F. Costanzo

Specific inhibition of Rous sarcoma virus byα-amanitin

The inhibition of the Rous sarcoma virus replication by α-amanitin suggests that the cellular RNA polymerase II may play a part at some stage of the viral replication.

Modifications of cellular RNA-polymerase II after infection with frog virus 3.

RNA-polymerase II extracted from FV3-infected and uninfected BHK cells were compared by measuring their abilities to bind [3-H]-amanitin and ribonucleoside triphosphates. Binding sites for [3-H]-amanitin and the dissociation constant of the complex between [3H]-amanitin and RNA-polymerase II were significantly modified following FV3 infection. The apparent Kms for ribonucleoside triphosphates remained unchanged.

Early Ultrastructural Changes Induced in BHK Cell Nuclei by Frog Virus 3. A Possible Mechanism for the Impairment of Cellular DNA Synthesis

Summary Evidence is presented that, in FV-3 infected BHK cell nuclei, the inhibition of RNA synthesis is paralleled by chromatin condensation. Inhibition of DNA synthesis could be due to the unavailability of the condensed chromatin to act as template.

Further characterization of virus obtained from herpes simplex virus type 1 recurrences and primary infections. Influence of the temperature of incubation upon glycoprotein synthesis and virus release: brief report

SummaryThe virus contained in clinical isolates of herpes simplex virus type 1 (HSV-1) which have not undergone previousin vitro passages (new isolates) differs from HSV-1 prototype strains with respect to infected cell glycoprotein pattern, and, most probably efficiency of virus egress at 37° C. The differences can be abolished by lowering the temperature of incubation to 33° C. A few tissue culture passages cause the conversion of the original virus to a virus undistinguishable from HSV-1 prototype strains with respect to the parameters mentioned above.

Enhanced inhibition of RNA synthesis by amanitins in in vitro cultured cells

The inhibition of RNA synthesis by α-amanitin on vitro cultured cells is very slow. The action of various analogues of the toxin was tested and some of them proved more effective. Moreover pretreatment of cell cultures with DEAE-dextran greatly enhanced the effect of β-amanitin.

Influence of genetic and physiological properties of the host cell on the cytopathic expression of herpes simplex virus

SummaryTwo plaque morphology variants, a cell aggregating variant and a syncytial variant, were isolated from MDBK cells infected with the MP mutant of herpes simplex virus, type 1. The variants differed in the polypeptides produced in infected MDBK cells. The properties of the variants were stable on passage in cells and both variants produced only syncytia in KB and HEp-2 cells. The physiological state of MDBK cells influenced the cytopathological expression of the infecting virus, so that, under certain conditions, each variant could shift from one type of plaque morphology to the other. However, attempts to correlate this plaque morphology shift with a difference in the glycopolypeptides synthesized in the infected cells were unsuccessful.

Restriction of herpes simplex virus by ama 1 cells. An analysis of viral macromolecule synthesis

SummaryAma 1 cells, an α-amanitin-resistant subline of CHO cells, restricted herpes simplex virus-1 and -2 replication. The infection was characterized by i) induction of typical cytopathology; ii) appearance of all the major virus proteins, glycoproteins and DNA earlier than in HEp-2 cells, followed by shut off of virus macromolecule synthesis; iii) defective maturation of viral particles, i.e. scarce assembly and lack of envelopment. The early shut off of viral DNA and protein synthesis, and the altered glycoprotein pattern may account for herpes simplex virus restriction.