Enterovirus 68 pathophysiology: Difference between revisions
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Due to being acid-labile, EV-68 is not shed in feces like other enteroviruses. [[Transmission]] of EV-68 is not as well-understood as those 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 when an infected person coughs, sneezes, or touches contaminated surfaces. | Due to being acid-labile, EV-68 is not shed in feces like other enteroviruses. [[Transmission]] of EV-68 is not as well-understood as those 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 when an infected person coughs, sneezes, or touches contaminated surfaces. | ||
==References== | ==References== | ||
Revision as of 13:49, 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:[3]
- 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
However, EV-68 shows less tropism for endothelial cells than EV-70 or EV-94, which makes the secondary site infections less common for EV-68.[1]
Transmission
Due to being acid-labile, EV-68 is not shed in feces like other enteroviruses. Transmission of EV-68 is not as well-understood as those 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 when an infected person coughs, sneezes, or touches contaminated surfaces.
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.