Enterovirus 68 pathophysiology: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
EV-68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining, EV-68 is acid-labile, which reduces its ability to colonize the [[gastrointestinal]] mucosa. It has been implicated in [[respiratory infections]] and in very rare occasions in [[CNS]] disease. This property of EV-68 sets it apart from other [[enterovirus]]es.<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> | EV-68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining enteroviruses in its class, EV-68 is acid-labile, which reduces its ability to colonize the [[gastrointestinal]] mucosa. It has been implicated in [[respiratory infections]] and in very rare occasions in [[CNS]] disease. This property of EV-68 sets it apart from other [[enterovirus]]es.<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> | ||
The virus shows optimal growth at lower temperatures, making the [[respiratory tract]] an adequate host for [[viral replication]]. Besides the cells of the [[respiratory]] mucosa, EV-68 also shows [[tropism]] for [[leukocytes]]. The virus binds receptors on the [[lymphocyte]] surface containing sialic-acid in order to access the cytoplasm.<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 capable of migrating 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]] limits their function, thereby facilitating viral replication and 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> | The virus shows optimal growth at lower temperatures, making the [[respiratory tract]] an adequate host for [[viral replication]]. Besides the cells of the [[respiratory]] mucosa, EV-68 also shows [[tropism]] for [[leukocytes]]. The virus binds receptors on the [[lymphocyte]] surface containing sialic-acid in order to access the cytoplasm.<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 capable of migrating 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]] limits their function, thereby facilitating viral replication and 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]] that provide | EV-68 also replicates inside [[endothelial cells]] that provide the required increase in viral load for the virus to infect [[parenchymal]] tissue, and gain access to secondary sites.<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> The virus also promotes the activation of [[endothelial cells]] leading to chemoattraction of further [[leukocytes]]. | ||
However, EV-68 shows less [[tropism]] for [[endothelial cells]] than EV-70 or EV-94, which makes | However, EV-68 shows less [[tropism]] for [[endothelial cells]] than EV-70 or EV-94, which makes [[infection]] of secondary sites less common.<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> | ||
===Immune Response=== | ===Immune Response=== | ||
| Line 22: | Line 19: | ||
===Transmission=== | ===Transmission=== | ||
Given its acid-lability, EV-68 is not shed in feces like other [[enteroviruses]]. [[Transmission]] of EV-68 is not as well-understood as that of other [[enterovirus]]es. EV-D68 causes [[respiratory disease]], and the virus can be found in [[respiratory]] [[secretions]] such as [[saliva]], nasal mucus, or [[sputum]]. The [[virus]] likely spreads from person to person via respiratory aerosols.<ref name=CDC>{{cite web | title = Enterovirus D68 | url = http://www.cdc.gov/non-polio-enterovirus/about/EV-D68.html }}</ref> [[Transmission]] of the virus is noted to occur more frequently between the months of August and November.<ref name="pmid24324030">{{cite journal| author=Lu QB, Wo Y, Wang HY, Wei MT, Zhang L, Yang H et al.| title=Detection of enterovirus 68 as one of the commonest types of enterovirus found in patients with acute respiratory tract infection in China. | journal=J Med Microbiol | year= 2014 | volume= 63 | issue= Pt 3 | pages= 408-14 | pmid=24324030 | doi=10.1099/jmm.0.068247-0 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24324030 }} </ref> | |||
==References== | ==References== | ||
Revision as of 22:39, 10 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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Overview
Unlike other enteroviruses, enterovirus 68 (EV-68) causes respiratory disease. Its cellular tropism, optimal growth at lower temperatures, and acid-lability are responsible for infection of cells in the respiratory mucosa and leukocytes. The virus is able to replicate inside leukocytes, which allows it to infect the parenchymal tissue; to increase its viral load, spreading to other regions; and to activate endothelial cells that attract more leukocytes to the infection site. Although viral transmission is not fully understood, the virus can be found in respiratory secretions and may be spread from person to person, when an infected person coughs, sneezes, or touches contaminated surfaces.
Pathogenesis
EV-68 belongs to the Human Enterovirus D species (HEV-D), along with EV-70 and EV-94. Unlike the remaining enteroviruses in its class, EV-68 is acid-labile, which reduces its ability to colonize the gastrointestinal mucosa. It has been implicated in respiratory infections and in very rare occasions in CNS disease. This property of EV-68 sets it apart from other enteroviruses.[1]
The virus shows optimal growth at lower temperatures, making the respiratory tract an adequate host for viral replication. Besides the cells of the respiratory mucosa, EV-68 also shows tropism for leukocytes. The virus binds receptors on the lymphocyte surface containing sialic-acid in order to access the cytoplasm.[2] Since leukocytes are capable of migrating to other tissues, by infecting these cells, the virus gains access to secondary sites.[1] Viral replication inside leukocytes limits their function, thereby facilitating viral replication and spread.[3]
EV-68 also replicates inside endothelial cells that provide the required increase in viral load for the virus to infect parenchymal tissue, and gain access to secondary sites.[3] The virus also promotes the activation of endothelial cells leading to chemoattraction of further leukocytes.
However, EV-68 shows less tropism for endothelial cells than EV-70 or EV-94, which makes infection of secondary sites less common.[1]
Immune Response
The immune response towards EV-68 is not fully understood. Viral clearance is achieved by an adequate T and B-cell response that contain and eliminate the virus. B lymphocytes, along with tissue macrophages contain the pathogen, while T lymphocytes penetrate the areas of infection, causing tissue damage. Tissue damage may lead to cell death of the affected areas.[4]
Transmission
Given its acid-lability, EV-68 is not shed in feces like other enteroviruses. Transmission of EV-68 is not as well-understood as that of other enteroviruses. EV-D68 causes respiratory disease, and the virus can be found in respiratory secretions such as saliva, nasal mucus, or sputum. The virus likely spreads from person to person via respiratory aerosols.[5] Transmission of the virus is noted to occur more frequently between the months of August and November.[6]
References
- ↑ 1.0 1.1 1.2 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.
- ↑ 3.0 3.1 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.
- ↑ Kreuter JD, Barnes A, McCarthy JE, Schwartzman JD, Oberste MS, Rhodes CH; et al. (2011). "A fatal central nervous system enterovirus 68 infection". Arch Pathol Lab Med. 135 (6): 793–6. doi:10.1043/2010-0174-CR.1. PMID 21631275.
- ↑ "Enterovirus D68".
- ↑ Lu QB, Wo Y, Wang HY, Wei MT, Zhang L, Yang H; et al. (2014). "Detection of enterovirus 68 as one of the commonest types of enterovirus found in patients with acute respiratory tract infection in China". J Med Microbiol. 63 (Pt 3): 408–14. doi:10.1099/jmm.0.068247-0. PMID 24324030.