Enterovirus 68 pathophysiology: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
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HEV-D viruses have an unusually wide leukocyte tropism. | |||
However, the role of leukocytes in enterovirus pathogenesis is somewhat obscure. | |||
After primary infection of the gastrointestinal tract, the viremia could be started via leukocytes if the virus was able to infect the dendritic cells and/or macrophages of Payer’s patches. | |||
Leukocytes may also serve as an additional reservoir for virus replication, thereby lengthening the viremic phase and increasing the amount of virus in circulation. Accordingly, a correla- tion between poliovirus neurovirulence and replication efficiency in monocytes has been observed [Freistadt and Eberle, 1996]. Tissue migrating leukocytes may also provide a virus with an access to secondary target tissues. Viral replication in leukocytes is also likely to affect the host immune system [Kramer et al., 2007, 2008]. At least some enteroviruses (e.g., CBV-3, CBV-4, and PV-1) are able to induce proinflammatory cytokine expression in human leukocytes [Henke et al., 1992; Vreugdenhil et al., 2000]. This can cause and/or maintain local inflammation in the secondary target tissues, thus contributing to immune-mediated chronic diseases such as T1D. | |||
It seems there are considerable differences between the abilities of different enterovirus serotypes to infect and replicate in leukocytes. Poliovirus is able to infect the monocytic fraction of peripheral blood mononuclear cells [Eberle et al., 1995], monocytic and granulocytic cell lines [Fagreus et al., 1981; Kitamura et al., 1985; Okada et al., 1987; Roivainen and Hovi, 1989; Freistadt and Eberle, 1996; Vuorinen et al., 1999], and monocyte- derived dendritic cells and macrophages [Wahid et al., 2005]. However, both T and B cells seem to be resistant to poliovirus infection [Okada et al., 1987; Vuorinen | |||
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Revision as of 23:09, 8 September 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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