Norovirus

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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]

Overview

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

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]

Virology

Transmission

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]

Classification

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).

Structure

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 (1.21Template:E to 1.41 Template:E 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

Gallery

References

  1. ↑ 1.0 1.1 "Norovirus - NHS Choices". Nhs.uk. 2014-01-20. Retrieved 2014-02-09.
  2. ↑ 2.0 2.1 Morillo SG, Timenetsky Mdo C (2011). "Norovirus: an overview". Revista Da Associação Médica Brasileira (1992). 57 (4): 453–8. doi:10.1016/s0104-4230(11)70094-x. PMID 21876931.
  3. ↑ Goodgame R (2006). "Norovirus gastroenteritis". Curr Gastroenterol Rep. 8 (5): 401–08. doi:10.1007/s11894-006-0026-4. PMID 16968608.
  4. ↑ Said MA, Perl TM, Sears CL (November 2008). "Healthcare epidemiology: gastrointestinal flu: norovirus in health care and long-term care facilities". Clinical Infectious Diseases. 47 (9): 1202–8. doi:10.1086/592299. PMID 18808354.
  5. ↑ Debbink K, Lindesmith LC, Donaldson EF, Baric RS (2012). "Norovirus Immunity and the Great Escape". PLoS Pathog. 8 (10): e1002921. doi:10.1371/journal.ppat.1002921.
  6. ↑ Jimenez L, Chiang M (2006). "Virucidal activity of a quaternary ammonium compound disinfectant against feline calicivirus: a surrogate for norovirus". Am J Infect Control. 34 (5): 269–73. doi:10.1016/j.ajic.2005.11.009. PMID 16765204.
  7. ↑ Lindesmith L, Moe C, Lependu J, Frelinger JA, Treanor J, Baric RS (2005). "Cellular and Humoral Immunity following Snow Mountain Virus Challenge". J. Virol. 79 (5): 2900–9. doi:10.1128/JVI.79.5.2900-2909.2005. PMC 548455. PMID 15709009.
  8. ↑ 8.0 8.1 Leon, Juan (2008). "Chapter 9". In Vajdy, Michael. Immunity Against Mucosal Pathogens. Springer. p. 232. ISBN 9781402084126.
  9. ↑ Noda M, Fukuda S, Nishio O (2007). "Statistical analysis of attack rate in norovirus foodborne outbreaks". Int J Food Microbiol. 122 (1–2): 216–20. doi:10.1016/j.ijfoodmicro.2007.11.073. PMID 18177970.
  10. ↑ Koopmans M, Duizer E (2004). "Foodborne viruses: an emerging problem". Int. J. Food Microbiol. 90 (1): 23–41. doi:10.1016/S0168-1605(03)00169-7. PMID 14672828.
  11. ↑ Lindesmith L, Moe C, Marionneau S, Ruvoen N, Jiang X, Lindblad L, Stewart P, LePendu J, Baric R (2003). "Human susceptibility and resistance to Norwalk virus infection". Nat. Med. 9 (5): 548–53. doi:10.1038/nm860. PMID 12692541.
  12. ↑ Widdowson MA, Sulka A, Bulens SN, Beard RS, Chaves SS, Hammond R, Salehi ED, Swanson E, Totaro J, Woron R, Mead PS, Bresee JS, Monroe SS, Glass RI (2005). "Norovirus and foodborne disease, United States, 1991–2000". Emerging Infect. Dis. 11 (1): 95–102. doi:10.3201/eid1101.040426. PMC 3294339. PMID 15705329.
  13. ↑ "Norovirus: Technical Fact Sheet". National Center for Infectious Diseases, CDC.
  14. ↑ Moore MD, Goulter RM, Jaykus L (April 2015). "Human Norovirus as a Foodborne Pathogen: Challenges and Developments". Annual Review of Food Science and Technology (2015). 6 (1): 411–33. doi:10.1146/annurev-food-022814-015643.
  15. ↑ "I've lost my appetite...": New Scientist article on spread of viral food poisoning across a restaurant by eating near where someone has vomited
  16. ↑ Atmar RL, Opekun AR, Gilger MA, Estes MK, Crawford SE, Neill FH, Graham DY (October 2008). "Norwalk Virus Shedding after Experimental Human Infection". Emerging Infect. Dis. 14 (10): 1553–7. doi:10.3201/eid1410.080117. PMC 2609865. PMID 18826818.
  17. ↑ Marks PJ, Vipond IB, Carlisle D, Deakin D, Fey RE, Caul EO (June 2000). "Evidence for airborne transmission of Norwalk-like virus (NLV) in a hotel restaurant". Epidemiol. Infect. 124 (3): 481–487. doi:10.1017/s0950268899003805. PMC 2810934. PMID 10982072.
  18. ↑ Marks PJ, Vipond IB, Regan FM, Wedgwood K, Fey RE, Caul EO (Aug 2003). "A school outbreak of Norwalk-like virus: evidence for airborne transmission". Epidemiol. Infect. 131 (1): 727–736. doi:10.1017/s0950268803008689. PMC 2870014. PMID 12948373.
  19. ↑ Heijne JC, Teunis P, Morroy G, Wijkmans C, Oostveen S, Duizer E, Kretzschmar M, Wallinga J (2009). "Enhanced Hygiene Measures and Norovirus Transmission during an Outbreak" (PDF). Emerg. Infect. Dis. 15 (1): 24–30. doi:10.3201/1501.080299. PMC 2660689. PMID 19116045.
  20. ↑ Hedberg CW, Osterholm MT (1993). "Outbreaks of food-borne and waterborne viral gastroenteritis". Clin. Microbiol. Rev. 6 (3): 199–210. PMC 358282. PMID 8395330.
  21. ↑ Shellfish consumption and the risk of norovirus infection
  22. ↑ Parashar UD, Monroe SS (2001). ""Norwalk-like viruses" as a cause of foodborne disease outbreaks". Rev. Med. Virol. 11 (4): 243–52. doi:10.1002/rmv.321. PMID 11479930.
  23. ↑ 23.0 23.1 Department of Health and Ageing Norovirus laboratory case definition
  24. ↑ Eric B. Carstens; King, Andrew; Elliot Lefkowitz; Adams, Michael Ian (2011). Virus Taxonomy: Ninth Report of the International Committee on Taxonomy of Viruses. Amsterdam: Elsevier. pp. 981–982. ISBN 0-12-384684-6.
  25. ↑ Ramirez S, Giammanco GM, De Grazia S, Colomba C, Martella V, Arista S (2008). "Genotyping of GII.4 and GIIb norovirus RT-PCR amplicons by RFLP analysis". J. Virol. Methods. 147 (2): 250–6. doi:10.1016/j.jviromet.2007.09.005. PMID 17953996.
  26. ↑ Vinjé J, Green J, Lewis DC, Gallimore CI, Brown DW, Koopmans MP (2000). "Genetic polymorphism across regions of the three open reading frames of "Norwalk-like viruses"". Arch. Virol. 145 (2): 223–41. doi:10.1007/s007050050020. PMID 10752550.
  27. ↑ Noel JS, Fankhauser RL, Ando T, Monroe SS, Glass RI (2000). "Identification of a distinct common strain of "Norwalk-like viruses" having a global distribution". J. Infect. Dis. 179 (6): 1334–44. doi:10.1086/314783. PMID 10228052.
  28. ↑ Tu ET, Bull RA, Greening GE, Hewitt J, Lyon MJ, Marshall JA, McIver CJ, Rawlinson WD, White PA (2008). "Epidemics of gastroenteritis during 2006 were associated with the spread of norovirus GII.4 variants 2006a and 2006b". Clin. Infect. Dis. 46 (3): 413–20. doi:10.1086/525259. PMID 18177226.
  29. ↑ Shirato H (2011). "Norovirus and histo-blood group antigens". Japanese Journal of Infectious Diseases. 64 (2): 95–103. PMID 21519121.
  30. ↑ McCartney SA, Thackray LB, Gitlin L, Gilfillan S, Virgin HW, Virgin Iv HW, Colonna M (July 18, 2008). Baric, Ralph S., ed. "MDA-5 Recognition of a Murine Norovirus". PLoS Pathog. 4 (7): e1000108. doi:10.1371/journal.ppat.1000108. PMC 2443291. PMID 18636103.
  31. ↑ Researchers Discover Primary Sensor That Detects Stomach Viruses Newswise, Retrieved on July 20, 2008.
  32. ↑ 32.0 32.1 32.2 "Viral Zone". ExPASy. Retrieved 15 June 2015.
  33. ↑ Prasad BV, Crawford S, Lawton JA, Pesavento J, Hardy M, Estes MK (2001). "Structural studies on gastroenteritis viruses". Novartis Found. Symp. Novartis Foundation Symposia. 238: 26–37, discussion 37–46. doi:10.1002/0470846534.ch3. ISBN 978-0-470-84653-7. PMID 11444031.
  34. ↑ Clarke IN, Lambden PR (2000). "Organization and expression of calicivirus genes". J. Infect. Dis. 181 Suppl 2: S309–16. doi:10.1086/315575. PMID 10804143.
  35. ↑ Tan M, Hegde RS, Jiang X (2004). "The P Domain of Norovirus Capsid Protein Forms Dimer and Binds to Histo-Blood Group Antigen Receptors". J. Virol. 78 (12): 6233–42. doi:10.1128/JVI.78.12.6233-6242.2004. PMC 416535. PMID 15163716.
  36. ↑ Tan M, Huang PW, Meller J, Zhong WM, Farkas T, Jiang X (2004). "Mutations within the P2 domain of norovirus capsid affect binding to human histo-blood group antigens: evidence for a binding pocket". J. Virol. 78 (6): 3201. doi:10.1128/JVI.78.6.3201.2004.
  37. ↑ Cao S, Lou Z, Tan M, Chen Y, Liu Y, Zhang Z, Zhang XC, Jiang X, Li X, Rao Z (2007). "Structural Basis for the Recognition of Blood Group Trisaccharides by Norovirus". J. Virol. 81 (11): 5949–57. doi:10.1128/JVI.00219-07. PMC 1900264. PMID 17392366.
  38. ↑ Lundborg M, Ali E, Widmalm G (2013). "An in silico virtual screening study for the design of norovirus inhibitors: fragment-based molecular docking and binding free energy calculations". Carbohydr Res. 378: 133–8. doi:10.1016/j.carres.2013.03.012. PMID 23582100.
  39. ↑ Victoria M, Miagostovich MP, Ferreira MS, Vieira CB, Fioretti JM, Leite JP, Colina R, Cristina J (2009). "Bayesian coalescent inference reveals high evolutionary rates and expansion of Norovirus populations". Infect Genet Evol. 9 (5): 927–932. doi:10.1016/j.meegid.2009.06.014. PMID 19559104.
  40. ↑ 40.0 40.1 40.2 40.3 40.4 40.5 40.6 "Public Health Image Library (PHIL)".


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