Coxsackie Viral Infection of the Aorta of Man

Ge, Burch; Jm, Harb; Hiramoto, Y.

doi:10.1097/00007611-197402000-00010

Cited by 5 publications

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“…In some cases, microvasculature and arterial endothelial cells differ in the degree of tight junction function and in their responsiveness to calcium ionophores [23]. Furthermore, myocarditis and dilated cardiomyopathy are often associated with CVB infection and CVB may infect aortic endothelial cells during cardiac infections [24], [25]. Interestingly, we observed the depletion of Ca i 2+ in response to CVB exposure of HAEC similar to that observed in HBMEC (Figure 2B, C).…”

Section: Resultssupporting

confidence: 72%

Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells

et al. 2010

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Group B coxsackieviruses (CVB) are associated with viral-induced heart disease and are among the leading causes of aseptic meningitis worldwide. Here we show that CVB entry into polarized brain microvasculature and aortic endothelial cells triggers a depletion of intracellular calcium stores initiated through viral attachment to the apical attachment factor decay-accelerating factor. Calcium release was dependent upon a signaling cascade that required the activity of the Src family of tyrosine kinases, phospholipase C, and the inositol 1,4,5-trisphosphate receptor isoform 3. CVB-mediated calcium release was required for the activation of calpain-2, a calcium-dependent cysteine protease, which controlled the vesicular trafficking of internalized CVB particles. These data point to a specific role for calcium signaling in CVB entry into polarized endothelial monolayers and highlight the unique signaling mechanisms used by these viruses to cross endothelial barriers.

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Section: Resultssupporting

confidence: 72%

Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells

et al. 2010

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Aneurysmal Subarachnoid Hemorrhage and Viral Infection

Timmons¹,

Donnan²,

Whisnant³

et al. 1986

Arch Neurol

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Coxsackievirus Group B Replication in Cultured Fetal Baboon Aortic Smooth Muscle Cells

Godeny

Gauntt

Sprague

et al. 1986

Journal of Medical Virology

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All six coxsackievirus B (CVB) serotypes replicated to various extents in fetal baboon aortic smooth muscle cells (SMC) in culture. CVB3 and CVB4 replicated to the highest titers and induced no cytopathology at the level of light microscopy. Maximum yields of CVB3 were produced between 12 and 24 hr postinoculation. Up to 15% of SMC cells became infected, as determined by immunofluorescence assays with anti-CVB3 antiserum, yet overall cell division in infected cultures did not differ from infected SMC cultures. Electron microscopy of CVB3-inoculated SMC cultures revealed changes in some cells: viruslike particles, secondary lysosomes containing dense bodies, and peripheral nuclear chromatin condensation. CVB3 replicated well in SMC passages up to the eighth, but did not replicate in eleventh-passage cells. Because of the cardiotropic and myotropic potential of this virus and its ability to replicate in aortic SMC with associated ultrastructural alterations, CVB3 (and other CVB) should be further examined as an etiologic agent(s) that could induce atherosclerosis.

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Coxsackie Viral Infection of the Aorta of Man

Cited by 5 publications

References 0 publications

Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells

Release of Intracellular Calcium Stores Facilitates Coxsackievirus Entry into Polarized Endothelial Cells

Aneurysmal Subarachnoid Hemorrhage and Viral Infection

Coxsackievirus Group B Replication in Cultured Fetal Baboon Aortic Smooth Muscle Cells

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