Norwalk virus norovirus

Facts About Noroviruses on Cruise Ships. Follow these tips to prevent norovirus at youth camps. Learn about food safety practices that can help prevent these outbreaks. Ways to Prevent Foodborne Norovirus Outbreaks. Skip directly to site content Skip directly to page options Skip directly to A-Z link. Section Navigation. Facebook Twitter LinkedIn Syndicate. Preventing Norovirus.

Minus Related Pages. You can help protect yourself and others from norovirus by washing your hands thoroughly with soap and water and following other simple prevention tips. Practice proper hand hygiene Wash your hands thoroughly with soap and water especially after using the toilet or changing diapers, always before eating, preparing, or handling food, and before giving yourself or someone else medicine. When you are sick, do not prepare food or care for others You should not prepare food for others or provide healthcare while you are sick and for at least two days after symptoms stop.

Furthermore, the development of a humanized immunodeficient murine model of human norovirus infection may also prove useful although perhaps only to a limited extent. Despite this manipulation, infection by the oral route was entirely unsuccessful, and intraperitoneal inoculation with a strain of human norovirus GII. Some insights into norovirus infection may, however, be obtained from studies of murine models utilizing MNVs.

MNVs are widespread in laboratory mice, and in contrast to human noroviruses, they can be propagated in tissue culture Although MNV produces little or no outward signs of infection in wild-type laboratory mice , knockout studies indicate that both innate and adaptive immunity play critical roles in the control of MNV infection. Particularly important are type 1 and type 2 interferons , — , dendritic cell functions , — , and the production of neutralizing antibody , — As such, MNVs may provide some important understanding of human norovirus infection that would not otherwise be possible to obtain Almost 4 decades ago, Parrino and colleagues challenged and then rechallenged, after an interval of 27 to 42 months, 12 volunteers with stool filtrates containing the norovirus GI.

Six subjects developed symptoms of gastroenteritis after the initial challenge, and each of these subjects also became ill upon rechallenge. In contrast, none of the 6 subjects who remained asymptomatic upon initial challenge became ill after rechallenge. Four of the six patients who developed symptoms were challenged a third time 4 to 8 weeks after the second challenge, and only one patient became ill.

The investigators concluded that they had demonstrated the presence of short-term but the absence of long-term immunity to Norwalk virus infection. This conclusion does not, however, address the 6 subjects who failed to become ill after either the first or second challenge, a finding that suggested the possibility that some individuals are intrinsically resistant to Norwalk virus infection. Five years later, the discovery of familial clustering of infection, with some related groups having apparent resistance, was also observed in a large community outbreak traced to a swimming pool These observations suggested the possibility that some individuals possess inherited protection against norovirus infection.

Subsequent investigations determined that the reason for this inherited resistance lies in the natural variability of histo-blood group antigens HBGAs and their expression on the mucosal epithelial surface of the gastrointestinal tract HBGAs are oligosaccharide epitopes whose diversity results from the sequential addition of monosaccharides to glycan precursors , The A and B red cell antigens are synthesized from a common intermediate molecule, the H substance, of which there are 3 types, but with the final fucosylated product having the same terminal disaccharide.

While the FUT1 gene is expressed in erythroid progenitor cells, FUT2 is expressed mostly in mucosal epithelial cells from which the enzymatic gene product is secreted into surrounding secretions such as saliva and breast milk. Lewis antigens are also present on mucosal surfaces and are secreted into the surrounding milieu.

The resultant absence of HBGAs at mucosal surfaces and in surrounding secretions that characterize the nonsecretor phenotype plays a key role in protection against infection by most noroviruses, as demonstrated in challenge studies , — and analyses of outbreaks, as reviewed by Rydell and colleagues They also bind to epithelial cells of the gastroduodenal mucosa of individuals who are secretors but not to those of nonsecretors Thus, it appears that norovirus is among organisms, such as Helicobacter pylori , that utilize HBGAs expressed in the gastrointestinal tract as cell surface receptors Given the multiplicity of viral strains and of HBGAs, it is not surprising that there are diverse patterns of individual strain associations with individual HBGAs.

In a study involving 14 norovirus strains, Huang et al. While there was some clustering of binding patterns depending on the phylogenetic relatedness of the viruses, both patterns could be found among both GI and GII viruses. While initial studies indicated that a nonsecretor status seemed to provide total resistance to norovirus-associated illness, the degree of protection has now been demonstrated to be less than absolute.

Examples of infection in nonsecretors include ones due to norovirus GII. In fact, combining the data from two GI. In addition, binding to human Caco-2 intestinal cells by GII. The receptors for these viruses remain unknown.

In addition, inherited factors other than HBGAs may affect susceptibility to norovirus infection. In addition to resistance to infection based on secretor status, norovirus infection results in adaptive immunity to homotypic viral challenge, albeit of relatively short duration, as was first reported by Parrino and colleagues in and subsequently confirmed However, the relevance of many challenge experiments has been questioned because the inocula used in this and many other studies were likely several orders of magnitude higher than that required for infection, and as a consequence, the duration of immunity in the natural setting may be significantly longer than that estimated from these experiments.

On the other hand, the potential for natural exposure to much larger numbers of viral particles is significant. Thus, 1 ml of virus-containing vomitus from symptomatically infected subjects contained a median of 41, genomic equivalents The norovirus load in feces is much higher and appears to be genogroup dependent, with reported medians of 8. It is therefore possible that estimates from observational studies of natural infection may provide the best estimates of the duration of immunity.

Thus, mathematical modeling taking into account observational data describing the age-specific incidence of norovirus disease, seasonality, and population immunity led to an estimated duration of immunity of 4.

Complicating the determination of immunity duration by examination of naturally acquired infections is the fact that immunity may be strain specific, and any analysis is potentially confounded by the multiple genogroups, genotypes, and strains of virus, together with the continuing evolution of the virus.

Thus, administration of stool filtrates from two distinct outbreaks to prison volunteers led to a lack of cross-protection between the Norwalk and Hawaii strains , now known to be prototypes of GI and GII noroviruses, respectively. While the inability to culture the virus in vitro precludes the ability to detect neutralizing antibody by classical methods, the prevention of binding of norovirus-derived VLPs or P particles to HBGA blocking antibody is believed to be an accurate surrogate of neutralization , In a volunteer study, preexisting antibody did not protect against disease resulting from an initial challenge, but a correlation with protection emerged after subsequent rechallenges However, others have reported that preexisting antibody provides at least partial protection against naturally acquired infection , The appearance of IgA antibody against norovirus in saliva by day 5 after challenge of genetically susceptible individuals correlated with protection , as did an early Th1 lymphocyte response High prechallenge titers of blocking antibodies also correlate with protection against experimental challenge Volunteers challenged with a GII.

A similar pattern of cross-reactivity was seen with T cells exposed to Snow Mountain virus, which elicited a predominantly Th1 response. The IgG antibody response to challenge with different GI strains results in variable heterotypic responses that are likely determined by an individual's history of natural exposure to noroviruses and deceptive imprinting e.

Antibodies to antigens other than those of the viral capsid also result from viral challenge. Three-fourths of volunteers challenged with GI. The viral capsid protein VP1 has 3 structural domains, with the shell S being the core from which 2 other domains, P1 and P2, protrude P2 is the most exposed portion and is likely the major point of contact with HBGA ligands and with neutralizing antibody 22 , 88 , , — In addition, mutations and recombination events involving P2 can significantly affect antigen properties and interactions with HBGAs In contrast, there has been only limited evolution of GI viruses over the last 4 decades There have been 7 different GII.

Thus, on average, new variants of GII. Evidence indicates that new variants emerge under positive selection 25 , likely as a result of the pressure exerted by the development of herd immunity as larger portions of the population experience infection, with resultant viral antigenic drift 20 , , — While norovirus evolution is believed to result from the selective pressure of the immune system, Schorn and colleagues demonstrated amino acid changes in P2 and P during individual chronic infections due to GII.

Others evaluating two hematopoietic stem cell transplant recipients and one small bowel transplant recipient chronically infected with GII. The immune selection of norovirus variants has important implications for vaccine development. There are strong public health and economic arguments in support of the potential benefits of the development of an effective norovirus vaccine. Thus, despite the biological obstacles to vaccine development, which require dealing with the complex matrix of inherited human traits and variability among noroviruses Table 10 , the potential benefits would appear to be well worth the effort.

Table 11 summarizes clinical studies on norovirus vaccines. Most efforts at vaccine development are now focusing on the use of VLPs as the immunogen Furthermore, VLP vaccines have a successful history in the prevention of hepatitis B virus and of human papillomavirus infection Intravenous administration of Norwalk virus to chimpanzees led to the appearance of virus in feces along with liver and duodenal and jejunal tissues , but all animals remained asymptomatic Intramuscular inoculation of other chimpanzees with VLPs derived from Norwalk virus protected against intravenous challenge with the same virus 6 and 18 months later, together with the development of blockade antibodies.

These data provide evidence of homologous but not heterologous resistance and indicate that norovirus-derived VLP inoculation may produce homologous immunity. Despite all the potential obstacles to the development of an effective vaccine, the interest is high, and by , Herbst-Kralovetz and colleagues were able to list 12 phase 1 trials that had reported the immunogenicity of plant or insect cell-derived norovirus VLPs after mucosal delivery Both oral and intranasal administrations have been shown to elicit antibody responses , — El-Kamary and colleagues reported the results of two of these trials in that same year These investigators administered GI.

The majority of circulating IgA norovirus antigen-specific cells carried markers indicative of homing to mucosal tissues alone or to mucosal and lymphoid tissues.

This GI. Two doses of each vaccine were administered intranasally 3 weeks apart. Thus, this proof-of-concept trial demonstrated the ability of an intranasal vaccine to provide a degree of short-term protection against illness after homotypic challenge. A systemically administered bivalent vaccine has also been evaluated in humans. Healthy adults were randomized to receive either placebo or a bivalent GI.

The GII. The primary composite endpoint of reduction in any type of gastroenteritis or norovirus case ascertainment was not achieved. There is interest in the development of norovirus vaccines to be given in combination with other immunogens. Many factors will need to be effectively addressed for the development of a useful norovirus vaccine Given our current understanding of the virus and the host response to it, such a vaccine will almost certainly be multivalent and, as is the case with influenza virus, may require frequent reformulations in response to viral evolution.

Norovirus is an important cause of morbidity due to acute gastroenteritis both within health care institutions and in the broader community. Although mortality is typically limited to the extremes of age, the disease exacts a significant toll on the health care system. Therapeutic management is usually supportive, and advances in molecular diagnostics may lead to the earlier identification of outbreaks and a reduction in person-to-person transmissions, particularly in vulnerable patient populations.

Ongoing global reporting initiatives will be enhanced by improved diagnostic methods. Additionally, global control efforts will benefit from the growing knowledge of the clinical implications of various norovirus strains.

Several advances into understanding the relationship among the viral strain, the host human blood group antigen type, and disease susceptibility have recently been elucidated, but this work has not yet been extended to clinical practice. The interplay of norovirus and host immunity still poses many unanswered questions.

Areas of future research may overcome technical limitations, such as the inability to cultivate norovirus in vitro , and may elucidate a way to directly measure neutralizing antibodies, which could pave the way for vaccine development.

The recent demonstration of infectability of B cells by the human norovirus GII. Several additional factors, such as inherited host variability, noroviral genogroup diversity, and ongoing viral evolution, will continue to complicate the process of vaccine development. Until a broadly effective, sustainable vaccine is developed, outbreak management will depend primarily on infection control efforts. Elizabeth Robilotti , M.

Robilotti's research focuses on the epidemiology of health care-associated infections and the impact of antimicrobial stewardship training and practice. Stan Deresinski , M. He has published more than peer-reviewed papers covering a broad area of Infectious Diseases and is currently Editor of Infectious Disease Alert and a Section Editor of Clinical Infectious Diseases.

Benjamin A. Pinsky , M. Pinsky's research focuses on the development and application of molecular techniques to improve the diagnosis and management of infectious diseases. National Center for Biotechnology Information , U. Journal List Clin Microbiol Rev v. Clin Microbiol Rev. Author information Copyright and License information Disclaimer. Corresponding author. Address correspondence to Benjamin A. Pinsky, ude.

Clin Microbiol Rev — All Rights Reserved. This article has been cited by other articles in PMC. Open in a separate window. FIG 1. FIG 2. Symptomatic Infection Incubation period. Signs, symptoms, and disease course. Reference Location Population No. Complications: severe disease and mortality at the extremes of age. Norovirus in immunocompromised hosts.

Unusual manifestations of norovirus infection. Waterborne Outbreaks Norovirus was first reported as the causative agent of a waterborne gastrointestinal disease outbreak by Kaplan et al.

Food, Restaurants, and Catering Food presents two distinct models for norovirus transmission. Sporadic Disease Caliciviruses, especially noroviruses, are important causes of sporadic gastrointestinal disease. OUTBREAKS Norovirus outbreaks have been reported in a variety of settings and are uniquely suited to areas of close living quarters, shared dining facilities, and difficult environmental maintenance.

Health Care Settings Norovirus is frequently implicated in hospital ward and nursing home outbreaks. Schools Schools and day care settings are frequently implicated in acute gastrointestinal outbreaks.

Military Norovirus is a major cause of morbidity in military training centers and fields of operation for many of the same reasons that it causes disease in civilian settings: close living quarters, the low viral inoculum required for infection, persistent viral shedding, viral resistance to disinfection, and environmental durability 41 , Cruise Ships and Resorts Numerous well-publicized norovirus outbreaks have been associated with cruise ships dating back several decades , — Outbreak Reporting Systems Once norovirus was recognized as a major etiologic agent of acute gastroenteritis and a significant cause of morbidity and cost within health care systems, several countries developed robust surveillance networks to monitor norovirus activity and outbreaks.

Criterion Description 1 Vomiting in more than half of symptomatic cases 2 Mean or median incubation period of 24 to 48 h 3 Mean or median duration of illness of 12 to 60 h 4 No bacterial pathogen isolated in stool culture.

Specimen Collection Interpretation of norovirus diagnostic testing relies upon the quality of the specimens submitted for analysis and therefore requires that appropriate specimens are properly collected and handled Norovirus Antigen Detection Enzyme immunoassays.

Rapid immunochromatographic assays. Sensitivity and specificity were calculated by using both prospective and retrospective samples. Isothermal amplification. Staff and Patient Policies An efficient response to a suspected norovirus outbreak is predicated on preexisting staff training and the rapid initiation of outbreak management policies, although evidence in support of these practices is minimal and based substantially on descriptive studies and single-institution reports.

Long-Term-Care and Other Facilities The policies employed in acute-care settings, such as patient cohorting, activity restrictions, and work restrictions for ill and exposed staff members, have been adapted to long-term-care facilities Hand Hygiene One of the primary recommended control strategies to interrupt norovirus transmission during outbreaks is appropriate hand hygiene, although this is based primarily on descriptive data Environmental Disinfection Environmental persistence of norovirus has been reported in several settings, and its role in propagating outbreaks has been described in settings ranging from health care environments to food products and preparation sites to a concert hall , — Animal Models Although no animal model to date has been entirely satisfactory, it has been demonstrated that chimpanzees can be successfully infected with GI.

Human Host Factors in Susceptibility and Resistance to Norovirus Infection Almost 4 decades ago, Parrino and colleagues challenged and then rechallenged, after an interval of 27 to 42 months, 12 volunteers with stool filtrates containing the norovirus GI.

Immune Selection and Development of Viral Diversity The viral capsid protein VP1 has 3 structural domains, with the shell S being the core from which 2 other domains, P1 and P2, protrude Obstacle to norovirus vaccine development Inability to cultivate norovirus in vitro Inability to directly measure neutralizing antibody Inherited host variability, especially with regard to HBGA Multiple viral genogroups and genotypes and their continued evolution Limited heterotypic immunity Likely need for continuing vaccine reformulation Uncertain duration of immunity Incomplete understanding of the role of cellular immunity Possible acceleration of viral evolution in response to a vaccinated population Uncertain efficacy in most vulnerable individuals, including young children, the elderly, and the immunocompromised.

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Lancet — What are the symptoms? How soon after exposure do symptoms appear? The incubation period is one to two days. What is the treatment for norovirus infection? How can norovirus infection be prevented? The following recommendations may reduce the risk of acquiring or spreading the infection: Wash hands thoroughly after each toilet visit and before and after preparing food.

People who experience nausea, vomiting or diarrhea should not attend school or work and should not handle food for others while ill. Avoid drinking untreated water. Cook shellfish thoroughly before eating.

Revised: October