.^[29] For murine norovirus (MNV), a model for human norovirus (HuNoV), entry involves receptor-mediated endocytosis via proteinaceous receptors like CD300lf, often in a cholesterol-dependent and pH-independent manner, though HuNoV entry details remain partially unclear due to cultivation challenges.^[30] Following endocytosis, uncoating occurs in endosomes, releasing the positive-sense single-stranded RNA genome into the cytoplasm, facilitated by low pH or other conformational changes in the capsid.^[31] Upon release, the genomic RNA, linked at its 5' end to the viral protein VPg (NS5), directly serves as mRNA for translation by host ribosomes, recruiting eukaryotic initiation factors like eIF4E and eIF4G via VPg to initiate cap-independent translation.^[30] This produces a large polyprotein from open reading frame 1 (ORF1), which is cleaved by the viral 3C-like protease NS6 into mature non-structural proteins: NS1/2 (p48), NTPase/helicase NS3, membrane remodeler NS4 (p22), VPg (NS5), protease NS6, and RNA-dependent RNA polymerase (RdRp) NS7.^[31] These proteins form replication complexes by recruiting and modifying host membranes, such as endoplasmic reticulum-derived vesicles, into perinuclear membranous webs that support RNA synthesis and shield double-stranded RNA intermediates from innate immune detection.^[30] Replication proceeds with NS7 RdRp, primed by VPg, synthesizing a negative-sense RNA intermediate from the positive-sense template, followed by production of new positive-sense genomic RNA and subgenomic RNA via premature termination or internal ribosome entry-like mechanisms on the negative strand; the subgenomic RNA encodes the structural proteins VP1 and VP2.^[29] NS3 provides helicase activity to unwind RNA, while NS4 induces vesicle formation for complex assembly, and NS1/2 contributes to replication complex formation by interacting with host membranes.^[31] Recent structural studies (2025) have elucidated the NS3 protein's role in RNA remodeling, while imaging in enteroids has identified specific replication hubs.^[32]^[33] New virions assemble in the cytoplasm as VP1 self-assembles into T=3 icosahedral capsids, stabilized by VP2, which encapsidate the positive-sense RNA; egress occurs primarily through cell lysis induced by apoptosis or non-lytic exocytosis via extracellular vesicles, with MNV demonstrating pro-apoptotic roles for NS3 and NS4.^[30] The full intracellular cycle typically completes in 6-12 hours per round in permissive models, leading to high viral yields of up to 10^{11} particles per gram of feces during peak shedding.^[29] Studying HuNoV replication has been hindered by the lack of robust cell culture systems until the development of human intestinal enteroids (HIEs) derived from stem cells, which support propagation including continuous passaging for some strains following recent advances (as of 2025) and reveal bile acid dependency for certain genogroups; MNV models complement this by replicating efficiently in macrophages and dendritic cells, evading autophagy through NS1/2 modulation to enable persistence.^[30]^[34]

Transmission and epidemiology

Transmission routes

Norovirus primarily spreads through the fecal-oral route, involving the ingestion of viral particles from contaminated sources such as food, water, or surfaces.^[35] This transmission occurs via direct person-to-person contact, particularly in close-quarters settings, or indirectly through contact with fomites like doorknobs, utensils, or linens contaminated by feces or vomit from infected individuals.^[8] The virus exhibits high infectivity, with an infectious dose for 50% of exposed individuals (ID₅₀) as low as 18 viral particles for certain strains like Norwalk virus.^[36] Its environmental stability contributes to persistence, allowing survival in chlorinated water at concentrations up to 10 ppm for several hours, which exceeds typical levels in treated drinking water.^[37] Foodborne transmission is a major pathway, often involving shellfish harvested from contaminated waters, ready-to-eat salads, or contamination by infected food handlers during preparation.^[38] In the United States, norovirus accounts for approximately 50% of food-related outbreak illnesses.^[38] Aerosolization of vomitus during vomiting episodes can propel infectious particles into the air, facilitating spread via airborne droplets or surface deposition, especially in confined spaces like cruise ships where air currents distribute the virus.^[39] Transmission rates peak during winter months (November to April) in the Northern Hemisphere, coinciding with increased indoor crowding that amplifies contact opportunities.^[40] Outbreaks are particularly frequent in densely populated environments such as schools, nursing homes, and long-term care facilities, where shared facilities heighten exposure risks.^[38] Although norovirus shows genetic similarities between human and animal strains—such as those in pigs, dogs, and cattle—zoonotic transmission to humans remains rare, with no confirmed animal reservoir for human-adapted genotypes.^[41] Potential spillover events have been hypothesized but lack robust evidence.^[23] Following the COVID-19 pandemic, enhanced hygiene practices like frequent handwashing and surface disinfection initially reduced norovirus transmission by over 80% in some regions.^[42] However, as these measures waned, outbreaks reemerged and persisted through 2024-2025, with over 2,600 reported in the United States from August 2024 to July 2025.^[43]

Global epidemiology

Norovirus is the leading cause of acute gastroenteritis worldwide, responsible for an estimated 685 million cases annually, including 200 million among children under 5 years of age, and approximately 200,000 deaths, with the majority occurring in young children in low-income countries.^[4]^[40] The virus imposes a substantial global economic burden, estimated at $60 billion per year in healthcare costs and lost productivity.^[40] In the United States, norovirus causes 19 to 21 million illnesses each year, resulting in roughly 109,000 hospitalizations and 900 deaths, predominantly among adults aged 65 years and older.^[40] The annual economic impact in the US exceeds $10 billion, driven largely by medical expenses and productivity losses from sporadic community cases.^[44] Norovirus is the primary etiologic agent in outbreaks of gastroenteritis, accounting for about 50% of all such outbreaks in the US and up to 80% of non-foodborne outbreaks in long-term care facilities.^[38]^[45] Genogroup II genotype 4 (GII.4) strains have historically dominated, causing 60-70% of infections, though emerging variants like GII.17 have recently increased in prevalence.^[46] Vulnerable populations include young children, older adults, and immunocompromised individuals, who face higher risks of severe outcomes; the disease burden is amplified in regions with poor sanitation and low-income settings.^[7]^[2] Epidemiological trends indicate a rise in norovirus prominence following widespread rotavirus vaccination, which has reduced rotavirus cases and elevated norovirus as the leading viral cause of gastroenteritis in pediatric populations.^[47] Surges in infections were reported across Europe, Asia, and the US during the 2024-2025 season, linked to the emergence of new variants such as GII.17, which accounted for over 70% of US outbreaks by early 2025. GII.17 continued to dominate in the early 2025-2026 season, accounting for the majority of typed outbreaks as of September 2025.^[17]^[48] Surveillance efforts, including the CDC's NoroSTAT network, monitor outbreaks in real-time across participating states, revealing approximately 2,500-2,700 annual reports, though underreporting is substantial, with only about 1.5% of infections typically tested and confirmed.^[43]^[49] The virus exhibits pronounced seasonality in temperate climates, with peaks during winter months attributed to indoor crowding, lower temperatures, and reduced humidity that favor transmission and environmental persistence.^[50]^[51] This pattern contributes to higher incidence in developed regions with cold winters, while year-round transmission predominates in tropical areas with suboptimal sanitation.^[52]

Human genetic factors

Human genetic factors play a crucial role in determining susceptibility to norovirus infection and disease severity, primarily through variations in genes controlling the expression of histo-blood group antigens (HBGAs), which serve as viral attachment sites. The FUT2 gene encodes α1,2-fucosyltransferase, an enzyme essential for synthesizing HBGAs on mucosal surfaces. Individuals homozygous for loss-of-function alleles in FUT2, known as non-secretors, comprise approximately 15-20% of the global population and exhibit resistance to infection by most norovirus strains, particularly those in genogroups GI and GII that rely on HBGA binding.^[53] This Mendelian trait was first identified in controlled human challenge studies, where non-secretors remained uninfected despite exposure to epidemic GII.4 strains.^[54] The FUT3 gene, which encodes α1,3/4-fucosyltransferase responsible for Lewis antigen synthesis, further modulates susceptibility in secretors. Polymorphisms in FUT3 influence the expression of Lewis b antigens, affecting binding affinity for certain norovirus genotypes, such as GII.6 and some GII.4 variants, thereby altering infection risk in populations with varying Lewis phenotypes.^[55] Similarly, ABO blood group antigens interact with norovirus capsid proteins; a meta-analysis of multiple studies revealed that individuals with blood type O are more susceptible to GII.4 infections compared to non-O types, likely due to enhanced viral binding to unmodified H antigen precursors.^[56] Genome-wide association studies (GWAS) have confirmed FUT2 as the primary locus influencing diarrheal disease susceptibility, including norovirus, in young children, with additional signals suggesting polygenic contributions beyond HBGA pathways.^[57] Family and population studies indicate a substantial genetic component to norovirus susceptibility, with familial clustering observed in outbreak settings and GWAS highlighting heritable variance in infection risk. These factors explain heterogeneous attack rates during outbreaks, where non-secretor prevalence can reduce overall transmission by 20-30% in affected groups.^[58] Such insights support potential applications in personalized risk assessment, including genetic screening to identify resistant individuals in high-risk environments like healthcare facilities. Recent research in 2025 has elucidated interactions between FUT2 variants and host microbiome composition, showing that non-secretor status correlates with altered gut microbial diversity that may enhance innate immunity against norovirus, potentially modulating infection outcomes through indirect genetic-microbiome effects.^[59]

Diagnosis and management

Diagnosis

Diagnosis of norovirus infection often begins with clinical evaluation, relying on characteristic symptoms such as sudden-onset vomiting, watery diarrhea, nausea, and abdominal cramps, which typically last 1-3 days. In outbreak settings, criteria like the Kaplan criteria—requiring at least 50% of affected individuals to have vomiting, an incubation period of 24-48 hours, symptom duration of 12-60 hours, and absence of a bacterial pathogen—support a presumptive diagnosis. However, no unique clinical features reliably differentiate norovirus from other causes of acute gastroenteritis, such as rotavirus or bacterial infections, necessitating laboratory confirmation for definitive identification, particularly in epidemiological investigations.^[7]^[2] Laboratory diagnosis primarily involves molecular detection of viral RNA from stool or vomitus specimens, with reverse transcription quantitative polymerase chain reaction (RT-qPCR) serving as the gold standard due to its high sensitivity and specificity. RT-qPCR can detect as few as 10-100 viral genome copies per reaction and is widely available in public health and clinical laboratories. Assays typically target conserved regions of the RNA-dependent RNA polymerase (RdRp) gene in open reading frame 1 (ORF1) or the major capsid protein VP1 gene in ORF2, enabling detection of major genogroups I and II. For rapid point-of-care assessment in outbreaks, antigen detection via enzyme immunoassay (EIA) kits identifies viral proteins in stool samples, offering results within hours but with sensitivities of 50-80% compared to RT-qPCR; these are best used for initial screening and require molecular confirmation. Electron microscopy, once a foundational method, visualizes 27-40 nm non-enveloped virus particles but is seldom employed today owing to its low sensitivity (detecting only high-titer samples >10^5 particles/mL) and labor-intensive nature.^[20]^[7]^[60]^[61]^[62] Genotyping through sequencing enhances surveillance by identifying circulating strains, with Sanger sequencing or next-generation sequencing (NGS) applied to RT-qPCR amplicons from the polymerase-capsid junction for precise variant classification, such as GII.4 Sydney. Diagnostic challenges include the transient nature of viral shedding, which peaks within 48-72 hours of symptom onset and persists for 3-14 days in most immunocompetent individuals, potentially yielding false negatives if specimens are collected outside this window or if viral loads are low early in infection. The Centers for Disease Control and Prevention (CDC) recommends RT-qPCR testing for suspected outbreaks involving three or more cases to confirm norovirus and guide control measures. Multiplex gastrointestinal pathogen panels are used in syndromic testing to detect norovirus alongside other agents like rotavirus and Salmonella, where clinically appropriate.^[20]^[63]^[64]^[7]^[65]

Treatment

There is no specific antiviral treatment for norovirus infection, with management focusing on supportive care to alleviate symptoms and prevent complications such as dehydration.^[2] The primary intervention is rehydration, using oral rehydration solutions (ORS) containing electrolytes and glucose for mild to moderate cases, as recommended by the World Health Organization for effective fluid replacement in viral gastroenteritis.^[7] In severe dehydration, particularly when oral intake is not tolerated, intravenous fluids are administered to restore electrolyte balance and volume.^[7] Symptomatic relief may include antiemetics such as ondansetron to control vomiting, especially in children with acute gastroenteritis, which can reduce the need for hospitalization by improving oral intake.^[66] Anti-diarrheal agents like loperamide should be avoided, as they can prolong illness by inhibiting gut motility and potentially retaining viral particles or toxins.^[67] For nutritional support, breastfeeding should continue in infants to maintain hydration and immunity, while older patients may transition to a bland diet (e.g., bananas, rice, applesauce, toast) once vomiting subsides, avoiding fatty or spicy foods to ease gastrointestinal recovery.^[68] Hospitalization is indicated for severe dehydration, intractable vomiting persisting beyond 24 hours, or in high-risk groups such as infants, elderly individuals, or immunocompromised patients, where intravenous therapy and monitoring are essential.^[7] Antibiotics have no role in routine norovirus management, as it is a viral infection, but may be used if a secondary bacterial infection is confirmed.^[7] Both WHO and CDC guidelines prioritize maintaining electrolyte balance through rehydration to support self-limiting recovery.^[7] Experimental therapies, such as nitazoxanide, have demonstrated in vitro inhibition of norovirus replication by activating host antiviral pathways, but phase II clinical trials in transplant recipients have shown limited efficacy, with inconclusive results on symptom resolution as of 2025. Other investigational approaches include adoptive T lymphocyte administration for chronic norovirus infection in immunocompromised patients.^[69]^[70]^[71] Most individuals (approximately 99%) recover fully within 1-3 days with supportive care, though mortality is less than 0.1% in developed countries; rates are higher among malnourished children in low-resource settings due to exacerbated dehydration and impaired immune response.^[2]^[40]^[72]

Prevention and control

Hygiene and disinfection

Effective hand hygiene is a cornerstone of norovirus prevention, with washing hands with soap and water for at least 20 seconds being essential, particularly after using the toilet, changing diapers, or before preparing food, as this physically removes the virus from the skin.^[73] Alcohol-based hand sanitizers are ineffective against norovirus due to its non-enveloped structure, which resists alcohol's disruptive action, achieving less than 1 log10 reduction in viral titer even at concentrations up to 70%.^[74] In contrast, soap and water can reduce norovirus by over 1 log10 through mechanical removal.^[75] For surface disinfection, chlorine bleach solutions at concentrations of 1,000–5,000 ppm (equivalent to 5–25 tablespoons of 5–6% household bleach per gallon of water) are highly effective, requiring a contact time of 5–10 minutes to achieve greater than 3 log10 reduction in norovirus infectivity.^[73] Alternatives include peracetic acid-based disinfectants, which inactivate norovirus at concentrations around 100–200 ppm with similar contact times, and accelerated hydrogen peroxide formulations (0.5–7%), which denature the viral capsid effectively on non-porous surfaces.^[76] When cleaning vomit or fecal matter in homes or during outbreaks, first absorb the material with disposable towels or paper, wearing gloves to avoid aerosolization, then wash the area with detergent and water before applying the disinfectant.^[77] Contaminated laundry should be washed separately in hot water at 60°C (140°F) with detergent, followed by tumble drying on high heat, to ensure viral inactivation without risking cross-contamination.^[78] In food handling, thorough washing of fruits and vegetables under running water removes potential norovirus contamination from surfaces, while shellfish such as oysters must be cooked to an internal temperature of at least 63°C (145°F) to kill the virus, as steaming alone may be insufficient.^[5] Bare-hand contact with ready-to-eat foods should be avoided to prevent transmission, using gloves or utensils instead.^[79] The Centers for Disease Control and Prevention guidelines emphasize integrating soap-and-water handwashing with targeted disinfection using bleach or approved alternatives in high-risk settings like households with outbreaks or food preparation areas to maximize interruption of transmission.^[73] A key challenge is norovirus's environmental stability, as it can persist on hard surfaces at room temperature for up to 7 weeks, necessitating prompt and thorough cleaning to mitigate prolonged risk.^[79]

Institutional and food safety measures

In healthcare facilities, isolation of confirmed or suspected norovirus cases is a cornerstone of outbreak control, with patients placed on Contact Precautions in single-occupancy rooms to minimize transmission.^[65] Symptomatic healthcare staff must be excluded from work for at least 48 to 72 hours after symptoms resolve, and cohort nursing—assigning dedicated staff to affected patients—is recommended to limit cross-contamination.^[73] Terminal cleaning of affected areas using bleach-based disinfectants (typically 1,000–5,000 ppm sodium hypochlorite) is essential, as norovirus is resistant to many standard cleaners, and this process should follow thorough removal of organic matter.^[80] In the food industry, Hazard Analysis and Critical Control Points (HACCP) plans are implemented to identify and mitigate norovirus risks throughout production, processing, and distribution, particularly in high-risk sectors like shellfish harvesting.^[81] Worker health policies mandate exclusion from food handling for at least 48 hours after symptoms subside, along with prohibitions on bare-hand contact with ready-to-eat foods to prevent fecal-oral contamination.^[81] Supplier testing for norovirus in shellfish, often via PCR assays on water and harvest areas, ensures compliance with safety thresholds before market entry.^[82] For community settings such as schools and cruise ships, facility closure during active outbreaks is advised to halt spread, coupled with enhanced ventilation to dilute airborne aerosols from vomiting. Health authorities must be notified if more than five cases occur within 72 hours, triggering enhanced surveillance and response protocols; on cruise ships, this includes pre-embarkation screening and isolation of ill passengers.^[83]^[84] Wastewater treatment for norovirus requires advanced methods beyond chlorination, which is often ineffective alone due to the virus's resistance and clustering.^[85] Ultraviolet (UV) irradiation or advanced oxidation processes, such as UV combined with hydrogen peroxide, achieve significant inactivation by damaging viral RNA, with log reductions of 3–5 in secondary effluents.^[86]^[87] Regulatory frameworks bolster these measures; the U.S. Food and Drug Administration's 2025 strategy for imported produce emphasizes prevention of norovirus contamination in berries through enhanced grower training, water quality monitoring, and import testing.^[88] In the European Union, the Rapid Alert System for Food and Feed (RASFF) facilitates rapid notifications of norovirus outbreaks linked to food, enabling swift recalls and border controls, with over 40 alerts annually for viral contaminants.^[89]^[90] Implementation of these institutional protocols has demonstrated effectiveness, with studies showing outbreak reductions of up to 56% in healthcare settings through ward closures and enhanced cleaning, though compliance challenges like staff shortages persist.^[91] Environmental sampling using real-time reverse transcription PCR (RT-PCR) on high-touch surfaces enables early detection of norovirus RNA, supporting preemptive facility closures before symptomatic cases surge.^[92]^[93]

Vaccine development

Vaccine development for norovirus focuses on preventing outbreaks in high-risk populations, including older adults, young children, healthcare workers, and military personnel, where the virus causes significant morbidity and economic burden.^[94] Efforts prioritize broad coverage against dominant strains such as GII.4, responsible for most epidemics, and GI.1, a common cause of sporadic cases, to address the virus's global impact.^[94] Key vaccine platforms include virus-like particles (VLPs) derived from the major capsid protein VP1, which self-assemble into non-infectious structures mimicking the native virion to elicit immune responses without replication risks. Takeda's bivalent VLP vaccine candidate, now developed by HilleVax as HIL-214, targets GI.1 and GII.4 strains and has advanced through clinical testing.^[95] Oral platforms, such as Vaxart's VXA-G1.1-NN tablet vaccine using a non-replicating adenoviral vector expressing norovirus antigens, aim to induce mucosal immunity at the site of infection.^[96] Emerging mRNA-based approaches, like Moderna's trivalent mRNA-1403 encoding VP1 from multiple genotypes, leverage lipid nanoparticle delivery refined during COVID-19 vaccine development to target diverse strains.^[97] Clinical trials have demonstrated promising efficacy. In a phase 2b challenge study (2019-2020), the bivalent VLP vaccine (TAK-214) showed 66% efficacy against moderate-to-severe acute gastroenteritis and 52% against any illness caused by GII.4, with reduced vomiting and stool output in protected participants.^[98] Proof-of-concept in adults from prior TAK-214 studies has informed HilleVax's ongoing exploration of HIL-214 development in adults following the discontinuation of infant trials.^[99] Moderna's mRNA-1403 entered phase 3 in 2024, enrolling over 20,000 adults to evaluate efficacy against moderate-to-severe gastroenteritis; the trial experienced a clinical hold in February 2025 due to a reported case of Guillain-Barré syndrome but resumed enrollment later that year, with completion anticipated by 2027.^[100]^[101] Vaxart's oral candidate significantly reduced viral shedding and infection rates in a 2025 phase 2b challenge study, highlighting mucosal protection.^[102] Major challenges include norovirus's high genetic and antigenic diversity across genogroups and genotypes, necessitating multivalent designs to cover evolving variants like GII.4 sub-clades.^[94] No established immune correlates of protection exist, complicating endpoint selection; while blocking antibodies against histo-blood group antigen binding show promise, they do not fully predict outcomes.^[103] The inability to cultivate human norovirus in vitro hinders potency assays, relying instead on surrogate measures like VLP immunogenicity in animal models or mouse histopathology.^[94] Adjuvants play a critical role in enhancing responses; AS01B, combining monophosphoryl lipid A and QS-21, boosts T-cell and antibody production in VLP formulations, improving durability against diverse strains.^[104] Mucosal delivery routes, such as oral or intranasal, promote secretory IgA production in the gut, essential for blocking initial infection, as seen in Vaxart's platform where post-vaccination IgA titers correlated with reduced shedding.^[96] Preclinical evaluation often uses gnotobiotic piglets, which recapitulate human norovirus infection, diarrhea, and shedding due to physiological similarities, allowing challenge studies to assess vaccine-induced protection against GII strains.^[105] Prospects include potential WHO prequalification by 2027 if phase 3 trials succeed, enabling integration into routine immunization in low-income countries where norovirus causes disproportionate child mortality.^[97] However, equity concerns persist, as high development costs and cold-chain requirements may limit access in resource-poor settings without global partnerships.^[106] In 2024, preclinical mRNA candidates expanded using COVID-19 platform adaptations, offering scalable production for multivalent formulations.^[107]

Historical aspects

Discovery and early research

The illness caused by norovirus was first recognized in 1929 as "winter vomiting disease" in the United Kingdom, characterized by seasonal outbreaks of acute gastroenteritis with prominent vomiting.^[108] In November 1968, an outbreak of acute nonbacterial gastroenteritis affected approximately 50% of students and staff at Bronson Elementary School in Norwalk, Ohio; investigators from the Centers for Disease Control and Prevention collected stool samples and prepared a filtrate that was later shown to transmit the illness to volunteers.^[109] This filtrate, termed the Norwalk virus, marked the first isolation of the pathogen responsible for such outbreaks.^[110] In 1972, Albert Z. Kapikian and colleagues at the National Institutes of Health used immune electron microscopy to visualize 27-nm virus-like particles in the infectious Norwalk stool filtrate, confirming it as a small round-structured virus (SRSV) and establishing its etiologic role through serologic responses in affected individuals.^[111] This technique, involving aggregation of viral particles with convalescent sera, became the primary diagnostic method for norovirus and related SRSVs in the ensuing decades due to the virus's inability to be cultured in conventional cell lines.^[112] Early research faced significant challenges, including the lack of a cell culture system; despite numerous attempts with various tissue and organ cultures from the 1940s onward, norovirus remained uncultivable until the development of a murine norovirus model in 2004, which allowed initial studies of replication and pathogenesis.^[110] Human norovirus cultivation was not achieved until the 2010s using intestinal organoids and B-cell lines.^[113] In the 1990s, molecular advances accelerated research; the full genome of Norwalk virus was cloned in 1990, revealing a positive-sense single-stranded RNA of approximately 7.5 kb with three open reading frames (ORF1 encoding nonstructural proteins, ORF2 for the major capsid protein, and ORF3 for a minor structural protein).^[114] Sequencing of related SRSVs, such as Hawaii virus in 1993, demonstrated genetic polymorphism and sequence similarity to known caliciviruses, leading to the classification of these agents within the family Caliciviridae and the eventual establishment of the genus Norovirus. Key milestones included the 2002 discovery that Norwalk virus-like particles bind histo-blood group antigens (HBGAs) on gastrointestinal epithelial cells, identifying them as critical receptors for infection and explaining host susceptibility patterns. The 2004 isolation of murine norovirus provided the first small-animal model for studying norovirus biology, immunity, and antiviral strategies in a cultivable system.^[115] Research on norovirus was supported by the National Institutes of Health, particularly through the Laboratory of Infectious Diseases starting in the 1970s, enabling foundational epidemiologic and virologic studies.^[110] The field shifted to a molecular era in the 2000s with genomic sequencing, reverse genetics for murine strains, and receptor insights, transforming understanding from descriptive epidemiology to mechanistic investigations.^[112]

Notable outbreaks and public health impact

Norovirus imposes a substantial public health burden worldwide, serving as the leading cause of acute gastroenteritis and the predominant agent in foodborne illness outbreaks. In the United States, it is estimated to cause 19–21 million cases annually, resulting in 109,000 hospitalizations and 900 deaths, along with approximately 465,000 emergency department visits and 2.3 million outpatient visits, with associated healthcare costs and lost productivity for foodborne cases estimated at $2 billion each year.^[40] Globally, norovirus was estimated in 2015 to account for approximately 685 million cases of diarrhea and 200,000 deaths annually, disproportionately affecting young children, the elderly, and immunocompromised individuals, while contributing to 18% of all foodborne disease cases and an economic toll of around $60 billion due to medical expenses and productivity losses.^[116] The virus's impact is amplified by its high transmissibility in semi-closed settings such as healthcare facilities, schools, and long-term care institutions, where outbreaks can rapidly affect vulnerable populations and strain resources. In the U.S., norovirus is responsible for about 2,500 reported outbreaks each year, comprising roughly 50% of foodborne outbreaks and leading to significant morbidity in these environments. Internationally, it drives seasonal epidemics, particularly during winter months in temperate regions, and poses ongoing challenges in low-resource settings where access to clean water and sanitation is limited, exacerbating dehydration risks in children under five, who bear nearly one-third of foodborne-related deaths.^[38]^[4]^[117] Historically, the first documented major outbreak occurred in 1968 in Norwalk, Ohio, where the virus—initially termed the Norwalk agent—was identified after affecting over 200 people, primarily schoolchildren, with symptoms of vomiting and diarrhea; this event marked the virus's discovery via immune electron microscopy and laid the foundation for its classification as a calicivirus. Subsequent global pandemics emerged from evolving genotypes, such as the GII.4 US95/96 variant in the late 1990s, which caused widespread outbreaks across multiple continents, including a surge in the U.S. and Europe, and the GII.4 Farmington Hills strain in 2002–2003, responsible for numerous institutional outbreaks. More recently, the GII.4 Sydney variant dominated U.S. outbreaks in 2012–2013, accounting for over 50% of cases and highlighting the virus's antigenic drift; subsequent variants, such as GII.17 in 2014–2015 and ongoing GII.4 strains, have continued to drive global outbreaks.^[110]^[118] Notable modern outbreaks often occur on cruise ships, where confined spaces facilitate rapid spread; for instance, in 2025, the U.S. Centers for Disease Control and Prevention (CDC) reported 20 gastrointestinal outbreaks on vessels, 16 confirmed as norovirus (as of November 2025), including one on the Royal Caribbean's Serenade of the Seas affecting nearly 100 passengers and crew with vomiting and diarrhea. Foodborne incidents have also been prominent, with 1,008 norovirus-linked outbreaks reported in the U.S. from 2009–2012, often traced to contaminated produce, shellfish, or deli meats prepared by infected food handlers. Institutional settings saw clusters like three college campus outbreaks in 2008 across California, Michigan, and Wisconsin, sickening hundreds of students. These events underscore norovirus's role in amplifying healthcare burdens, with outbreaks in nursing homes and hospitals frequently leading to extended stays and increased mortality among the elderly.^[83]^[119]^[120]

References

[1]
Viral Gastroenteritis - StatPearls - NCBI Bookshelf - NIH
May 4, 2025 · Norovirus presents most commonly with abdominal cramps and nausea, followed by vomiting and diarrhea. Onset can be abrupt. Symptoms also include ...
[2]
About Norovirus - CDC
Apr 24, 2024 · Norovirus is a very contagious virus that causes vomiting and diarrhea. It is sometimes called the "stomach flu" or the "stomach bug."Laboratory Testing for Norovirus · Site Index | Norovirus | CDC
[3]
Diarrhoeal disease - World Health Organization (WHO)
Mar 7, 2024 · Among children under 5 years of age, the most common viral pathogens are rotavirus, norovirus, adenovirus and astrovirus. Bacterial ...
[4]
Norovirus Gastroenteritis - PMC - NIH
Incubation period, 10–51 hr. ; Symptoms, Sudden onset of vomiting (more common in children) and diarrhea (more common in adults). Diarrheal stools usually ...Missing: differences | Show results with:differences
[5]
Norovirus - StatPearls - NCBI Bookshelf - NIH
Feb 17, 2025 · Common symptoms include nausea, vomiting, abdominal pain and cramping, diarrhea, myalgias, headache, and chills. Some patients report a ...
[6]
Norovirus | Yellow Book - CDC
Apr 23, 2025 · Infected people usually experience acute onset of vomiting and non-bloody diarrhea. The incubation period ranges from 12 to 48 hours. Other ...
[7]
A narrative review of norovirus epidemiology, biology, and ... - NIH
May 29, 2024 · Norovirus AGE symptoms usually emerge ~ 1 day after exposure, although a small number of cases exhibit symptoms in as few as 0.5 days.
[8]
Norovirus-associated neurological manifestations - PubMed Central
Clinical features of norovirus infection are nausea, vomiting, fever, abdominal pain, and mild self-limited non-bloody diarrhea. Notably, the phrase “stomach ...
[9]
https://pmc.ncbi.nlm.nih.gov/articles/PMC11137017/
[10]
https://pmc.ncbi.nlm.nih.gov/articles/PMC10501950/
[11]
https://doi.org/10.1016/j.tim.2005.04.004
[12]
https://doi.org/10.1128/JVI.76.23.12335-12343.2002
[13]
https://doi.org/10.1136/gut.2008.160150
[14]
https://doi.org/10.1128/JVI.79.5.2900-2909.2005
[15]
https://doi.org/10.1016/j.coviro.2019.04.001
[16]
Updated classification of norovirus genogroups and genotypes - PMC
The genus Norovirus in the family Caliciviridae consists of a genetically diverse group of viruses infecting a wide range of mammalian host species that include ...
[17]
Laboratory Testing for Norovirus - CDC
Apr 24, 2024 · Noroviruses are now classified into ten genogroups (GI-GX) and 48 genotypes. Some genotypes were reclassified, for example, GII.15 became a new ...
[18]
Molecular Evolution and Epidemiology of Norovirus GII.4 Viruses in ...
Feb 26, 2025 · The mean estimated rate of GII.4 molecular evolution was 5.56 × 10−3 substitutions per site per year. The most common recent ancestor for all ...
[19]
Noroviruses: Evolutionary Dynamics, Epidemiology, Pathogenesis ...
May 29, 2024 · The pathogenic mechanisms of human norovirus infection are poorly understood because of the difficulty in cultivating the virus in the ...
[20]
Animals as Reservoir for Human Norovirus - PMC - PubMed Central
Viruses from genogroups GI, GII and GIV are known to infect humans. Animal noroviruses including viruses found in pigs, dogs, and cats are closely related to ...
[21]
Increasing Predominance of Norovirus GII.17 over GII.4 ... - CDC
Jun 2, 2025 · In April 2024, the percentage of GII.17 outbreaks increased to 47.4%, overtaking GII.4 outbreaks (23.7%), and from May 2024 through March 2025, ...
[22]
Atomic structure of the predominant GII.4 human norovirus capsid ...
Mar 10, 2022 · Noroviruses (NoVs), belonging to the genus Norovirus in the Caliciviridae family, are nonenveloped, positive-sense single-stranded RNA viruses ...
[23]
High-resolution cryo-EM structures of outbreak strain human ... - PNAS
Jun 10, 2019 · The norovirus genomes encode two structural proteins, one major capsid protein (VP1) that forms the icosahedral shell enclosing the genome and ...Abstract · Sign Up For Pnas Alerts · Results And Discussion
[24]
A narrative review of norovirus epidemiology, biology, and ... - Nature
May 29, 2024 · Increases in norovirus incidence have been shown in multiple countries with the emergence of GII.2[P16] in 2015–2016 and GII.17[P17] in 2014– ...
[25]
Pathogenesis of Noroviruses, Emerging RNA Viruses - PMC - NIH
This review summarizes the current understanding of norovirus pathogenesis from the histological to the molecular level, including contributions from new model ...
[26]
Norovirus: An Overview of Virology and Preventative Measures - PMC
Dec 16, 2022 · The pathogenesis of Nov suggests a broadening and blunting of the intestinal villi, crypt-cell hyperplasia and cytoplasmic vacuolization of the ...
[27]
Noroviruses—The State of the Art, Nearly Fifty Years after Their ...
We provide an updated overview of norovirus phylogeny, genome organisation, virion morphology, the replicative cycle, and clinical disease.
[28]
Human Norovirus Proteins: Implications in the Replicative Cycle ...
Jun 16, 2020 · This review examines exhaustively the functions of both HuNoV structural and non-structural proteins and their possible role within the viral replicative cycle.
[29]
How Norovirus Spreads - CDC
Apr 24, 2024 · You can get norovirus by accidentally getting tiny particles of feces (poop) or vomit in your mouth from a person infected with norovirus.
[30]
Evaluation of the 50% Infectious Dose of Human Norovirus Cin-2 in ...
In humans, the ID50 of Norwalk virus was identified to be between 18 and 2800 genomic equivalents [25,26].
[31]
Disease information about norovirus - ECDC - European Union
Jun 26, 2017 · Noroviruses are highly contagious and 10-100 viral particles may be sufficient to infect an individual. They are transmitted primarily through ...Missing: ID50 | Show results with:ID50
[32]
Norovirus Outbreaks - CDC
Most norovirus outbreaks happen when infected people spread the virus to others through direct contact. Norovirus outbreaks have been reported in many settings.Missing: overview | Show results with:overview
[33]
Aerosol Transmission of Norovirus - PMC - NIH
Jan 19, 2024 · The most common symptoms of the NoV infection are diarrhea and vomiting. The infectious dose of NoV is very low, as little as 18 viral particles ...
[34]
Norovirus Facts and Stats - CDC
May 8, 2024 · Norovirus is the leading cause of vomiting and diarrhea from acute gastroenteritis among people of all ages in the United States.Missing: overview | Show results with:overview
[35]
What Is the Reservoir of Emergent Human Norovirus Strains? - PMC
Noroviruses display tight species specificity and there is no evidence supporting zoonotic transmission, so an animal reservoir is considered unlikely.
[36]
Reduction in Sporadic Norovirus Infections Following the Start ... - NIH
COVID-19 health safety measures including stay-at-home orders, social distancing, and hand hygiene were temporally associated with a decline in norovirus ...
[37]
NoroSTAT Data | Norovirus - CDC
Sep 5, 2025 · A seasonal year's line that consistently falls above the gray or blue areas, especially during the peak of the season (December to March), might ...Missing: winter | Show results with:winter
[38]
Norovirus - Immunization, Vaccines and Biologicals
The Immunization, Vaccines and Biologicals department is responsible for targeting vaccine-preventable diseases, guiding immunization research and establishing ...
[39]
The Clinical and Economic Burden of Norovirus Gastroenteritis ... - NIH
Jul 16, 2020 · We estimate that norovirus costs $10.6 billion annually, based on the latest US incidence estimate. Sporadic community cases represented >90% and productivity ...
[40]
Norovirus in Nursing Homes: Even More Transmissible Than ...
Aug 11, 2015 · Figures from the CDC show that 80% of all nonfoodborne norovirus outbreaks in the United States from 2009 to 2012 occurred in long-term care ...Missing: elderly | Show results with:elderly
[41]
Genetic characterization of norovirus GII.4 variants circulating in ...
Oct 17, 2018 · Genogroup II genotype 4 (GII.4) is the most prevalent, comprising many variants which have caused 62% to 80% of all NoV outbreaks globally since ...
[42]
Burden of Norovirus and Rotavirus in Children after Rotavirus ... - NIH
Recent data suggest that the relative burden of norovirus versus rotavirus in children with AGE may be changing after widespread adoption of rotavirus vaccine.
[43]
Staying Healthy: Norovirus Infections Surge in 2025 - AllCare Health
Jan 6, 2025 · Underreporting: Only an estimated 1.5% of infections are officially tested and confirmed, suggesting a larger, unmeasured disease burden.
[44]
Norovirus seasonality and the potential impact of climate change
Whether or not climate change could influence the seasonal patterns of norovirus infection, by impacting on its transmission, geographic distribution and ...
[45]
Absolute Humidity Influences the Seasonal Persistence and ...
Norovirus (NoV) is one of the main causative agents of acute gastroenteritis worldwide. In temperate climates, outbreaks peak during the winter season.
[46]
A Systematic Review and Meta-Analysis of the Global Seasonality of ...
Oct 2, 2013 · Norovirus cases and outbreaks exhibited a clear seasonality across most of the locations in this study (Figure 2), with a peak in winter months ...
[47]
Genetic Susceptibility to Human Norovirus Infection: An Update
Mar 6, 2019 · The so-called non-secretors, having an inactivated FUT2 enzyme, do not express blood group antigens and are resistant to several norovirus ...
[48]
Mendelian resistance to human norovirus infections - PubMed
... in particular secretor status controlled by the alpha1,2fucosyltransferase FUT2 gene determine susceptibility to norovirus infections, with nonsecretors (FUT2 ...
[49]
FUT2, Secretor Status and FUT3 Polymorphisms of Children with ...
Sep 25, 2020 · Our results reinforce the current knowledge that secretors are more susceptible to infection by both rotavirus and norovirus than non-secretors.
[50]
ABO blood group-associated susceptibility to norovirus infection
However, blood type O appeared to be more susceptible to norovirus infection. Keywords: ABO blood group; Meta-analysis; Norovirus. Copyright © 2020 Elsevier ...
[51]
A genome-wide association meta-analysis of diarrhoeal disease in ...
Sep 15, 2016 · This genome-wide association meta-analysis suggests the implication of the FUT2 gene in diarrhoeal disease in young children from the general population.
[52]
Innate Susceptibility to Norovirus Infections Influenced by FUT2 ...
Jun 1, 2015 · " Susceptibility to some noroviruses depends on FUT2 secretor status, but the population impact of this association is not established.
[53]
Exploring deleterious non-synonymous SNPs in FUT2 gene, and ...
Mar 26, 2025 · Non-synonymous SNPs in FUT2 gene have been reported to be associated with the norovirus susceptibility and gut microbiota composition.<|control11|><|separator|>
[54]
Optimization of a real-time RT-PCR assay reveals an increase of ...
Most real-time RT-PCR assays for GI and GII norovirus target the RNA polymerase-capsid junction (ORF1-ORF2 junction), which is the most highly conserved region ...
[55]
Diagnostic Accuracy and Analytical Sensitivity of IDEIA Norovirus ...
The sensitivity and specificity of the EIA were 57.6% and 91.9%, respectively. The sensitivity for detecting NoV in fecal samples from outbreaks improved from ...
[56]
Norovirus: Epidemiology Clinical Features and Laboratory Diagnostics
FDA-approved diagnostic procedures for norovirus are based on the detection of virus in stool samples by enzyme immunoassays (EIA) or reverse transcription ...
[57]
[PDF] Using a Universal Primer-Independent Next-Generation Sequencing ...
Conventional norovirus detection and genotyping have involved RT-PCR amplification and Sanger sequencing of partial regions of polymerase and capsid sequences ...
[58]
Norwalk Virus Shedding after Experimental Human Infection - CDC
Virus shedding was first detected by antigen ELISA ≈33 hours (median 42 hours) after inoculation and lasted 10 days (median 7 days) after inoculation.Missing: false | Show results with:false
[59]
II. Summary of Recommendations | Infection Control - CDC
Mar 21, 2024 · 1. Avoid exposure to vomitus or diarrhea. Place patients on Contact Precautions in a single occupancy room if they have symptoms consistent with ...Missing: overview | Show results with:overview
[60]
Norovirus Outbreak 2025: Key Symptoms and Prevention Tips
Jan 29, 2025 · Norovirus is the leading cause of viral gastroenteritis worldwide, responsible for an estimated 19-21 million cases of illness in the United ...
[61]
Antiemetics for reducing vomiting related to acute gastroenteritis in ...
A single oral dose of ondansetron given to children with mild to moderate dehydration can control vomiting, avoid hospitalization and intravenous fluid ...
[62]
Infectious Diarrhea - IDSA
Oct 19, 2017 · Loperamide may be given to immunocompetent adults with acute watery diarrhea (weak, moderate), but should be avoided at any age in suspected or ...
[63]
Viral gastroenteritis (stomach flu) - Diagnosis & treatment - Mayo Clinic
You might find that you can eat bland, easy-to-digest foods at first, such as soda crackers, soup, oats, noodles, bananas and rice. Stop eating if your nausea ...
[64]
Nitazoxanide Inhibits Human Norovirus Replication and Synergizes ...
Nitazoxanide Inhibits Human Norovirus Replication and Synergizes with Ribavirin by Activation of Cellular Antiviral Response - PMC.
[65]
NNITS-Nitazoxanide for Norovirus in Transplant Patients Study
This is a phase 2 multi-center, double-blind, placebo-controlled study of the efficacy and safety of nitazoxanide for the treatment of solid organ and ...
[66]
The Effect of Malnutrition on Norovirus Infection - PMC - NIH
Mar 4, 2014 · Our results reveal that malnutrition is associated with more severe norovirus infections as defined by weight loss, impaired control of norovirus infections.Missing: mortality | Show results with:mortality
[67]
How to Prevent Norovirus - CDC
Jan 13, 2025 · Prevention steps and strategies: If you are sick, do not prepare, handle food, or care for others. Wait at least 2 days (48 hours) after symptoms stop.Norovirus at Youth Camps · Norovirus Fact Sheet for Food...<|separator|>
[68]
Effectiveness of Liquid Soap and Hand Sanitizer against Norwalk ...
Despite the promise of alcohol-based sanitizers for the control of pathogen transmission, they may be relatively ineffective against the HuNoV, reinforcing the ...
[69]
handwashing is more effective than alcohol-based hand disinfectants
Conclusions. Washing hands with soap and water is better than using alcohol-based hand disinfectants in removing noroviruses from hands.
[70]
EPA's Registered Antimicrobial Products Effective Against Norovirus ...
EPA Registered Hospital Disinfectants Effective Against Norovirus (Norwalk-like virus) ... Hydrogen peroxide; Peroxyacetic acid (Peracetic acid), Maguard 1522 ...
[71]
Step-by-step guide to norovirus cleanup | UMN Extension
Cleaning and disinfecting surfaces immediately after a vomiting or diarrhea event is critical to removing and destroying norovirus.
[72]
[PDF] Noroviruses - OSHA
Stability of Chlorine Bleach Once opened, bottles of household bleach will lose effectiveness after 30 days. Use a new unopened bottle of bleach every 30 days ...
[73]
Norovirus Fact Sheet for Food Workers - CDC
May 8, 2024 · Norovirus spreads easily and can make you very sick with diarrhea, vomiting, and stomach pain. All food workers should know how to prevent the ...Text Equivalent · Norovirus: Facts For Food... · 4 Tips To Prevent Norovirus...
[74]
Infection control for norovirus - PMC - NIH
Norovirus infections are notoriously difficult to prevent and control, owing to their low infectious dose, high shedding titre, and environmental stability.
[75]
Norovirus Prevention and Control Guidelines for Healthcare Settings
Apr 12, 2024 · CDC provides information on infection control and clinical safety to help reduce the risk of infections among healthcare workers, patients, and visitors.
[76]
[PDF] Using Food Safety Management Systems to Reduce norovirus - FDA
Employee Health Policies. • Employees practice proper handwashing. • Employees do not contact ready-to-eat food with bare hands. • Responsibilities of the ...
[77]
[PDF] Regulator Call to Action on Norovirus 2017 - FDA
Key provisions to combat norovirus at retail include employee health policies, hand washing and handling practices, prevention of cross-contamination, and ...
[78]
Outbreaks on Cruise Ships in VSP's Jurisdiction - CDC
Oct 21, 2025 · Learn more about outbreaks of gastrointestinal (GI) illness on cruise ships in the Vessel Sanitation Program's (VSP) jurisdiction.Missing: schools | Show results with:schools
[79]
[PDF] Guidance for the Management of Norovirus Infection in Cruise Ships
The purpose of this document is to set out guidance for health professionals, port health and other agency staff and the crew of affected vessels for the ...
[80]
Disinfection techniques of human norovirus in municipal wastewater
In this mini-review, conventional disinfection techniques adopted in wastewater treatment plants including chemical disinfection and UV irradiation are ...
[81]
Recent Update on UV Disinfection to Fulfill the ... - ACS Publications
Ultraviolet (UV) radiation alone or in combination with other oxidation processes is increasingly being considered for water disinfection because of ...
[82]
Advanced Oxidation Processes for Water and Wastewater Viral ...
Jun 14, 2021 · One of the most widely used AOP is the UV/H2O2. Such a process has been shown to be highly efficient for the treatment of burdened wastewater ...
[83]
Outbreaks Associated with Fresh and Frozen Berries - FDA
Jan 17, 2025 · The FDA developed a FDA Employee Health Policy Tool as part of Healthy People 2030's norovirus workgroup initiative to reduce norovirus through ...Missing: HACCP | Show results with:HACCP
[84]
RASFF - Food Safety - European Commission
The Rapid Alert System for Food and Feed (RASFF) was established to ensure the exchange of information between member countries to support swift reaction by ...RASFF Window - Search · Alert and Cooperation Network · RASFF Window
[85]
Foodborne Norovirus State of Affairs in the EU Rapid Alert System ...
Nov 25, 2017 · The European Union Rapid Alert System for Food and Feed (EU RASFF) database is an invaluable instrument for analyzing notifications ...
[86]
Cost-effectiveness of Ward Closure to Control Outbreaks of ...
Dec 19, 2015 · Ward closure leads to higher costs but reduces the number of new outbreaks by 6%–56% and the number of clinical cases by 1%–55%, depending on the efficacy of ...
[87]
Norovirus detection in environmental samples ... - ScienceDirect.com
Environmental samples were positive for norovirus in 31 (67.4%) outbreaks. Norovirus was most frequently detected on elevator buttons (4/17, 24%), toilet ...Missing: preemptive | Show results with:preemptive
[88]
Norovirus Detection in Environmental Samples from Norovirus ... - NIH
This report conveys the norovirus detection rates and viral loads in different environmental sites in 45 norovirus outbreaks in Beijing Municipality from ...Missing: preemptive | Show results with:preemptive
[89]
Norovirus Vaccines: Current Clinical Development and Challenges
Dec 19, 2021 · Several major barriers were noted during the development of a norovirus vaccine. Noroviruses are known for their wide genetic and antigenic ...
[90]
Clinical Development of the Takeda Norovirus Virus-Like Particles ...
Takeda vaccines is developing a bivalent, adjuvanted, norovirus vaccine candidate based on virus-like particles (VLPs) from a GI.1 strain, and a consensus ...
[91]
An oral norovirus vaccine generates mucosal immunity and reduces ...
May 14, 2025 · VXA-G1.1-NN was safe and well tolerated, conferred protection against norovirus GI.1 challenge, and reduced viral shedding in stool and emesis.
[92]
The Impact of Norovirus on Children and Adolescents - NIH
Aug 13, 2025 · Beyond its health impact, norovirus also imposes a substantial economic burden. Globally, it is estimated to cause approximately $4.2 billion in ...
[93]
Efficacy of an intramuscular bivalent norovirus GI. 1/GII. 4 virus-like ...
Sep 22, 2020 · We performed this first-in-human efficacy trial of Takeda's bivalent norovirus vaccine candidate (TAK-214) against moderate or severe acute gastroenteritis ( ...
[94]
Pipeline - HilleVax
Our initial program is a VLP based vaccine candidate in development for the prevention of acute gastroenteritis caused by norovirus.
[95]
https://academic.oup.com/ofid/article/3/suppl_1/742/2637130
[96]
Norovirus vaccine produces mucosal immunity in phase 2b trial
May 29, 2025 · An oral tablet norovirus vaccine generated mucosal immunity and reduced viral shedding in participants in a new phase 2 placebo-controlled challenge study.
[97]
Norovirus vaccines: Correlates of protection, challenges and ...
An important challenge hampering the formulation of NoV vaccines is the diversity of the virus. ... genetic variation and escape mutants on the efficacy of these ...
[98]
Thin-film freeze-drying of a bivalent Norovirus vaccine while ...
Nov 20, 2021 · Liquid AS01B/OVA vaccine formulations were prepared using sucrose, trehalose dihydrate, or D-mannitol as a stabilizer at total lipids to ...
[99]
Human norovirus animal model essential for vaccine development
Dec 29, 2021 · ... gnotobiotic pigs make excellent human norovirus animal models. ... gnotobiotic pig model of human norovirus infection and diarrhoea for vaccine ...
[100]
Vaccine value profile for norovirus - PMC - PubMed Central
Oct 6, 2023 · Norovirus vaccine stakeholders are thought to include global health organizations, low-income countries ... equity, feasibility, etc.
[101]
The Long Road to a Norovirus Vaccine: How Close Are We?
Apr 10, 2025 · However, in February 2025, the FDA paused the trial due to a Guillain-Barré syndrome case—a setback that raises questions about next steps.
[102]
Norovirus - PMC - PubMed Central - NIH
Mild diarrhea, with 4 to 6 loose stools, lasted 24 h, while low-grade fever lasted only 8 to 12 h. Other symptoms were anorexia, moderately severe abdominal ...
[103]
Updated Norovirus Outbreak Management and Disease Prevention ...
Mar 4, 2011 · Summary. Noroviruses are the most common cause of epidemic gastroenteritis, responsible for at least 50% of all gastroenteritis outbreaks ...Missing: overview | Show results with:overview
[104]
The Discovery of the 27-nm Norwalk Virus: An Historic Perspective
One of the four outbreaks took place in an elementary school in Norwalk, Ohio, in October 1968, and was investigated by the Centers for Disease Control [20].
[105]
Visualization by Immune Electron Microscopy of a 27-nm Particle ...
A 27-nm particle was observed by immune electron microscopy in an infectious stool filtrate derived from an outbreak in Norwalk, Ohio, of acute infectious.
[106]
The discovery of the 27-nm Norwalk virus: an historic perspective
In 1972, a 27-nm virus-like particle was discovered by use of immune electron microscopy (IEM) in an infectious stool filtrate derived from an outbreak of ...
[107]
In Vitro Replication of Human Norovirus - PMC - NIH
This review will highlight ways in which previous research guided and impacted the development of HuNoV culture systems and discuss ways in which more recent ...
[108]
Norwalk virus genome cloning and characterization - PubMed
Norwalk virus contains a single-stranded RNA genome of positive sense, with a polyadenylated tail at the 3' end and a size of at least 7.5 kilobases.Missing: Green et al norovirus
[109]
Murine Norovirus: a Model System To Study Norovirus Biology and ...
The MNV model system provides the first opportunity to understand the relationship between basic mechanisms of norovirus replication in tissue culture and ...
[110]
Norovirus Disease in the United States - PMC - NIH
Norovirus causes an average of 570–800 deaths, 56,000–71,000 hospitalizations, 400,000 emergency department visits, 1.7–1.9 million outpatient visits, and 19–21 ...Methods And Findings · Laboratory-Confirmed... · Figure 1
[111]
WHO's first ever global estimates of foodborne diseases find ...
Dec 3, 2015 · Children are at particular risk of foodborne diarrhoeal diseases, with 220 million falling ill and 96 000 dying every year. Diarrhoea is often ...
[112]
Food safety - World Health Organization (WHO)
Oct 4, 2024 · Norovirus is a common cause of foodborne infections that is characterized by nausea, explosive vomiting, watery diarrhoea and abdominal pain. ...
[113]
Review Evolution of norovirus - ScienceDirect.com
4 variants include US 96, which caused a pandemic in the late 1990s [22, 23], Farmington Hills 2002 [24, 25], Hunter 2004 [26], Den Haag 2006b [9, 27], New ...
[114]
Foodborne Norovirus Outbreaks — United States, 2009–2012 - CDC
Jun 6, 2014 · Transmission of norovirus occurs primarily via the fecal-oral route, including direct person-to-person contact, consumption of contaminated ...
[115]
Norovirus Outbreaks on Three College Campuses - CDC
Oct 9, 2009 · During fall 2008, three norovirus outbreaks occurring on college campuses in California, Michigan, and Wisconsin were reported to CDC.