Use of fluorescent-antibody staining of cytocentrifuge-prepared smears in combination with cell culture for direct detection of respiratory viruses.

Over a 3-year period, 1,003 respiratory samples were collected and examined for selected respiratory viruses with cytocentrifuged prepared smears stained with fluorescently labeled antibodies (IFA) in conjunction with cell culture. IFA results were compared with results obtained by cell culture. Viruses were isolated or detected by direct means in 401 samples.

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.

Effect of influenza virus strains on lipid metabolism of infected HEK cells.

We have shown previously that in infected HEL cells varicella-zoster virus (VZV) causes a shift from polar to neutral lipid synthesis and that some strains of the virus depressed total lipid synthesis. In this report we show that VZV produces a similar effect on the lipid metabolism of infected human embryonic kidney cells. The pattern of lipid synthesis in human embryonic kidney cells infected with either of two strains of influenza type A virus was similar to that of control uninfected cells, whereas the greatest difference and the pattern closest to that seen with VZV was produced by influenza type B strains.

Differentiation of strains of varicella-zoster virus by changes in neutral lipid metabolism in infected cells.

Eleven isolates of varicella-zoster virus were tested for their effects on the incorporation of [14C]acetate into lipids in infected human embryonic lung cells. By relative percent, all virus isolates demonstrated a shift from polar lipid synthesis to neutral lipid, especially triglyceride, synthesis. By data expressed as counts per minute per microgram of protein, the VZV strains could be separated into two groups: those strains which depressed lipid synthesis and those strains which did not depress, and may even have stimulated, lipid, especially triglyceride, synthesis.

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.

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.

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.

Enzymatic basis for the selective inhibition of varicella-zoster virus by 5-halogenated analogues of deoxycytidine.

5-Bromodeoxycytidine (BrdC) and 5-iododeoxycytidine, at a concentration of 100 mug/ml, effectively inhibit the replication of varicella-zoster (VZ) virus in tissue culture. No toxicity could be demonstrated in uninfected cells under the same conditions. Studies on the enzymatic basis for this selective inhibition were undertaken.

Demonstration of oncogenic potential of mammalian cells transformed by DNA-containing viruses following photodynamic inactivation.

The oncogenic properties of hamster embryo cells transformed by herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) and SV40 virus following photodynamic inactivation using neutral red were determined by subcutaneous inoculation into newborn Syrian hamsters. Cells transformed by all three viruses produced palpable tumors after different latent periods. Histopathological examination showed that HSV-2 tumors were fibrosarcomas and metastases were often seen in the lungs.

Stimulation of adenovirus replication in simian cells in the absence of a helper virus by pretreatment of the cells with iododeoxyuridine.

Pretreatment of African green monkey kidney cells with 50 mu g of 5'-iododeoxyruidine (IUdR) per ml can modify their susceptibility to the replication of human adenovirus type 7 in the absence of simian virus 40 (SV40) although this enhancement of adenovirus replication is not as efficient as that of the helper SV40 virus. Since the number of infectious centers remains unchanged after IUdR pretreatment whereas the burst size of virus from each infected cell increases, the IUdR appears to allow each infected cell to produce more virus. Cell DNA synthesis appears to be stimulated in IUdR pretreated cells infected with adenovirus 7, but the host cell DNA synthesized is small enough to remain in the Hirt supernatant fluid.

Replication and complementation of human adenoviruses and simian papovavirus at an elevated temperature.

The simian papovavirus SV40 replicated as well in simian cells incubated at 41 C as in cells incubated at 37 C, although the latent period was shortened at the elevated temperature. Human adenoviruses differed in their responses to the elevated temperature. Some serotypes, such as 3, 4, 5, 7, 8, 16, and 21, replicated as well, or almost as efficiently, in human cells incubated at 41 C as in cells incubated at 37 C, whereas with other serotypes, such as 1, 2, 6, 12, and 14, maximal yields in cultures incubated at 41 C were much lower than the yields from companion cultures incubated at 37 C.

Variation in the oncogenic potential of human adenoviruses carrying a defective SV40 genome (PARA).

The acquisition of the defective SV40 genome by a variety of human adenovirus serotypes by the process of transcapsidation has resulted in the addition of oncogenic potential for newborn hamsters to the previously nononcogenic adenovirus types 1, 2, 5, and 6. These serotypes have previously been grouped together by the high GC content of their DNA. Transcapsidation of the SV40 genome to weakly oncogenic adenovirus types 3, 14, 16, and 21 has failed to increase their oncogenic potential although the parent adenovirus type 7 carrying PARA is highly oncogenic.