The effects of cytomegalovirus infection on polar lipids and neutral lipids in cultured human cells.

The effects of infection by the human cytomegaloviruses Ad-169 on the incorporation of [14C]acetate into the polar and neutral lipids of human embryonic lung cells and human saphenous vein smooth muscle cells were compared to [14C]acetate incorporation in mock-infected control cells. Cytomegalovirus infection caused a shift in the relative amounts of polar and neutral lipids, with infected cells having lower amounts of polar lipids and higher amounts of neutral lipids than mock-infected controls. When neutral lipids were separated into diglyceride (DG), cholesterol (C), fatty acid, triglyceride (TG) and cholesterol ester (CE) components, Ad-169-infected cells had lower levels of incorporation of label into CE, TG, and DG fractions, and higher levels of label incorporation into C than mock-infected cells.

Variation in human herpesvirus susceptibility to enhancement by the pesticide carbaryl.

The ability of various human herpesviruses to be enhanced by the pretreatment of human embryonic lung cells with the pesticide carbaryl (1-naphthyl-N-methyl-carbamate) differs according to the virus tested. Different strains of varicella-zoster virus produced different patterns of susceptibility to enhancement. Laboratory-adapted strains were less sensitive to enhancement than were wild-type strains recently isolated from clinical specimens. The related human herpes simplex viruses types 1 and 2 and cytomegalovirus were negative for susceptibility to enhancement when either laboratory-adapted or wild-type strains were tested. No difference in the pattern of susceptibility was detected whether virus yields were determined by cell-associated or cell-free virus assay or when the input multiplicity was varied 10-fold.

Characterization of varicella-zoster virus enhancement by the pesticide carbaryl.

Further characterization of the viral enhancement system of varicella-zoster virus by the pesticide carbaryl (1-naphthyl-N-methylcarbamate) is presented. It was necessary to expose cells to the enhancing chemical during the period of virus replication to detect enhancement. The optimum time for the pretreatment is 20 to 24 h. Maximum enhancement of virus expression occurs 48 to 72 h post-inoculation. Treated cells cannot pass on to daughter cells the ability to produce increased amounts of virus. alpha-Naphthol, a metabolite of carbaryl, is also capable of enhancing virus replication; Guthion, another pesticide tested, did not enhance varicella-zoster virus. The stable cell line HEP-2 can be used in place of human embryonic lung cells to detect enhancement. Differences in enhancement levels were not due to cell lot, cell passage, or a change in the stability of the cell membrane to sonic disruption.

Enhancement of varicella-zoster virus replication in cultured human embryonic lung cells treated with the pesticide carbaryl.

In studies designed to determine the factors responsible for control of herpesvirus replicaton in an infected cell, we examined the interaction of varicella-zoster (VZ) virus-infected human embryonic lung cells with the pesticide carbaryl. The replication of the cell-associated VZ virus was enhanced 2- to 13-fold as compared to control cultures in Sevin 4 Oil-treated cultures and in cultures treated with the pesticide's active ingredient, carbaryl. The replication of VZ virus in cultures teated with the base oil plus inert ingredients found in the pesticide formulation was not enhanced. Possible differences in cytotoxicity induced by Seven 4 Oil, pure carbaryl, or the base oil preparation were ruled out since treated and control cultures were shown to have similar numbers of viable cells when measured by trypan blue exclusion tests or by the ability of treated cells to form foci. A dose response study showed a decrease in viral enhancement in cells treated with decreasing carbaryl concentrations.