Norovirus infection pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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.
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,[7] and it can survive for months, maybe even years in contaminated still water.[8] A study done in 2006 found the virus on several surfaces used for food preparation 7 days after contamination.[9]
Genetics
A non functional fucosyltransferase FUT2 provides high protection from the most common norovirus GII.4.[10] 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.[11] Non-secretors can still produce ABH antigens in erythrocytes as the precursor is formed by FUT1.[12] Some norovirus genotypes (GI.3) can infect non-secretors.[13]
Of individuals who are secretor positive, those with blood type O were more likely to be infected and B less likely.[14][15][16]
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.
- ↑ 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)