The inhibition of influenza virus RNA synthesis by actinomycin D and cycloheximide

Pons, Marcel W.

doi:10.1016/0042-6822(73)90372-3

Cited by 64 publications

(38 citation statements)

References 13 publications

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“…Studies on influenza virus indicate that an event early in its replicative cycle occurs in the nucleus of the cell and actinomycin D blocks this event. Transcription of influenza virus RNA cannot be detected in cells infected with the virus and treated with actinomycin D during the first 2 h after infection (Bean & Simpson, 1973;Pons, 1973;Stephenson & Dimmock, 1975 ). The drug does not inhibit influenza virus replication if added late in the replicative cycle (Barry et al 1962).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Pichinde Virus Replication by Actinomycin D

Rawls

Banerjee

Mcmillan

et al. 1976

Journal of General Virology

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SUMMARYThe yields of Pichinde virus, a member of the arenavirus group, were markedly inhibited when infected BHK 21 cells were incubated in the presence of o'4 to 4 #g/ml of actinomycin D. Maximal inhibition was observed when actinomycin D was added after the adsorption of virus to cultures; however, addition of drug as late as 12 h after infection reduced the 24 h yield by 5 ° ~. Virus antigen synthesis, as measured by complement fixation and immunodiffusion, was not dramatically reduced by actinomycin D. The expression of virus antigens on the surface of infected cells was greater on cells treated with actinomycin D than on untreated cells. Putative defective particles with a density of Pichinde virus were not detected in fluids of cultures incubated with actinomycin D and 3H-amino acids. Actinomycin D appears to inhibit Pichinde virus late in the replicative cycle. The observations raise the possibility that the drug inhibits the synthesis of proteins of the host cell membrane which are required for virus maturation.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Pichinde Virus Replication by Actinomycin D

Rawls

Banerjee

Mcmillan

et al. 1976

Journal of General Virology

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“…4C). Previous reports showed that CHX suppresses viral protein synthesis and thereby represses vRNA replication (9,33). Therefore, we could examine the viral transcription level without amplification of the viral genome in the presence of CHX.…”

Section: Synthesis Of Viral Rnas In Ts53 Virus-infected Cellsmentioning

confidence: 99%

Involvement of Influenza Virus PA Subunit in Assembly of Functional RNA Polymerase Complexes

Kawaguchi

Naito

Nagata

2005

J Virol

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“…1, except that the cells were not treated with antiscru M. The cells were fixed with cold acetone 4 hr (1), 7 hr (2, 4), and 12 hr (3, 5) after infection. (14,17). cRNA is synthesized mainly early in infection, while most of the virion RNA (vRNA) is synthesized late during infection (3,6,17).…”

Section: Hamaguchi Et Almentioning

confidence: 99%

Analysis of Nuclear Accumulation of Influenza Nucleoprotein Antigen in the Presence of p‐Fluorophenylalanine

Hamaguchi

Maeno

Nagai

et al. 1980

Microbiology and Immunology

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When p-fluorophenylalanine (FPA) was added to influenza virus RI/5+-infected cells 4 hr after infection, virus-specific proteins were synthesized but infectious progeny virus was not produced. In these cells, synthesis of viral RNA was strongly inhibited and nucleoprotein (NP) antigen was found predominantly in the nucleus in contrast to untreated cells in which NP antigen was distributed throughout the whole cell. The intracellular location and migration of NP were examined by isotope labeling followed by fractionation of infected cells. In untreated cells, a large portion of the NP was present in the cytoplasm and most of it was detected in the form of ribonucleoprotein (RNP). In contrast, in FPAtreated cells little viral RNP was detectable and NP was present predominantly in the nucleus in a nonassembled, soluble form. When FPA was removed from the culture, synthesis of viral RNA was soon restored and a large amount of viral RNP appeared in the cytoplasm; this was followed by the production of infectious virus. The results of the experiments suggest that the NP synthesized in the presence of FPA is not assembled into viral RNP because of the lack of available RNA, and such NP migrates readily into the nucleus and accumulates there.Influenza ribonucleoprotein (RNP) consists of multiple molecules of nucleoprotein (NP) and one segment of virion RNA (vRNA) or cRNA complementary to vRNA (2, 15). Intracellular development of RNP has been studied extensively by immunofluorescence (1,4,5,10,11,16,21). The NP antigen appears first in the nucleus and later becomes distributed throughout the cytoplasm. However, under certain conditions such as an abortive infection in L cells (4), virus growth in the presence of p-fluorophenylalanine (FPA) (21) or infection with von Magnus-type incomplete virus (16), NP antigen remains in the nucleus throughout the infection. The mechanism by which NP antigen remains in the nucleus is not yet clear,

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The inhibition of influenza virus RNA synthesis by actinomycin D and cycloheximide

Cited by 64 publications

References 13 publications

Inhibition of Pichinde Virus Replication by Actinomycin D

Inhibition of Pichinde Virus Replication by Actinomycin D

Involvement of Influenza Virus PA Subunit in Assembly of Functional RNA Polymerase Complexes

Analysis of Nuclear Accumulation of Influenza Nucleoprotein Antigen in the Presence of p‐Fluorophenylalanine

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