No abstract

1H-benz[f]indene-1.3(2H)dione-bis-amidinohydrazone (benzhydrazone) inhibited incorporation of 14C-glucosamine, 14C-fucose and 14C-mannose into glycoproteins of HEp-2 cells infected with various strains of herpes simplex virus 1 (HSV-1) and impaired RNA and protein synthesis to a low extent. These biochemical effects are very similar to those induced by glycosylation inhibitors such as tunicamycin, D-glucosamine and 2-deoxy-D-glucose. In contrast to these inhibitors, benzhydrazone reduced HSV glycoprotein synthesis selectively since it did not significantly modify i) the saccharide uptake into glycoproteins of uninfected and of Sindbis virus-infected cells, ii) viral growth and cell fusion in paramyxovirus-infected cells, two activities which depend on viral glycoprotein synthesis. Benzhydrazone had only minor effects on the overall metabolism of uninfected cells, since it did not alter cell growth rate, and amino acid, uridine, and hexose incorporations were about 80% those of untreated cells.

The analysis of 23 clinical isolates of herpes simplex virus type 1 (HSV-1) showed that 15 of 15 isolates that had undergone a few passages in tissue culture (fresh isolates) and two of eight isolates that had never been passaged (new isolates) were composed of a mixed population with respect to plaque morphology in Vero cells. Cloning and characterization of 10 large plaque viruses (L variants) and nine small plaque viruses (S variants), obtained from seven different isolates, showed the following. BamHI DNA restriction patterns of the L and the S variants from a single isolate differed only with respect to the electrophoretic mobility of the fragments that contain reiteration of specific sequences; they did not differ regarding the presence or the absence of restriction endonuclease cleavage sites. The L and S variants differed with respect to the electrophoretic profiles of infected cell glycoproteins, thermosensitivity of growth and plaquing efficiency at 39 degrees C, and, at least in the case of the two couples of variants that we tested, pathogenicity for the mouse. The hypothesis that the L variants might arise from the S variant during in vivo replication is discussed.

Die Reaktion von Aminoguanidinhydrochlorid (II) mit den Carbonylverbindungen (I), (IVa), (Va), (VIa) bzw. (VII) ergibt die Amidinohydrazon‐Derivate (III), (IVb) (60% Ausb.), (Vb) (60%), (VIb) (55%) bzw. (VIII), die überwiegend als Hydrate oder Dihydrate isoliert werden.

The RNA polymerase activity present in the cytoplasm of BHK cells infected with vaccinia virus is not affected by rifampicin or by a-amanitin. The rifamycins, a group of broad-spectrum antibiotics, have been shown to block bacterial ribonucleic acid (RNA) synthesis (7, 25) by in