Enterovirus 68 pathophysiology
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
Pathogenesis
Enterovirus 68 (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 rare occasions with CNS involvement. This characteristic of EV-68 sets its pathogenesis apart from that of other enteroviruses.[1]
Besides the cells of the respiratory mucosa, EV-68 also shows tropism for leukocytes. For that it uses receptors on the lymphocyte surface containing sialic-acid.[2] Since leukocytes are capable 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, facilitating 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 secondary site infections less common in EV-68 infection.[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
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 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, when an infected person coughs, sneezes, or touches contaminated surfaces.[5] Transmission of the virus was 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.