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Vesicular stomatitis virus synthesis

Talib, S., and J.E. Hearst. 1983. Initiation of RNA synthesis in vitro by vesicular stomatitis virus Single internal initiation in the presence of aurintricarboxylic acid and vanadyl ribonucleoside complexes. Nucleic Acids Res 11 7031. [Pg.106]

Baltimore D, Huang AS, Stampfer M (1970) Ribonucleic acid synthesis of vesicular stomatitis virus, 11. An RNA polymerase in the virion. Proc Natl Acad Sci USA 66 572-576. [Pg.339]

The first synthesis of racemic [9-(2,3-dihydroxypropyl)adenine] DHPA, C H N O was reported in 1965 (59), and the synthesis of the (R)- and (5)-enantiomers of DHPA was reported later (60). Subsequendy (5)-DHPA [54262-83-8] (29) was shown to be active against a broad range of DNA and RNA vimses including vaccinia, HSV-1, HSV-2, measles, and vesicular stomatitis viruses. The racemic mixture, (R,3)-DHPA [55904-02-4] was almost as active as the (3)-enantiomer. However, the (R)-isomer of DHPA was inactive as an antiviral agent. [Pg.308]

The antiviral activity of (5)-DHPA in vivo was assessed in mice inoculated intranasally with vesicular stomatitis virus ( 5)-DHPA significandy increased survival from the infection. (3)-DHPA did not significandy reduce DNA, RNA, or protein synthesis and is not a substrate for adenosine deaminase of either bacterial or mammalian origin. However, (5)-DHPA strongly inhibits deamination of adenosine and ara-A by adenosine deaminase. Its mode of action may be inhibition of X-adenosyl-L-homocysteine hydrolase (61). Inhibition of SAH hydrolase results in the accumulation of SAH, which is a product inhibitor of 5-adenosyhnethionine-dependent methylation reactions. Such methylations are required for the maturation of vital mRNA, and hence inhibitors of SAH hydrolase may be expected to block virus replication by interference with viral mRNA methylation. [Pg.308]

Huang AS, Wagner RR (1965) Inhibition of cellular RNA synthesis by non-rephcating vesicular stomatitis virus. Proc Natl Acad Sci USA 54 1579 Hully JR, Chang L, Schwall RH, Widmer HR, Terrell TG, Gillett NA (1994) Induction of apoptosis in the murine liver with recombinant human activin A. Hepatology 20 854-861... [Pg.143]

The trienamide onnamide A (43) is a metabolite isolated from the marine sponge Theonella sp. found in Okinawan waters [84]. It belongs to the pederin family like mycalamides and theopederins [85], and shows a potent antiviral activity against herpes simplex virus type-1, vesicular stomatitis virus, and coronavirus A-59. The complete determination of the structure was carried out during the total synthesis of onnamide A (43)... [Pg.393]

The following aspects of viral glycoproteins have been reviewed glycoprotein and protein precursors to plasma membranes in vesicular stomatitis virus infected HeLa cells,membrane glycoproteins of enveloped viruses, membrane assembly, including the synthesis and intracellular processing of vesicular stomatitis virus, and the structure and replication of a-viruses. ... [Pg.315]

It has been reported [20] that a mixture of A A and A G dimers, or the individual G G dimer, produce effects on the mitotic activity of a human amniotic cell line, and a transient effect on the reproduction of the RNA viruses, polio virus and vesicular stomatitis virus, grown on these cells. These effects may be attributable to the utilisation of the dimers in RNA synthesis of the cells and the viruses. A similar effect on RNA synthesis may also be produced in experiments [20] demonstrating a cytotoxic... [Pg.506]

Apparently related to the problem of host cell protein synthesis inhibition by viruses is the phenomenon of viral interference. In some cases, superinfection of a cell already infected with one virus does not affect the yield of the original virus. In other cases, however, the superinfecting virus completely inhibits translation of the original viral mRRA. Such is the case for superinfection of vesicular stomatitis virus (VSV)-infected cells by poliovirus (32). The kinetics and general properties of the shut-off of VSY protein synthesis appear to be the same as the shut-off of cellular protein synthesis after poliovirus infection... [Pg.82]

MDDD, J.A. and SmyiMERS, D.F. Protein synthesis in vesicular stomatitis virus-infected HeLa cells. Virology,(l970), 18,... [Pg.95]

It has been realized for some time that viral multiplication can occur with only minimal cytopathic effects (Choppin, 1964). Conversely, considerable cytopathology can result from infection with a virus, the multiplication of which is restricted in that host. Cantell et al. (1962) were perhaps the first to describe that L cells could be destroyed by large doses of a UV-irradiated virus, vesicular stomatitis virus, in the absence of a detectable synthesis of viral antigen this toxic activity could not be separated from the viral particle. We shall discuss in a later chapter why this does not prove the absence of viral replicative functions or that preformed virion components are necessarily cytotoxic. However, it is quite clear that early interactions... [Pg.6]

All functions of a cell need not remain intact to retain susceptibility to viral infections. However, loss of certain functions will predispose to resistance to certain viruses and not others. For example, cells enucleated by cytochalasin B will support the replication of vesicular stomatitis virus but not influenza virus, which also fails to inhibit protein synthesis in enucleated cells (Follett et al., 1974). [Pg.7]

The feature common to the cytotoxic effects brought on by nonreplicating influenza virus, poxvirus, and defective-interfering vesicular stomatitis virus is the high multiplicity of infection required. This has led to the assumption that the toxic effect is caused by one or more components of the parental input virion, most likely protein in origin. However, Cordell-Stewart and Taylor (1971, 1973) have provided evidence that the double-stranded viral RNA isolated from cells infected with bovine enterovirus causes a rapid cytopathic effect as determined by trypan-blue uptake or Cr release from affected Ehrlich ascites tumor cells or L1210 cells toxic effects are reduced or do not occur in cells exposed to single-stranded or heat-denatured double-stranded viral RNA and the toxic effect of bovine enteroviral double-stranded RNA is not abolished by inhibitors of protein synthesis such as puromycin or cycloheximide. [Pg.33]

However, the better authenticated cytotoxic components of virions are their proteins. As mentioned previously, the fiber antigen of adenoviruses has a marked cytotoxic effect as demonstrated by its capacity to inhibit division of KB cells, and to inhibit multiplication of adenovirus 5 and poliovirus in KB cells, as well as inhibiting RNA, DNA, and protein synthesis in uninfected and adenovirus-infected KB cells (Levine and Ginsberg, 1967). The isolated glycoprotein of vesicular stomatitis virus at exceedingly large concentrations significantly impairs macromolecular synthesis of BHK-21 cells (McSharry and Choppin, 1978) and can be assumed to have a cytotoxic effect. [Pg.33]

Baxt, B., and Bablanian, R., 1976, Mechanism of vesicular stomatitis virus-induced cytopathic effects. II. Inhibition of macromolecular synthesis induced by infectious and defective-interfering particles, Virology 72 383. [Pg.53]

Farmilo, A. J., and Stanners, C. P., 1972, Mutant of vesicular stomatitis virus which allows DNA synthesis and division in cells synthesizing viral RNA, J. Virol. 10 605. [Pg.55]

Marvaldi, J. L., Lucas-Lenard, J., Sekellick, M. J., and Marcus, P. I., 1977, Cell killing by viruses. IV. Cell killing and protein synthesis inhibition by vesicular stomatitis virus require the same gene functions. Virology 79 267. [Pg.59]

McAllister, P. E., and Wagner, R. R., 1976, Differential inhibition of host protein synthesis in L cells infected with RNA temperature-sensitive mutants of vesicular stomatitis virus, J. Virol. 18 550. [Pg.60]

Schnitzlein, W. M., O Banion, M. K., Poirot, M. K., and Reichmann, M. E., 1983, Effect of intracellular vesicular stomatitis virus mRNA concentration on the inhibition of host cell protein synthesis, J. Virol. 45 206. [Pg.62]

Wagner, R. R., and Huang, A. S., 1966, Inhibition of RNA and interferon synthesis in Krebs-2 cells infected with vesicular stomatitis virus. Virology 28 1. [Pg.63]

Yaoi, Y., Mitsui, H., and Amano, M., 1970, Effect of UV-irradiated vesicular stomatitis virus on nucleic acid synthesis in chick embryo cells, J. Gen. Virol. 8 165. [Pg.63]

Lodish, H. F., and Froshauer, S., 1977, Rates of initiation of protein synthesis by two purified species of vesicular stomatitis virus messenger RNA, J. Biol. Chem. 252 8804. [Pg.167]

Lodish, H. F., and Porter, M., 1980, Translational control of protein synthesis after infection by vesicular stomatitis virus, J. Virol. 36 719. [Pg.167]


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See also in sourсe #XX -- [ Pg.183 , Pg.241 ]




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