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- W2053797162 abstract "Based on well-documented data showing that bioactive ions (such as Ca2+, PO4-, etc.) released by BCPC induce various cell responses and on the significance of herpes outbreaks in human pathology, we investigated whether BCPC can modify cell response to HSV-1 infection. The roles of some physical and chemical properties of ceramics were evaluated using three BCPC samples--French commercial macro-microporous (FR) and two Bulgarian microporous laboratory samples--one of which was modified with magnesium (BG and BG + Mg). Samples only washed in 0.9% NaCl were designated as nonconditioned while those resuspended in cell growth medium for 10 days after washing were designated as conditioned. Experiments were done on cells from the continuous MDBK line precultured on BCPC surfaces for different time intervals and thereafter HSV-1 infected. The yield of infectious virus progeny, measured as virus titers, was the parameter used to determine the cell response to HSV-1 infection mediated by BCPC as compared to that of the virus control, that is, virus yield in cells cultured without BCPC. The data obtained show that all three nonconditioned BCPC samples were able to modify cells to resist HSV-1 infection. The prolongation of the resistant state depended on the specific physical and chemical properties of the particular BCPC sample: as the data show that the conditioning procedure (1) increased the ability of BG + Mg to promote cell resistance, and (2) reduced the ability of FR samples to modify cells to resist HSV-1 infection. The data obtained show that apart from Ca2+ and PO4-, ions of biometals such as Mg2+ also are responsible for the induction and maintenance of cell resistance to HSV-1 infection." @default.
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- W2053797162 date "2001-01-01" @default.
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- W2053797162 title "Cell response to herpes simplex virus type 1 infection mediated by biphasic calcium-phosphate ceramics:In vitro approach" @default.
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- W2053797162 doi "https://doi.org/10.1002/1097-4636(200111)57:2<232::aid-jbm1163>3.0.co;2-b" @default.
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