Parotitis pathophysiology: Difference between revisions
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**[[Mumps]] [[virus]] is a member of the [[paramyoxoviridae]] family with a single-strand, negative-sense [[RNA]] [[molecule]]. | **[[Mumps]] [[virus]] is a member of the [[paramyoxoviridae]] family with a single-strand, negative-sense [[RNA]] [[molecule]]. | ||
**The [[mumps]] HN and F [[glycoproteins]] reach the surface of the infected host [[cell]] through the [[Endoplasmic reticulum|endoplasmic reticulum]] and [[Golgi complex]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **The [[mumps]] HN and F [[glycoproteins]] reach the surface of the infected host [[cell]] through the [[Endoplasmic reticulum|endoplasmic reticulum]] and [[Golgi complex]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**[[Virions]] emerge from the infected [[cells]] due to the [[M protein]] facilitating the localization of the [[viral]] | **[[Virions]] emerge from the infected [[cells]] due to the [[M protein]] facilitating the localization of the [[viral]] ribonucleic proteins onto the host [[cell]] [[membrane]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**The [[virus]] binds with the neighboring host [[cell|cells]] via [[Sialic acids|sialic acid]] through HN [[glycoprotein]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **The [[virus]] binds with the neighboring host [[cell|cells]] via [[Sialic acids|sialic acid]] through HN [[glycoprotein]].<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
**Both HN and F [[glycoproteins]] mediate the fusion of virus and host [[cell]], as well as [[cell]] and [[cell]]-[[membrane]] fusion, to perpetuate the spread of the [[virus]] throughout the host.<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | **Both HN and F [[glycoproteins]] mediate the fusion of virus and host [[cell]], as well as [[cell]] and [[cell]]-[[membrane]] fusion, to perpetuate the spread of the [[virus]] throughout the host.<ref name="pmid25229387">{{cite journal |vauthors=Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP |title=Molecular biology, pathogenesis and pathology of mumps virus |journal=J. Pathol. |volume=235 |issue=2 |pages=242–52 |year=2015 |pmid=25229387 |pmc=4268314 |doi=10.1002/path.4445 |url=}}</ref> | ||
Revision as of 20:27, 1 March 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
Acute infection can occur in any salivary gland but the most commonly affected one is the parotid. This is thought to be due to a combination of anatomic and physiologic factors. The saliva from the parotid is less mucoid than that from the other salivary glands. IgA, lysozyme and sialic acid are all found in smaller amounts in the more viscous parotid secretions. These substances are thought to help fight off ascending bacterial infection. Bacterial parotitis is generally unilateral in adults (75-90%), while viral is generally bilateral. Though 80-90% of salivary calculi occur in the Wharton’s duct of the submandibular gland, the parotid remains the most common site of acute suppurative salivary infection. The secretions from the submandibular gland are more alkaline, thought to result in a higher concentration of insoluble calcium phosphate.
Pathogenesis
Viral Parotitis
- Viral parotitis is caused by the infiltration of respiratory droplets containing the mumps virus.[1]
- Mumps virus is a member of the paramyoxoviridae family with a single-strand, negative-sense RNA molecule.
- The mumps HN and F glycoproteins reach the surface of the infected host cell through the endoplasmic reticulum and Golgi complex.[2]
- Virions emerge from the infected cells due to the M protein facilitating the localization of the viral ribonucleic proteins onto the host cell membrane.[2]
- The virus binds with the neighboring host cells via sialic acid through HN glycoprotein.[2]
- Both HN and F glycoproteins mediate the fusion of virus and host cell, as well as cell and cell-membrane fusion, to perpetuate the spread of the virus throughout the host.[2]
- The virus replicates in the nasopharynx and regional lymph nodes.[2]
- Upon replication, viremia occurs for three to five days, spreading to the salivary glands.[2]
- Parotitis results from the inflammatory response the the presence of mumps virus in the salivary glands.
References
- ↑ Conly J, Johnston B (2007). "Is mumps making a comeback?". Can J Infect Dis Med Microbiol. 18 (1): 7–9. PMC 2542890. PMID 18923686.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Rubin S, Eckhaus M, Rennick LJ, Bamford CG, Duprex WP (2015). "Molecular biology, pathogenesis and pathology of mumps virus". J. Pathol. 235 (2): 242–52. doi:10.1002/path.4445. PMC 4268314. PMID 25229387.