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This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Norovirus infection.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Norovirus is the cause of norovirus infection. Noroviruses (genus Norovirus) are a group of related, single-stranded RNA, nonenveloped viruses that cause acute gastroenteritis in humans. Noroviruses belong to the family Caliciviridae.


Norovirus, sometimes known as the winter vomiting bug[1], is the most common cause of viral gastroenteritis in humans. It affects people of all ages.[2] The virus is transmitted by fecal–oral route contaminated food or water, by person-to-person contact,[3] and via aerosolization of the virus and subsequent contamination of surfaces.[4] The virus affects around 267 million people and causes over 200,000 deaths each year; these deaths are usually in less developed countries and in the very young, elderly and immunosuppressed.[5]

Norovirus infection is characterized by nausea, vomiting, watery diarrhea, abdominal pain, and in some cases, loss of taste. General lethargy, weakness, muscle aches, headache, and low-grade fever may occur. The disease is usually self-limiting, and severe illness is rare. Although having norovirus can be unpleasant, it is not usually dangerous and most who contract it make a full recovery within a couple of days.[1] Norovirus is rapidly inactivated by either sufficient heating or by chlorine-based disinfectants and polyquaternary amines, but the virus is less susceptible to alcohols and detergents.[6]

After infection, immunity to norovirus is usually incomplete and temporary,[7] with one publication drawing the conclusion that protective immunity to the same strain of norovirus lasts for six months, but that all such immunity is gone after two years.[8] Outbreaks of norovirus infection often occur in closed or semiclosed communities, such as long-term care facilities, overnight camps, hospitals, schools, prisons, dormitories, and cruise ships, where the infection spreads very rapidly either by person-to-person transmission or through contaminated food.[9] Many norovirus outbreaks have been traced to food that was handled by one infected person.[10]

The genus name Norovirus is derived from Norwalk virus, the only species of the genus. The species causes approximately 90% of epidemic nonbacterial outbreaks of gastroenteritis around the world,[11] and may be responsible for 50% of all foodborne outbreaks of gastroenteritis in the United States.[12][13]



Noroviruses are transmitted directly from person to person (62–84% of all reported outbreaks)[14] and indirectly via contaminated water and food. They are extremely contagious, and fewer than twenty virus particles can cause an infection[2] (some research suggests as few as five).[8] Transmission can be aerosolized when those stricken with the illness vomit, and can be aerosolized by a toilet flush when vomit or diarrhea is present; infection can follow eating food or breathing air near an episode of vomiting, even if cleaned up.[15] The viruses continue to be shed after symptoms have subsided and shedding can still be detected many weeks after infection.[16]

Vomiting, in particular, transmits infection effectively, and appears to allow airborne transmission. In one incident, a person who vomited spread infection right across a restaurant, suggesting that many unexplained cases of food poisoning may have their source in vomit.[17] 126 people were dining at six tables in December 1998; one woman vomited onto the floor. Staff quickly cleaned up, and people continued eating. Three days later others started falling ill; 52 people reported a range of symptoms, from fever and nausea to vomiting and diarrhea. The cause was not immediately identified. Researchers plotted the seating arrangement: more than 90% of the people at the same table as the sick woman later reported becoming ill. There was a direct correlation between the risk of infection of people at other tables and how close they were to the sick woman. More than 70% of the diners at an adjacent table fell ill; at a table on the other side of the restaurant, the attack rate was still 25%. The outbreak was attributed to a Norwalk-like virus (norovirus). Other cases of transmission by vomit were later identified.[18]

In one outbreak at an international scout jamboree in the Netherlands, each person with gastroenteritis infected an average of 14 people before increased hygiene measures were put in place. Even after these new measures were enacted, an ill person still infected an average of 2.1 other people.[19] A CDC study of 11 outbreaks in New York State lists the suspected mode of transmission as person-to-person in seven outbreaks, foodborne in two, waterborne in one, and one unknown. The source of waterborne outbreaks may include water from municipal supplies, wells, recreational lakes, swimming pools and ice machines.[20]

Shellfish and salad ingredients are the foods most often implicated in norovirus outbreaks. Ingestion of shellfish that have not been sufficiently heated poses a high risk for norovirus infection.[21] Foods other than shellfish may be contaminated by infected food handlers.[22]


Noroviruses (NoV) are a genetically diverse group of single-stranded RNA, non-enveloped viruses belonging to the Caliciviridae family.[23] According to the International Committee on Taxonomy of Viruses, the genus Norovirus has one species, which is called Norwalk virus.[24]

Noroviruses commonly isolated in cases of acute gastroenteritis belong to two genogroups: genogroup I (GI) includes Norwalk virus, Desert Shield virus and Southampton virus; and II (GII), which includes Bristol virus, Lordsdale virus, Toronto virus, Mexico virus, Hawaii virus and Snow Mountain virus.[23]

Noroviruses can genetically be classified into five different genogroups (GI, GII, GIII, GIV, and GV), which can be further divided into different genetic clusters or genotypes. For example, genogroup II, the most prevalent human genogroup, presently contains 19 genotypes. Genogroups I, II and IV infect humans, whereas genogroup III infects bovine species, and genogroup V has recently been isolated in mice.[25]

Most noroviruses that infect humans belong to genogroups GI and GII.[26] Noroviruses from Genogroup II, genotype 4 (abbreviated as GII.4) account for the majority of adult outbreaks of gastroenteritis and often sweep across the globe.[27] Recent examples include US95/96-US strain, associated with global outbreaks in the mid- to late-1990s; Farmington Hills virus associated with outbreaks in Europe and the United States in 2002 and in 2004; and Hunter virus which was associated with outbreaks in Europe, Japan and Australasia. In 2006, there was another large increase in NoV infection around the globe.[28] Reports have shown a link between the expression of human histo-blood group antigens (HBGAs) and the susceptibility to norovirus infection. Studies have suggested the viral capsid of noroviruses may have evolved from selective pressure of human HBGAs.[29]

A 2008 study suggests the protein MDA-5 may be the primary immune sensor that detects the presence of noroviruses in the body.[30] Some people have common variations of the MDA-5 gene that could make them more susceptible to norovirus infection.[31]

A 2010 study suggested a specific genetic version of norovirus (which would not be distinguishable from other types of the virus using standard viral antibody tests) interacts with a specific mutation in the ATG16L1 gene to help trigger symptomatic Crohn's disease in mice that have been subjected to a chemical that causes intestinal injury similar to the process in humans. (There are other similar ways for such diseases to happen like this, and this study in itself does not prove norovirus causes Crohn's in humans).


Viruses in Norovirus are non-enveloped, with icosahedral geometries. Capsid diameters vary widely, from 23-40 nm in diameter. The larger capsids (38-40 nm) exhibit T=3 symmetry and are composed of 180 VP1 proteins. Small capsids (23 nm) show T=1 symmetry, and are composed of 60 VP1 proteins.[32] The virus particles demonstrate an amorphous surface structure when visualized using electron microscopy.[33]

Noroviruses contain a linear, non-segmented,[32] positive-sense RNA genome of approximately 7.5kbp, encoding a major structural protein (VP1) of about 58~60 kDa and a minor capsid protein (VP2).[34]

The most variable region of the viral capsid is the P2 domain, which contains antigen-presenting sites and carbohydrate-receptor binding regions.[35][36][37][38]

The estimated mutation rate (1.21×10−2 to 1.41 ×10−2 substitutions per site per year) in this virus is high even compared with other RNA viruses.[39]

Genus Structure Symmetry Capsid Genomic Arrangement Genomic Segmentation
Norovirus Icosahedral T=1, T=3 Non-Enveloped Linear Monopartite

Life Cycle

Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment to host receptors, which mediates endocytosis. Replication follows the positive stranded RNA virus replication model. Positive stranded RNA virus transcription is the method of transcription. Translation takes place by leaky scanning, and RNA termination-reinitiation. Human and mammals serve as the natural host. Transmission routes are fecal-oral and contamination.[32]

Genus Host Details Tissue Tropism Entry Details Release Details Replication Site Assembly Site Transmission
Norovirus Humans; mammals Intestinal epithelium Cell receptor endocytosis Lysis Cytoplasm Cytoplasm Oral-fecal



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