Enterovirus 68 pathophysiology: Difference between revisions
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Enterovirus 68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining, EV-69 is acid-labile, which reduces its ability to colonize the gastrointestinal mucosa. It has therefore been implicated in respiratory infections, and in rare occasions in [[CNS infection]]. This characteristic of EV-68 sets it apart from other enteroviruses, in what deals with its [[pathogenesis]] and infected cells.<ref name="pmid20872722">{{cite journal| author=Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V et al.| title=Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis. | journal=J Med Virol | year= 2010 | volume= 82 | issue= 11 | pages= 1940-9 | pmid=20872722 | doi=10.1002/jmv.21894 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20872722 }} </ref> | Enterovirus 68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining, EV-69 is acid-labile, which reduces its ability to colonize the gastrointestinal mucosa. It has therefore been implicated in respiratory infections, and in rare occasions in [[CNS infection]]. This characteristic of EV-68 sets it apart from other enteroviruses, in what deals with its [[pathogenesis]] and infected cells.<ref name="pmid20872722">{{cite journal| author=Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V et al.| title=Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis. | journal=J Med Virol | year= 2010 | volume= 82 | issue= 11 | pages= 1940-9 | pmid=20872722 | doi=10.1002/jmv.21894 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20872722 }} </ref> | ||
Besides cells of the respiratory mucosa, EV-68 also shows tropism for [[leukocytes]], using the receptors that contain sialic-acid in these cells.<ref name="pmid15919894">{{cite journal| author=Vlasak M, Roivainen M, Reithmayer M, Goesler I, Laine P, Snyers L et al.| title=The minor receptor group of human rhinovirus (HRV) includes HRV23 and HRV25, but the presence of a lysine in the VP1 HI loop is not sufficient for receptor binding. | journal=J Virol | year= 2005 | volume= 79 | issue= 12 | pages= 7389-95 | pmid=15919894 | doi=10.1128/JVI.79.12.7389-7395.2005 | pmc=PMC1143622 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15919894 }} </ref> Since [[leukocytes]] are able to migrate to other tissues, by infecting these cells the virus gains access to secondary sites.<ref name="pmid20872722">{{cite journal| author=Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V et al.| title=Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis. | journal=J Med Virol | year= 2010 | volume= 82 | issue= 11 | pages= 1940-9 | pmid=20872722 | doi=10.1002/jmv.21894 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20872722 }} </ref> Viral replication inside leukocytes is likely to affect their function, thereby jeopardizing immune system response towards the virus, which facilitates its spread.<ref name="pmid17298395">{{cite journal| author=Kramer M, Schulte BM, Toonen LW, de Bruijni MA, Galama JM, Adema GJ et al.| title=Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells. | journal=Cell Microbiol | year= 2007 | volume= 9 | issue= 6 | pages= 1507-18 | pmid=17298395 | doi=10.1111/j.1462-5822.2007.00888.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17298395 }} </ref> | Besides cells of the [[respiratory]] mucosa, EV-68 also shows [[tropism]] for [[leukocytes]], using the receptors that contain sialic-acid in these cells.<ref name="pmid15919894">{{cite journal| author=Vlasak M, Roivainen M, Reithmayer M, Goesler I, Laine P, Snyers L et al.| title=The minor receptor group of human rhinovirus (HRV) includes HRV23 and HRV25, but the presence of a lysine in the VP1 HI loop is not sufficient for receptor binding. | journal=J Virol | year= 2005 | volume= 79 | issue= 12 | pages= 7389-95 | pmid=15919894 | doi=10.1128/JVI.79.12.7389-7395.2005 | pmc=PMC1143622 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15919894 }} </ref> Since [[leukocytes]] are able to migrate to other tissues, by infecting these cells the virus gains access to secondary sites.<ref name="pmid20872722">{{cite journal| author=Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V et al.| title=Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis. | journal=J Med Virol | year= 2010 | volume= 82 | issue= 11 | pages= 1940-9 | pmid=20872722 | doi=10.1002/jmv.21894 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20872722 }} </ref> [[Viral replication]] inside leukocytes is likely to affect their function, thereby jeopardizing immune system response towards the virus, which facilitates its spread.<ref name="pmid17298395">{{cite journal| author=Kramer M, Schulte BM, Toonen LW, de Bruijni MA, Galama JM, Adema GJ et al.| title=Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells. | journal=Cell Microbiol | year= 2007 | volume= 9 | issue= 6 | pages= 1507-18 | pmid=17298395 | doi=10.1111/j.1462-5822.2007.00888.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17298395 }} </ref> | ||
EV-68 also replicates inside endothelial cells. By infecting these cells the virus is able to: | |||
* Infect the parenchymal tissue | |||
* Increase its probability of infecting secondary sites, due to the important increase in viral load in endothelial cells | |||
* Promote activation of [[endothelial cells]], which are responsible for chemoattraction of more leukocytes | |||
* Indirectly induce damage in parenchymal cells, due to the proinflammatory cytokines produces by the immune cells at this location | |||
Revision as of 13:11, 10 September 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Pathogenesis
Enterovirus 68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining, EV-69 is acid-labile, which reduces its ability to colonize the gastrointestinal mucosa. It has therefore been implicated in respiratory infections, and in rare occasions in CNS infection. This characteristic of EV-68 sets it apart from other enteroviruses, in what deals with its pathogenesis and infected cells.[1]
Besides cells of the respiratory mucosa, EV-68 also shows tropism for leukocytes, using the receptors that contain sialic-acid in these cells.[2] Since leukocytes are able to migrate to other tissues, by infecting these cells the virus gains access to secondary sites.[1] Viral replication inside leukocytes is likely to affect their function, thereby jeopardizing immune system response towards the virus, which facilitates its spread.[3]
EV-68 also replicates inside endothelial cells. By infecting these cells the virus is able to:
- Infect the parenchymal tissue
- Increase its probability of infecting secondary sites, due to the important increase in viral load in endothelial cells
- Promote activation of endothelial cells, which are responsible for chemoattraction of more leukocytes
- Indirectly induce damage in parenchymal cells, due to the proinflammatory cytokines produces by the immune cells at this location
Transmission
Life Cycle
References
- ↑ 1.0 1.1 Smura T, Ylipaasto P, Klemola P, Kaijalainen S, Kyllönen L, Sordi V; et al. (2010). "Cellular tropism of human enterovirus D species serotypes EV-94, EV-70, and EV-68 in vitro: implications for pathogenesis". J Med Virol. 82 (11): 1940–9. doi:10.1002/jmv.21894. PMID 20872722.
- ↑ Vlasak M, Roivainen M, Reithmayer M, Goesler I, Laine P, Snyers L; et al. (2005). "The minor receptor group of human rhinovirus (HRV) includes HRV23 and HRV25, but the presence of a lysine in the VP1 HI loop is not sufficient for receptor binding". J Virol. 79 (12): 7389–95. doi:10.1128/JVI.79.12.7389-7395.2005. PMC 1143622. PMID 15919894.
- ↑ Kramer M, Schulte BM, Toonen LW, de Bruijni MA, Galama JM, Adema GJ; et al. (2007). "Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells". Cell Microbiol. 9 (6): 1507–18. doi:10.1111/j.1462-5822.2007.00888.x. PMID 17298395.