Enterovirus 68 pathophysiology
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
|
Enterovirus 68 Microchapters | |
|
Diagnosis | |
|---|---|
|
Treatment | |
|
Case Studies | |
|
Enterovirus 68 pathophysiology On the Web | |
|
American Roentgen Ray Society Images of Enterovirus 68 pathophysiology | |
|
Risk calculators and risk factors for Enterovirus 68 pathophysiology | |
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]
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.