Interference between enteroviruses and conditions effecting its reversal

Cords, Carl E.; Holland, John J.

doi:10.1016/0042-6822(64)90007-8

Cited by 47 publications

(16 citation statements)

References 15 publications

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“…on the relative multiplicity of each virus used and the time when the second virus is added. This is in agreement with other reports on mixed infection experiments between enteroviruses (Cords & Holland, 1964) The effect of different monovalent ion concentrations in the culture medium of cells double-infected with EMC virus and poliovirus indicated that virus protein synthesis in these two viruses responds in a different way. In EMC virus-infected HeLa cells, a hypotonic medium inhibited virus protein synthesis, whereas some poliovirus translation took place under these conditions.…”

Section: Translation In Double-infected Cellssupporting

confidence: 82%

“…Early studies of mutual interference with different picornaviruses of the genus Enterovirus lead to the hypothesis that interference is due to a competition between the two viruses for metabolites or replicating sites (Cords & Holland, 1964). These results also indicated that the extent of the interference is dependent on the ratio of multiplicities of infection used and the time of challenge of the second virus (Cords & Holland, 1964).…”

Section: Introductionmentioning

confidence: 54%

“…These results also indicated that the extent of the interference is dependent on the ratio of multiplicities of infection used and the time of challenge of the second virus (Cords & Holland, 1964).…”

Section: Introductionmentioning

confidence: 61%

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Protein Synthesis in HeLa Cells Double-infected with Encephalomyocarditis Virus and Poliovirus

Alonso

Carrasco

1982

Journal of General Virology

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SUMMARYThe pattern of host, encephalomyocarditis (EMC) virus and poliovirus protein synthesis in HeLa cells double-infected with EMC virus and poliovirus has been examined. Both picornaviruses were able to block host translation after infection, although with different degrees of efficiency. In co-infection experiments, the inhibition of poliovirus protein synthesis by EMC virus and vice versa depended on the relative multiplicities of infection of each virus used. Under some conditions, double-infected HeLa cells simultaneously synthesized poliovirus and EMC virus proteins. In superinfection experiments, when the two viruses were added at different times, the pattern of the proteins synthesized depended on the time of addition of the second virus challenge. Poliovirus did not replicate when added 4 h after EMC virus. On the other hand, EMC virus replication was inhibited in cells preinfected with poliovirus. If co-infected cells were treated with guanidine from the beginning of the infection, only the synthesis of EMC virus proteins was apparent. However, if poliovirus was allowed to replicate for 4 h before guanidine addition, then the synthesis of EMC virus proteins was reduced, even though the translation of poliovirus mRNA was very much inhibited. EMC virus-infected HeLa cells exclusively synthesized cellular proteins in hypotonic media, whereas under hypertonic conditions only virus protein synthesis took place. In poliovirus-infected HeLa cells no cellular translation was detected under all ionic conditions tested. The ionic optimum of EMC virus and poliovirus protein synthesis was also different in cells infected with a single virus. However, in double-infected cells the monovalent ion optimum for translation of EMC virus and poliovirus mRNA was the same, although EMC virus protein synthesis was more resistant to inhibition by hypertonic media. No cellular protein synthesis was detected in double-infected HeLa cells under all the ionic conditions tested.

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Section: Translation In Double-infected Cellssupporting

confidence: 82%

Section: Introductionmentioning

confidence: 54%

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Protein Synthesis in HeLa Cells Double-infected with Encephalomyocarditis Virus and Poliovirus

Alonso

Carrasco

1982

Journal of General Virology

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“…The possible existence of limiting replication sites was discussed in earlier work (17), in which competition for such putative sites was considered to be an explanation for the interference of two viruses in double-infected cells. The view that preferential start sites for viral RNA replication exist is also supported by previous observations on the location of COPII-mediated vesicle formation in PV-infected and uninfected cells (48).…”

Section: Discussionmentioning

confidence: 99%

Recombination of Poliovirus RNA Proceeds in Mixed Replication Complexes Originating from Distinct Replication Start Sites

Egger

Bienz

2002

J Virol

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Genetic recombination occurs frequently during replication of picornaviruses. To explore the intracellular site and structures involved in recombination, HeLa cells were infected with poliovirus type 1 Mahoney and type 2 Sabin. The two genomes were located by fluorescent in situ hybridization and confocal microscopy. For hybridization, type-specific fluorescent riboprobes were used to visualize the same genomic region where, in parallel, recombination was demonstrated with type-specific reverse transcription-PCR and sequencing. The hybridization analysis indicated that >85% of the replication complexes contained both type 1 and type 2 RNA sequences aligned at a lateral distance of 50 nm or less. Sequential infection of cells ruled out the possibility that the high percentage of mixed replication complexes was due to aggregation of input virus. Visualization of input genomic RNA over time showed that the viral genomes migrated to relatively few distinct, and thus presumably specific, perinuclear sites where replication started. The first recombinant RNA strands could be detected concomitantly with the onset of RNA replication. The limited number of start sites for replication may be the reason for the observed preferential formation of mixed replication complexes, each accommodating several parental RNA strands and thus allowing recombination.Poliovirus (PV), the prototype member of the family Picornaviridae, represents in many respects the paradigm for research on other plus-strand RNA viruses. Among the fundamental insights gained by PV research is the first discovery of recombination between viral RNA genomes (30, 35). Since then, some light has been thrown on mechanistic aspects of recombination (for a review see references 1 and 57); however, it is not clear in which context of the elaborate structures comprising the viral RNA replication machinery, i.e., the replication complex (4,6,9,12,21,22,51,52), recombination can occur.PV RNA replication is preceded by translation of the incoming viral genome. Translation, initiated at the internal ribosomal entry site (IRES) (42, 43), was reported to be enhanced by binding of the cellular poly(rC) binding protein (PCBP) to the IRES (10,11,25) and, additionally at early stages, by an interaction of eIF4G with the IRES and the poly(A)-bound poly(A) binding protein (PABP) (50). A transition from translation to transcription was thought to be mediated by the newly synthesized viral protein 3CD, which, together with PCBP, binds to the 5Ј cloverleaf of the viral mRNA (23,24,39). Poly(A)-bound PABP then would attach to this complex, leading (again) to a 5Ј-3Ј interaction in the viral plus-strand RNA (29). This interaction was proposed to be a prerequisite for minus-strand RNA synthesis, the first step in genome replication (3,29,53). The second step in viral genome replication is plus-strand RNA synthesis, which proceeds, after multiple initiations, in the partially doublestranded replicative intermediate. The primer for RNA synthesis is VPgpUpU (41), which was found to be ...

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“…It is presently difficult to determine which of the early reports on viral interference were concerned with interferon production by the host or by other factors. It is apparent, however, that there are several types of viral interference that do not involve the mediation of interferon (5,7,12,(15)(16)(17) Cell cultures. Cell cultures were prepared from 10-day-old chick embryos.…”

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confidence: 99%

Interference Among Group a Arboviruses

Zebovitz¹,

Brown²

1967

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Interference among group A arboviruses is described which does not involve the mediation of interferon. Interference was observed only if the interfering virus had an advantage over the challenge virus, either in time or in multiplicity of infection. Adsorption, penetration, and uncoating of challenge virus did not appear to be inhibited, but the synthesis of infectious viral ribonucleic acid of the challenge virus was significantly retarded. It was shown with temperature-sensitive viruses or mutants that the replication of viral ribonucleic acid by the interfering virus was required to establish interference. A mechanism of interference based on a competition for replication sites or substrates is compared with other possible explanations.The practical and theoretical implications of viral interference have stimulated considerable interest in this research area. Many reports have been published since the discovery of interference in plant viruses (14) and in animal viruses (11). Those papers that appeared prior to the discovery of interferon (13) have been reviewed extensively by Henle (10) and Schlesinger (18). The role of interferon as an important factor in the development of nonspecific resistance of the host cells to superinfection with a second related or unrelated virus is now firmly established (6). It is presently difficult to determine which of the early reports on viral interference were concerned with interferon production by the host or by other factors. It is apparent, however, that there are several types of viral interference that do not involve the mediation of interferon (5,7,12,(15)(16)(17) Cell cultures. Cell cultures were prepared from 10-day-old chick embryos. The chick embryo (CE) monolayers were grown, in lactalbumin hydrolysate medium containing 10% calf serum, for 24 hr at 37 C before infection. Details of the preparation of monolayers, medium, and growth conditions were described in an earlier paper (22).Virus growth. Except where noted, CE cell monolayers in 60-mm plastic petri dishes were infected with a virus seed prepared as a 10% CE seed, or as undiluted tissue culture fluids obtained from infected CE monolayers. The virus was allowed to adsorb for 15 min at room temperature; the cells were washed twice with phosphate-buffered saline (PBS) at pH 7.4 to remove excess unattached virus, and were overlayered with 5 ml of lactalbumin hydrolysate medium containing 10% calf serum. The cultures were incubated at 37 C in a 5% C02-95% air incubator.When the interfering and challenge virus were simultaneously added to CE monolayers, the virus seeds were mixed before infection of the cells. When the challenge virus was added at some time after infection of the cells with the interfering virus, the culture medium was removed, the challenge virus was added, and, after a 15-min adsorption period at room temperature, the infected cells were washed twice with PBS and overlayered with the lactalbumin hydrolysate medium. The cultures were reincubated at 37 C and samples of the culture medium were ...

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Interference between enteroviruses and conditions effecting its reversal

Cited by 47 publications

References 15 publications

Protein Synthesis in HeLa Cells Double-infected with Encephalomyocarditis Virus and Poliovirus

Protein Synthesis in HeLa Cells Double-infected with Encephalomyocarditis Virus and Poliovirus

Recombination of Poliovirus RNA Proceeds in Mixed Replication Complexes Originating from Distinct Replication Start Sites

Interference Among Group a Arboviruses

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