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| __NOTOC__
| | #REDIRECT[[Measles virus]] |
| {{Measles}}
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| {{Taxobox2
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| | color = violet
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| | name = Measles
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| | image = Measles virus.JPG
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| | image_width = 180 px
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| | image_caption = Measles virus [[electron micrograph]]
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| | virus_group = v
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| | ordo = ''[[Mononegavirales]]''
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| | familia = ''[[Paramyxoviridae]]''
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| | subfamilia = ''[[Paramyxovirinae]]''
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| | genus = ''[[Morbillivirus]]''
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| | species = '''''Measles virus'''''
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| }}
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| {{CMG}}
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| ==Overview==
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| '''Measles virus''' ('''MeV''') is a single-stranded, negative-sense, enveloped RNA virus of the genus ''[[Morbillivirus]]'' within the family ''[[Paramyxoviridae]]''. Humans are the natural hosts of the virus; no animal reservoirs are known to exist.
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| ==Microbiology==
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| The measles virus is the cause of [[measles]], an infection of the [[respiratory system]]. Symptoms include [[fever]], [[cough]], [[runny nose]], [[red eyes]] and a generalized, [[maculopapular]], [[erythematous]] rash. The virus is highly contagious and is spread by coughing and sneezing via close personal contact or direct contact with secretions.
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| ==Replication cycle==
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| ===Entry===
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| The measles virus has two envelope glycoproteins on the viral surface - hemagglutinin (H) and membrane fusion protein (F). These proteins are responsible for host cell binding and invasion. Three receptors for the H protein have been identified to date: complement regulatory molecule [[CD46]], the [[signaling lymphocyte activation]] molecule (SLAM) and the cell adhesion molecule [[Nectin|Nectin-4]].<ref name=Lu2013>Lu G, Gao GF, Yan J (2013) The receptors and entry of measles virus: a review. Sheng Wu Gong Cheng Xue Bao 29(1):1–9</ref>
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| ==Evolution==
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| The measles virus evolved from the formerly widespread [[rinderpest]] virus, which infects cattle.<ref name="Furuse2010"/> [[Molecular phylogenetics|Sequence analysis]] has suggested that the two viruses most probably diverged in the 11th and 12th centuries, though the periods as early as the 5th century fall within the 95% [[confidence interval]] of these calculations.<ref name="Furuse2010">{{cite journal |author=Furuse Y, Suzuki A, Oshitani H |title=Origin of measles virus: divergence from rinderpest virus between the 11th and 12th centuries |journal=Virol. J. |volume=7 |pages=52 |year=2010 |pmid=20202190 |pmc=2838858 |doi=10.1186/1743-422X-7-52 }}</ref>
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| Other analysis has suggested that the divergence may be even older because of the technique's tendency to underestimate ages when strong [[purifying selection]] is in action.<ref>{{cite doi|10.1093/molbev/msr170|noedit}}</ref> There is some linguistic evidence for an earlier origin within the seventh century.<ref name="Griffin2007">{{cite book |author=Griffin DE |chapter=Measles Virus |editor=Martin, Malcolm A.; Knipe, David M.; Fields, Bernard N.; Howley, Peter M.; Griffin, Diane; Lamb, Robert |title=Fields' virology |publisher=Wolters Kluwer Health/Lippincott Williams & Wilkins |location=Philadelphia |year=2007 |isbn=0-7817-6060-7 |edition=5th}}</ref><ref name="McNeil1976">{{cite book |last=McNeil |first=W. |title=Plagues and Peoples |location=New York |publisher=Anchor Press/Doubleday |year=1976 |isbn=0-385-11256-4 }}</ref> The current epidemic strain evolved at the beginning of the 20th century—most probably between 1908 and 1943.<ref name="Pomeroy2008">{{cite journal |author=Pomeroy LW, Bjørnstad ON, Holmes EC |title=The evolutionary and epidemiological dynamics of the paramyxoviridae |journal=J. Mol. Evol. |volume=66 |issue=2 |pages=98–106 |date=February 2008 |pmid=18217182 |doi=10.1007/s00239-007-9040-x |pmc=3334863}}</ref>
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| ==Genotypes==
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| The WHO currently recognises 8 clades of measles (A–H). Subtypes are designed with numerals – A1, D2 etc. Currently a total of 23 subtypes are recognised. The sequencing of the 450 nucleotides that code for the C‐terminal 150 amino acids of N are the minimum amount of sequence data required for genotyping a measles virus isolate. The genotyping scheme was introduced in 1998 and extended in 2002 and 2003.
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| The major genotypes differ between countries and restatus of measles circulation within that country or region. Indigenous transmission of measles virus was interrupted in the United States and Australia by 2000 and the Americas by 2002.
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| * Measles virus (MV) is an enveloped, nonsegmented negative-stranded [[RNA virus]] of the [[Paramyxoviridae]] family, genus [[Morbillivirus]].
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| * It is 100–200 nm in diameter, with a core of single-stranded RNA, and is closely related to the rinderpest and canine distemper viruses.
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| * Two membrane envelope proteins are important in pathogenesis:
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| ** F (fusion) protein, which is responsible for fusion of virus and host cell membranes, viral penetration, and hemolysis.
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| ** H (hemagglutinin) protein, which is responsible for adsorption of virus to cells.
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| * There is only one antigenic type of measles virus. Although studies have documented changes in the H glycoprotein, these changes do not appear to be epidemiologically important (i.e., no change in vaccine efficacy has been observed).
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| * Measles virus is rapidly inactivated by heat, light, acidic pH, ether, and trypsin. It has a short survival time (less than 2 hours) in the air or on objects and surfaces.
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| ==References==
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| {{reflist|2}}
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| [[Category:primary care]]
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| [[Category:Pediatrics]]
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| [[Category:Dermatology]]
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| [[Category:Viral diseases]]
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| [[Category:Mononegavirales]]
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| [[Category:Infectious disease]]
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| [[Category:Ophthalmology]]
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| [[Category:Otolaryngology]]
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| [[Category:Pulmonology]]
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| [[Category:Disease]]
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| {{WH}}
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| {{WS}}
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