Norovirus infection pathophysiology: Difference between revisions
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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. Foods other than shellfish may be contaminated by infected food handlers.<ref name="pmid11479930">{{cite journal | |||
|author=Parashar UD, Monroe SS | |author=Parashar UD, Monroe SS | ||
|title="Norwalk-like viruses" as a cause of foodborne disease outbreaks | |title="Norwalk-like viruses" as a cause of foodborne disease outbreaks | ||
Revision as of 16:29, 26 December 2012
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Norovirus infection Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Norovirus infection pathophysiology On the Web |
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American Roentgen Ray Society Images of Norovirus infection pathophysiology |
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Risk calculators and risk factors for Norovirus infection pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Norovirus is a highly contagious virus. Anyone can get infected with norovirus and get sick. Also, one can get norovirus illness many times in life. One reason for this is that there are many different types of noroviruses. Being infected with one type of norovirus may not protect one against other types. Norovirus can be found in your stool (feces) even before one starts feeling sick. The virus can stay in stool for 2 weeks or more after one feels better.
Pathophysiology
Structure
Noroviruses contain a positive-sense RNA genome of approximately 7.5 kbp, encoding a major structural protein (VP1) of about 58~60 kDa and a minor capsid protein (VP2).[1] The virus particles demonstrate an amorphous surface structure when visualized using electron microscopy and are between 27-38 nm in size.[2] The most variable region of the viral capsid is the P2 domain, which contains antigen-presenting sites and carbohydrate-receptor binding regions.[3][4][5]
The estimated mutation rate (1.21 x 10−2 to 1.41 x 10−2 substitutions per site per year) in this virus is high even compared with other RNA viruses.[6]
Transmission
One is most contagious when sick with norovirus illness, and during the first 3 days after recovery from norovirus illness. One can become infected with norovirus by accidentally getting stool or vomit from infected people in mouth. This usually happens by eating food or drinking liquids that are contaminated with norovirus, touching surfaces or objects contaminated with norovirus then putting fingers in one's mouth, or having contact with someone who is infected with norovirus (for example, caring for or sharing food or eating utensils with someone with norovirus illness). Environmental and fomite contamination may also act as a source of infection. Good evidence exists for transmission due to aerosolization of vomitus that presumably results in droplets contaminating surfaces or entering the oral mucosa and being swallowed. No evidence suggests that infection occurs through the respiratory system.
Noroviruses are highly contagious and as few as 10 viral particles may be sufficient to infect an individual. During outbreaks of norovirus gastroenteritis, several modes of transmission have been documented; for example, initial foodborne transmission in a restaurant, followed by secondary person-to-person transmission to household contacts. Although presymptomatic viral shedding may occur, shedding usually begins with onset of symptoms and may continue for 2 weeks after recovery. It is unclear to what extent viral shedding over 72 hours after recovery signifies continued infectivity.
Noroviruses are transmitted directly from person to person and indirectly via contaminated water and food. They are highly contagious, and fewer than twenty virus particles can cause an infection.[7] Transmission occurs through ingesting contaminated food and water and by person-to-person spread. Transmission through fecal-oral 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.[8] The viruses continue to be shed after symptoms have subsided and shedding can still be detected many weeks after infection.[9]
Vomiting, in particular, transmits infection effectively. 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. 126 people were dining at six tables in December 1998; one woman vomited. 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 diarrhoea. The cause was not immediately identified. Researchers plotted the seating arrangement: more than 90% of the people on the same table as the sick woman later reported food poisoning. 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 on an adjacent table fell ill; at a table on the other side of the restaurant, the rate was still 25%. The outbreak is being blamed on a Norwalk-like virus (norovirus). Other cases of transmission by vomit were later identified. Bernard Betts, director of the Microbiology Research Unit at the University of York, said that clinical-standard hygiene was needed, even in restaurants, commenting "Just a single drop of material hitting a hard surface can produce an aerosol that travels a very long way." [10]
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.[11] 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.[12]
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. Foods other than shellfish may be contaminated by infected food handlers.[13]
Persistence
The norovirus can survive for long periods outside a human host depending on the surface and temperature conditions: 12 hours on hard surfaces, and up to 12 days on contaminated fabrics,[14] and it can survive for months, maybe even years in contaminated still water.[15] A study done in 2006 found the virus on several surfaces used for food preparation 7 days after contamination.[16]
Genetics
A non functional fucosyltransferase FUT2 provides high protection from the most common norovirus GII.4.[17] Functional FUT2 fucosyltransferase transferes a fucose sugar to the end of the Histo-blood group ABO(H) precursor in gastrointestinal cells as well as saliva glands. The ABH antigen produced is thought to act as receptors for human norovirus. Homozygous carriers of any nonsense mutation in the FUT2 gene are called non-secretors as no ABH antigen is produced. Approximately 20% of Caucasians are non-secretors due to the G428A and C571T nonsense mutations in FUT2 and therefore have strong although not absolute protection from the norovirus GII.4.[18] Non-secretors can still produce ABH antigens in erythrocytes as the precursor is formed by FUT1.[19] Some norovirus genotypes (GI.3) can infect non-secretors.[20]
Of individuals who are secretor positive, those with blood type O were more likely to be infected and B less likely.[21][22][23]
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.[24]
A 2008 study suggests the protein MDA-5 may be the primary immune sensor that detects the presence of noroviruses in the body.[25] Interestingly, some people have common variations of the MDA-5 gene that could make them more susceptible to norovirus infection.[26]
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).
References
- ↑ 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.
- ↑ 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.
- ↑ Jiang X, Tan M, Hegde RS (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.
- ↑ 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.
- ↑ Cao S, Lou ZY, Tan M, Chen YT, Liu YJ, Zhang ZS, Zhang XJC (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.
- ↑ 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.
- ↑ Morillo SG, Timenetsky Mdo C (2011). "Norovirus: an overview". Revista Da Associação Médica Brasileira (1992). 57 (4): 453–8. PMID 21876931. Unknown parameter
|month=ignored (help) - ↑ "I've lost my appetite...": New Scientist article on spread of viral food poisoning across a restaurant by eating near where someone has vomited
- ↑ Atmar RL, Opekun AR, Gilger MA; et al. (2008). "Norwalk Virus Shedding after Experimental Human Infection". Emerging Infect. Dis. 14 (10): 1553–7. doi:10.3201/eid1410.080117. PMC 2609865. PMID 18826818. Unknown parameter
|month=ignored (help) - ↑ New Scientist magazine: I've lost my appetitie. Issue 2255, 9 September 2000, p 7. Sourced from Epidemiology and Infection (vol 124, p 481). Article available online[1], full version only to subscribers
- ↑ Heijne JCM, Teunis P, Morroy G; et al. (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.
- ↑ Hedberg CW, Osterholm MT (1993). "Outbreaks of food-borne and waterborne viral gastroenteritis". Clin. Microbiol. Rev. 6 (3): 199–210. PMC 358282. PMID 8395330.
- ↑ 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.
- ↑ http://www.phac-aspc.gc.ca/id-mi/norovirus-eng.php
- ↑ http://blogs.scientificamerican.com/artful-amoeba/2012/01/17/misery-inducing-norovirus-can-survive-for-months-perhaps-years-in-drinking-water/
- ↑ http://www.ncbi.nlm.nih.gov/pubmed/16473426
- ↑ Carlsson B, Kindberg E, Buesa J, Rydell GE, Lidón MF, Montava R, Abu Mallouh R, Grahn A, Rodríguez-Díaz J, Bellido J, Arnedo A, Larson G, Svensson L. (2009). "The G428A Nonsense Mutation in FUT2 Provides Strong but Not Absolute Protection against Symptomatic GII.4 Norovirus Infection". PLOS one. doi:10.1371/journal.pone.0005593. PMID 19440360. Unknown parameter
|month=ignored (help) - ↑ Rydell GE, Kindberg E, Larson G, Svensson L (2011). "Susceptibility to winter vomiting disease: a sweet matter". Rev. Med. Virol. 21 (6): 370–82. doi:10.1002/rmv.704. PMID 22025362. Unknown parameter
|month=ignored (help) - ↑ Shirato H (2011). "Norovirus and histo-blood group antigens". Jpn. J. Infect. Dis. 64 (2): 95–103. PMID 21519121.
- ↑ Nordgren J, Kindberg E, Lindgren PE, Matussek A, Svensson L (2010). "Norovirus gastroenteritis outbreak with a secretor-independent susceptibility pattern, Sweden". Emerg. Infect. Dis. 16 (1): 81–7. doi:10.3201/eid1601.090633. PMID 20031047. Unknown parameter
|month=ignored (help) - ↑ "Norovirus and histo-blood group antigens". Retrieved 22 December 2012.
- ↑ Hutson, AM (July 2003). "Norwalk virus infection and disease is associated with ABO histo-blood group type". J. Infect. Dis. 188 (1): 176–7. doi:10.1086/375829. PMID 12825190. Unknown parameter
|coauthors=ignored (help) - ↑ Le Guyader FS, Krol J, Ambert-Balay K, Ruvoen-Clouet N, Desaubliaux B, Parnaudeau S, Le Saux JC, Ponge A, Pothier P, Atmar RL, Le Pendu J (2010). "Comprehensive Analysis of a Norovirus-Associated Gastroenteritis Outbreak, from the Environment to the Consumer". Journal of Clinical Microbiology. 48 (3): 915–20. doi:10.1128/JCM.01664-09. PMC 2832421. PMID 20053852. Unknown parameter
|month=ignored (help) - ↑ Shirato H (2011). "Norovirus and histo-blood group antigens". Japanese Journal of Infectious Diseases. 64 (2): 95–103. PMID 21519121.
- ↑ McCartney SA, Thackray LB, Gitlin L, Gilfillan S, 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. Unknown parameter
|unused_data=ignored (help) - ↑ Researchers Discover Primary Sensor That Detects Stomach Viruses Newswise, Retrieved on July 20, 2008.