Norovirus infection pathophysiology: Difference between revisions
| Line 62: | Line 62: | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
Noroviruses are highly transmissible since only 10 virions (ID50 = 10 virions) per individual is required to infect half proportion of those individuals. Norovirus is transmitted via aerosols, direct contact and fecal-oral routes. The virus is highly resistant to extremely low and/or high temperatures, high sugar concentrations, acidic environments, exposure to chlorine, antiseptic solutions and alcohol. The virus has an incubation period of about 1-2 days with symptoms lasting for about 1-3 days. It could remain contagious for up to 3 weeks. | Noroviruses are highly transmissible since only 10 virions (ID50 = 10 virions) per individual is required to infect half proportion of those individuals. Norovirus is transmitted via aerosols, direct contact and fecal-oral routes. The virus is highly resistant to extremely low and/or high temperatures, high sugar concentrations, acidic environments, exposure to chlorine, antiseptic solutions and alcohol. The virus has an incubation period of about 1-2 days with symptoms lasting for about 1-3 days. It could remain contagious for up to 3 weeks<ref name="pmid18837783">{{cite journal| author=Donaldson EF, Lindesmith LC, Lobue AD, Baric RS| title=Norovirus pathogenesis: mechanisms of persistence and immune evasion in human populations. | journal=Immunol Rev | year= 2008 | volume= 225 | issue= | pages= 190-211 | pmid=18837783 | doi=10.1111/j.1600-065X.2008.00680.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18837783 }} </ref>. Histoblood group antigens (HBGAs) are polymorphic receptors or cofactors of norovirus. Different genoclusters bind various HBGAs: Genogroup I viruses bind A and O antigens; genogroup II viruses mostly bind A and B antigens. Great diversity of norovirus strains and the lack of cross-strain or long-term immunity are the causes of recurrent infections<ref name="pmid12825167">{{cite journal| author=Huang P, Farkas T, Marionneau S, Zhong W, Ruvoën-Clouet N, Morrow AL | display-authors=etal| title=Noroviruses bind to human ABO, Lewis, and secretor histo-blood group antigens: identification of 4 distinct strain-specific patterns. | journal=J Infect Dis | year= 2003 | volume= 188 | issue= 1 | pages= 19-31 | pmid=12825167 | doi=10.1086/375742 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12825167 }} </ref>. | ||
==Genetics== | ==Genetics== | ||
Revision as of 17:46, 19 February 2021
|
Norovirus infection Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Norovirus infection pathophysiology On the Web |
|
American Roentgen Ray Society Images of Norovirus infection pathophysiology |
|
Risk calculators and risk factors for Norovirus infection pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Noroviruses are highly contagious, given that as few as 10 particles are enough to cause the disease, transmission is via the fecal-oral route and peaks during the period when symptoms are most severe, and up to 3 days after recovery. As many strains of noroviruses exist, immunity is not gained following an infection. A non-functional fucosyltransferase FUT2 mutation has been associated with protection against the most common norovirus strains as FUT2 is required for viral transport in the small intestine.
Pathophysiology
Physiology
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]
Pathogenesis
Noroviruses are highly transmissible since only 10 virions (ID50 = 10 virions) per individual is required to infect half proportion of those individuals. Norovirus is transmitted via aerosols, direct contact and fecal-oral routes. The virus is highly resistant to extremely low and/or high temperatures, high sugar concentrations, acidic environments, exposure to chlorine, antiseptic solutions and alcohol. The virus has an incubation period of about 1-2 days with symptoms lasting for about 1-3 days. It could remain contagious for up to 3 weeks[7]. Histoblood group antigens (HBGAs) are polymorphic receptors or cofactors of norovirus. Different genoclusters bind various HBGAs: Genogroup I viruses bind A and O antigens; genogroup II viruses mostly bind A and B antigens. Great diversity of norovirus strains and the lack of cross-strain or long-term immunity are the causes of recurrent infections[8].
Genetics
- A non-functional fucosyltransferase FUT2 provides high protection from the most common norovirus GII.4.[9]
- 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.[10]
- Non-secretors can still produce ABH antigens in erythrocytes as the precursor is formed by FUT1.[11] Some norovirus genotypes (GI.3) can infect non-secretors.[12]
- Of individuals who are secretor positive, those with blood type O were more likely to be infected and B less likely.[13][14][15]
- 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.[16]
- A 2008 study suggests the protein MDA-5 may be the primary immune sensor that detects the presence of noroviruses in the body.[17] Interestingly, some people have common variations of the MDA-5 gene that could make them more susceptible to norovirus infection.[18]
- 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).
Associated Conditions
Gross Pathology
Microscopic Pathology
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.
- ↑ Donaldson EF, Lindesmith LC, Lobue AD, Baric RS (2008). "Norovirus pathogenesis: mechanisms of persistence and immune evasion in human populations". Immunol Rev. 225: 190–211. doi:10.1111/j.1600-065X.2008.00680.x. PMID 18837783.
- ↑ Huang P, Farkas T, Marionneau S, Zhong W, Ruvoën-Clouet N, Morrow AL; et al. (2003). "Noroviruses bind to human ABO, Lewis, and secretor histo-blood group antigens: identification of 4 distinct strain-specific patterns". J Infect Dis. 188 (1): 19–31. doi:10.1086/375742. PMID 12825167.
- ↑ Carlsson B, Kindberg E, Buesa J, Rydell GE, Lidón MF, Montava R; et al. (2009). "The G428A nonsense mutation in FUT2 provides strong but not absolute protection against symptomatic GII.4 Norovirus infection". PLoS One. 4 (5): e5593. doi:10.1371/journal.pone.0005593. PMC 2680586. PMID 19440360.
- ↑ 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.
- ↑ 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. PMC 2874438. PMID 20031047.
- ↑ "Norovirus and histo-blood group antigens". Retrieved 22 December 2012.
- ↑ Hennessy EP, Green AD, Connor MP, Darby R, MacDonald P (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.
- ↑ Le Guyader FS, Krol J, Ambert-Balay K, Ruvoen-Clouet N, Desaubliaux B, Parnaudeau S; et al. (2010). "Comprehensive analysis of a norovirus-associated gastroenteritis outbreak, from the environment to the consumer". J Clin Microbiol. 48 (3): 915–20. doi:10.1128/JCM.01664-09. PMC 2832421. PMID 20053852.
- ↑ 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 HW, Virgin Iv HW; et al. (2008). "MDA-5 recognition of a murine norovirus". PLoS Pathog. 4 (7): e1000108. doi:10.1371/journal.ppat.1000108. PMC 2443291. PMID 18636103.
- ↑ Researchers Discover Primary Sensor That Detects Stomach Viruses Newswise, Retrieved on July 20, 2008.