Enterovirus 68 causes: Difference between revisions
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Since 1960, the genome of enterovirus 68 has underwent several rearrangements and deletions, particularly of the UTR, that have led to the classification of the virus into clades. Genomic variations within the IRES region may lead to different effects on virulence, however, in the particular case of enterovirus 68 spacer region, little is known about this impact. | Since 1960, the genome of enterovirus 68 has underwent several rearrangements and deletions, particularly of the UTR, that have led to the classification of the virus into clades. Genomic variations within the IRES region may lead to different effects on virulence, however, in the particular case of enterovirus 68 spacer region, little is known about this impact.<ref name="pmid22694903">{{cite journal| author=Tokarz R, Firth C, Madhi SA, Howie SR, Wu W, Sall AA et al.| title=Worldwide emergence of multiple clades of enterovirus 68. | journal=J Gen Virol | year= 2012 | volume= 93 | issue= Pt 9 | pages= 1952-8 | pmid=22694903 | doi=10.1099/vir.0.043935-0 | pmc=PMC3542132 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22694903 }} </ref> | ||
The spacer regions of [[rhinovirus]]es are small. It is important to notice that besides sharing cellular [[tropism]] for the [[respiratory epithelium]], enterovirus 68's spacer region, has been experiencing deletions throughout the years, towards the size of the one in [[rhinovirus]]es. The genome deletions seen in enterovirus 68 may also be responsible for changes in the virulence of the virus, justifying the recent outbreaks seen worldwide. | The spacer regions of [[rhinovirus]]es are small. It is important to notice that besides sharing cellular [[tropism]] for the [[respiratory epithelium]], enterovirus 68's spacer region, has been experiencing deletions throughout the years, towards the size of the one in [[rhinovirus]]es. The genome deletions seen in enterovirus 68 may also be responsible for changes in the virulence of the virus, justifying the recent outbreaks seen worldwide.<ref name="pmid22694903">{{cite journal| author=Tokarz R, Firth C, Madhi SA, Howie SR, Wu W, Sall AA et al.| title=Worldwide emergence of multiple clades of enterovirus 68. | journal=J Gen Virol | year= 2012 | volume= 93 | issue= Pt 9 | pages= 1952-8 | pmid=22694903 | doi=10.1099/vir.0.043935-0 | pmc=PMC3542132 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22694903 }} </ref> | ||
Revision as of 17:38, 8 September 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
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Enterovirus 68 Microchapters | |
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Diagnosis | |
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Treatment | |
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Case Studies | |
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Enterovirus 68 causes On the Web | |
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American Roentgen Ray Society Images of Enterovirus 68 causes | |
Overview
Taxonomy
Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Picornavirales; Picornaviridae; Enterovirus; Enterovirus D[1]
Biology
Enterovirus 68 is non-enveloped, positive-sense ssRNA enterovirus that belongs to the family Picornaviridae.[2] It belongs to serotype D, along with EV-D70, EV-D94 and EV-D-111. Contrarily to other viruses of the same genus, enterovirus 68 is acid-labile and is more related to rhinoviruses. Therefore it commonly causes respiratory illness.[3] Recently, several outbreaks in Japan, Netherlands, Philippines and in the USA, have implicated enterovirus 68 in respiratory disease.[2][4][5][6]
Genome
The common genome of an enterovirus is contained within an RNA strand of approximately 7500 nucleotides. It contains a single open reading frame (ORF) which encodes a polyprotein. Once translated, the polyprotein is processed, yielding different individual viral proteins. Two UTRs flank the ORF polyprotein on both sides, one of which contains an Internal Ribosome Entry Site (IRES).[7]
To distinguish the different serotypes in the genus enterovirus, a gene (VP1) which encodes 1 of the 4 capsid proteins, is used. Accordingly, the different enterovirus may be organized in the following serotypes:[8]
- HEV-A
- HEV-B
- HEV-C
- HEV-D
Since 1960, the genome of enterovirus 68 has underwent several rearrangements and deletions, particularly of the UTR, that have led to the classification of the virus into clades. Genomic variations within the IRES region may lead to different effects on virulence, however, in the particular case of enterovirus 68 spacer region, little is known about this impact.[2]
The spacer regions of rhinoviruses are small. It is important to notice that besides sharing cellular tropism for the respiratory epithelium, enterovirus 68's spacer region, has been experiencing deletions throughout the years, towards the size of the one in rhinoviruses. The genome deletions seen in enterovirus 68 may also be responsible for changes in the virulence of the virus, justifying the recent outbreaks seen worldwide.[2]
Tropism
Natural Reservoir
Origin and Serotypes
Based on their pathogenesis in humans and experimental animals, enteroviruses were originally divided into four species: poliovirus, coxsackie A virus, coxsackie B virus, and echovirus. However, further studies reported that some coxsackie and echoviruses have overlapping antigenic properties with respect to the diseases they caused in mice. As a result, they were all later described as enterovirus and numbered sequentially, beginning with EV68. Current classifications systems are based on molecular, antigenic as well as biological properties of these viruses. The enterovirus family is currently subgrouped into 5 categories: poliovirus, human enterovirus A (HEV-A), HEV-B, HEV-C and HEV-D. EV68 is one of the 3 serotypes of the HEV-D subgroup.[9]
Human rhinovirus 87 was isolated at the same time as EV68. Corn is a prototype of HRV87 and is very unique in its receptor quality. Cross neutralization and partial capsid sequence studies revealed that HRV-87 Corn belongs to the same group as EV68.[10] A study on 1962 isolates of EV68 reported the genome sequences of the 5′-non-translated (NTR) and 3D polymerase coding regions and complete VP1 capsid protein coding region sequence. These are closely related with the genome sequence of human rhinovirus 87 (HRV 87) and are consistent with the fact that the two viruses are closely related.
Identification of Isolates
Serotype specific rabbit antisera are used for typing of EV68 isolates. Partial sequencing of VP1 capsid gene, using primer 292 (5'-MIGCIGYIGARACNGG-3') and 222 (5'-CICCIGGIGGIAYRWACAT-3') is another method used for sequencing. The serotype is determined by comparing partial sequence of isolates with a database containing partial sequences of all known enterovirus serotypes.[11]
Two commercially available FDA approved multipathogen detection systems, Luminex xTAG RVP and Idaho Technologies Film Array Respiratory Panel are currently being used in the United States. Both techniques use broadly reactive primers that can pick both enterovirus as well as human rhinovirus.[12]
References
- ↑ "Enterovirus D68".
- ↑ 2.0 2.1 2.2 2.3 Tokarz R, Firth C, Madhi SA, Howie SR, Wu W, Sall AA; et al. (2012). "Worldwide emergence of multiple clades of enterovirus 68". J Gen Virol. 93 (Pt 9): 1952–8. doi:10.1099/vir.0.043935-0. PMC 3542132. PMID 22694903.
- ↑ Oberste MS, Maher K, Schnurr D, Flemister MR, Lovchik JC, Peters H; et al. (2004). "Enterovirus 68 is associated with respiratory illness and shares biological features with both the enteroviruses and the rhinoviruses". J Gen Virol. 85 (Pt 9): 2577–84. doi:10.1099/vir.0.79925-0. PMID 15302951.
- ↑ Hasegawa S, Hirano R, Okamoto-Nakagawa R, Ichiyama T, Shirabe K (2011). "Enterovirus 68 infection in children with asthma attacks: virus-induced asthma in Japanese children". Allergy. 66 (12): 1618–20. doi:10.1111/j.1398-9995.2011.02725.x. PMID 21958204.
- ↑ Kaida A, Kubo H, Sekiguchi J, Kohdera U, Togawa M, Shiomi M; et al. (2011). "Enterovirus 68 in children with acute respiratory tract infections, Osaka, Japan". Emerg Infect Dis. 17 (8): 1494–7. doi:10.3201/eid1708.110028. PMC 3381549. PMID 21801632.
- ↑ Jacobson LM, Redd JT, Schneider E, Lu X, Chern SW, Oberste MS; et al. (2012). "Outbreak of lower respiratory tract illness associated with human enterovirus 68 among American Indian children". Pediatr Infect Dis J. 31 (3): 309–12. doi:10.1097/INF.0b013e3182443eaf. PMID 22315004.
- ↑ Fields, Bernard (2001). Fields virology. Philadelphia: Lippincott Williams & Wilkins. ISBN 0781718325.
- ↑ Oberste MS, Maher K, Kilpatrick DR, Pallansch MA (1999). "Molecular evolution of the human enteroviruses: correlation of serotype with VP1 sequence and application to picornavirus classification". J Virol. 73 (3): 1941–8. PMC 104435. PMID 9971773.
- ↑ "ICTV Virus Taxonomy". Retrieved 28 February 2014.
- ↑ Ishiko, H.; Miura, R.; Shimada, Y.; Hayashi, A.; Nakajima, H.; Yamazaki, S.; Takeda, N. (2002). "Human rhinovirus 87 identified as human enterovirus 68 by VP4-based molecular diagnosis". Intervirology. 45 (3): 136–41. doi:65866 Check
|doi=value (help). PMID 12403917. - ↑ Oberste, MS.; Maher, K.; Schnurr, D.; Flemister, MR.; Lovchik, JC.; Peters, H.; Sessions, W.; Kirk, C.; Chatterjee, N. (2004). "Enterovirus 68 is associated with respiratory illness and shares biological features with both the enteroviruses and the rhinoviruses". J Gen Virol. 85 (Pt 9): 2577–84. doi:10.1099/vir.0.79925-0. PMID 15302951. Unknown parameter
|month=ignored (help) - ↑ "Clusters of acute respiratory illness associated with human enterovirus 68--Asia, Europe, and United States, 2008-2010". MMWR Morb Mortal Wkly Rep. 60 (38): 1301–4. 2011. PMID 21956405. Unknown parameter
|month=ignored (help)