Deoxyribonucleic Acid Replication in Simian Virus 40-Infected Cells

Ritzi, Earl M.; Levine, Arnold J.

doi:10.1128/jvi.5.6.686-692.1970

Cited by 69 publications

(10 citation statements)

References 20 publications

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“…5). These results are in agreement with previously published reports (Ritzi and Levine, 1969). With the in sitlr hybridization of (3H)-cRNA on similarly infected cells, the following observations can be made.…”

Section: Tinir Course Of Dna Synthesis and Niirltiplicity Of Infectionsupporting

confidence: 93%

Detection of virus‐specific DNA sequences by quantitative in situ hybridization during infection with SV40

Langelier

Mandeville

Simard

1975

Intl Journal of Cancer

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In situ hybridization has been used as a quantitative method to study the replication of SV40 during lytic infection. Various parameters have been defined such as fixation and denaturation of cytological preparations, concentration of complementary (3H)-cRNA and volume of buffer used for the hybridization reaction. When all these parameters are carefully controlled, a reproducibility of +/-10% can be obtained for the quantitative study of the system SV40-monkey kidney cells (CV-1). In this system, it is evident that the synthesis of viral DNA is not synchronized in confluent cells. Moreover, a proportion of 20 to 30% of cells are not labelled whatever the multiplicity of infection. In SV40-transformed cells, it was not possible to detect significantly the integrated genome due either to the small size of the genome or to the fact that the number of genome-equivalents integrated at the same place is too low to yield a radioactivitity superior to background level for long periods of exposure.

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Section: Tinir Course Of Dna Synthesis and Niirltiplicity Of Infectionsupporting

confidence: 93%

Detection of virus‐specific DNA sequences by quantitative in situ hybridization during infection with SV40

Langelier

Mandeville

Simard

1975

Intl Journal of Cancer

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“…That infected cells not only remain viable regardless of the input multiplicity or accumulation of virus (37) but are also in a phase in which their capacity to synthesize DNA is retained is also consistent with the findings of several workers who have measured the biosynthetic capacity of infected cells. The continued synthesis of viral DNA has also been reported by others (17,31,39,43). Preparation of nuclei (41) or cellular fractions (9, 12, 49) 33 to 48 h after infection which are active in in vitro DNA synthesis testifies to the continued presence of the machinery for DNA synthesis.…”

Section: Discussionmentioning

confidence: 61%

Simian Virus 40-Host Cell Interaction During Lytic Infection

Gershey

1979

J Virol

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Both exponentially growing and serum-arrested subcloned CV-1 cell cultures were infected with simian virus 40 (SV40). By 24 h after infection 96% of the nuclei of these permissive cells contained SV40 T-antigen. Analysis of the average DNA content per cell at various times after infection indicated that by 24 h most of the cells contained amounts of DNA similar to those normally found in G 2 cells. Analysis of cell cycle distributions indicated that a G 2 DNA complement was maintained by over 90% of the cells in the infected populations 24 to 48 h postinfection. Cells continued to synthesize SV40 DNA during the first 50 h after infection, and cytopathic effect was first observed 60 h after inoculation. After infection the number of mitotic cells that could be recovered by selective detachment decreased precipitously and was drastically reduced by 24 h. A study of the kinetics of decline in the number of mitotic cells suggests that this decline is related to an event during the cell cycle at or near the G 1 -S-phase border upon which commencement of SV40 DNA replication apparently depends. It was concluded that after SV40 infection, stationary cells are induced to cycle, and cycling cells complete one round of cellular DNA synthesis but do not divide. Although the infected cells continue to synthesize viral DNA, they do not appear able to reinitiate cellular DNA replication units. These results imply that the abundance of T-antigen (produced independently of cell cycle phase) in the presence of the enzymes required for continued DNA synthesis is not sufficient for reinitiation of cellular DNA synthesis.

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“…The percentage of cells actively synthesizing DNA at various times after polyoma infection is also presented in Figure 1 and shows that a significant increase in the percentage of cells having labeled nuclei also occurred after a lag of 15-20 hours. Although [aH]-thymidine autoradiography does not allow us to distinguish between viral and cellular DNA synthesis, other investigators have shown that both occur as a result of lytic infection (Dulbecco et al, 1965;Hirt, 1967;Ritzi and Levine, 1970;Sheinin, 1966). The results presented in Figure 1 show that the induction of dihydrofolate reductase synthesis following polyoma infection is accompanied by an increase in the percentage of cells that are actively engaged in DNA synthesis.…”

Section: Lytic Infection By Polyoma Virusmentioning

confidence: 89%

The effect of polyoma virus, serum factors, and dibutyryl cyclic AMP on dihydrofolate reductase synthesis, and the entry of quiescent cells into S phase

Gudewicz¹,

Morhenn²,

Kellems³

1981

Journal Cellular Physiology

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Three procedures were used to induced dihydrofolate reductase synthesis in quiescent cultures of methotrexate resistant mouse fibroblasts: 1) lytic infection with polyoma virus, 2) growth stimulation by replating cells at lower density in fresh cell culture medium, and 3) the addition of fresh medium to confluent cells. Following polyoma infection, an increase in the percentage of S-phase cells began at approximately 20 hours; dihydrofolate reductase synthesis also increased following a lag of 20 hours or more, and continued to increase throughout the late phase of lytic infection, reaching values nearly fivefold greater than that originally present in the quiescent cells. When quiescent cells received fresh medium (with or without replating), the percentage of cells in S phage began to increase by 10 hours and was accompanied by an increase in dihydrofolate reductase synthesis which reached a maximum by approximately 25 hours. These observations show that the initial entry of cells into S phase following mitogenic stimulation is associated with an induction of dihydrofolate reductase synthesis. Dibutyryl cyclic AMP blocked the stimulation of dihydrofolate reductase synthesis and the increase in the percentage of S-phase cells that resulted from the addition of fresh medium to confluent cells. When dibutyryl cyclic AMP was added at various times following the addition of fresh medium, the block in the induction of dihydrofolate reductase synthesis was correlated with a corresponding block in the increase in S-phase cells. These results suggest that dibutyryl cyclic AMP blocks cells at a point in G1 prior to either the induction of dihydrofolate reductase synthesis of the beginning of S phase. The relationship between the control of dihydrofolate reductase synthesis and entry into S phase suggests some form of coordinate control over these two parameters.

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Deoxyribonucleic Acid Replication in Simian Virus 40-Infected Cells

Cited by 69 publications

References 20 publications

Detection of virus‐specific DNA sequences by quantitative in situ hybridization during infection with SV40

Detection of virus‐specific DNA sequences by quantitative in situ hybridization during infection with SV40

Simian Virus 40-Host Cell Interaction During Lytic Infection

The effect of polyoma virus, serum factors, and dibutyryl cyclic AMP on dihydrofolate reductase synthesis, and the entry of quiescent cells into S phase

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