Intrinsic Interference: a New Type of Viral Interference

Marcus, Philip I.; Carver, David H.

doi:10.1128/jvi.1.2.334-343.1967

Cited by 64 publications

(25 citation statements)

References 18 publications

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“…2). This linear rate is approximately the same as that seen for Sindbis virus-induced intrinsic interference with NDV replication (14,18,29).…”

Section: Characterization Of Interference Inductionsupporting

confidence: 64%

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Mechanism of Sindbis Virus-Induced Intrinsic Interference with Vesicular Stomatitis Virus Replication

Hunt

Marcus

1974

J Virol

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Heterologous viral interference is induced by Sindbis virus against vesicular stomatitis virus (VSV) in a manner analogous to intrinsic interference with Newcastle disease virus replication. Interference in both systems (i) depends upon early expression of the inducing virus genome, (ii) shows similar kinetics of induction, (iii) does not involve interferon action, and (iv) appears to be manifest as an all-or-none effect. VSV can be added to the list of viruses blocked by intrinsic interference. Sindbis virus-induced intrinsic interference with VSV replication is not mediated through homotypic interference by defective interfering particles; rather, T-particle and B-particle synthesis is inhibited. Significantly, intrinsic interference has no effect on primary transcription directed by the virion-associated transcriptase in VSV-challenged cells. However, Sindbis virus appears to induce interference with the VSV-RNA synthesized subsequent to primary transcription, namely, that which is dependent on protein synthesis. Thus, the target of intrinsic interference appears to be a reaction subsequent to primary transcription but prior to the appearance of protein synthesis-dependent VSV RNA, secondary transcription.Virion-associated RNA transcriptases are presumably the first viral enzymes to function in the replication of negative-strand viruses (1). In addition, development of an interferonmediated antiviral state in cells correlates quantitatively with the inhibition of vesicular stomatitis virus (VSV) virion transcriptase activity (13, 15). The virion transcriptase of VSV thus appears to be a target of interferonmediated interference with replication of this virus. In contrast, interference with VSV replication by defective interfering particles of VSV, homotypic interference, does not affect the synthesis of VSV RNA by the virion-associated transcriptase (11). We have characterized, and describe herein, yet a third type of interference in which VSV transcriptase activity can be measured, viz., interference with VSV replication induced by Sindbis virus. Our results show that this heterotypic interference system is analogous to that described by Marcus and Carver (14) as intrinsic interference.In the absence of an assay for cells refractory to infection by VSV comparable to that used in the hemadsorption-negative plaque or cell test for viruses inducing intrinsic interference against Newcastle disease virus (NDV), inter-'Present address:

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“…2). This linear rate is approximately the same as that seen for Sindbis virus-induced intrinsic interference with NDV replication (14,18,29).…”

Section: Characterization Of Interference Inductionsupporting

confidence: 64%

“…To facilitate comparison of the results just presented with induction of intrinsic interference in the Sindbis-NDV system (14), a linear ordinate scale was used (percent inhibition of VSV PFP yield) (Fig. 2).…”

Section: Characterization Of Interference Inductionmentioning

confidence: 99%

Mechanism of Sindbis Virus-Induced Intrinsic Interference with Vesicular Stomatitis Virus Replication

Hunt

Marcus

1974

J Virol

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“…Initially it was observed in Newcastle disease virus (NDV) superinfection where the refractory state against NDV emerged exclusively in cells that experienced prior viral infection. The effect was due to molecules encoded by the virus (viral genome/proteins) and not to the intrinsic capacity of cells (138). Later this was also observed in FMDV, where the attenuated A24 Cruzeiro strain interfered with the multiplication of a homologous wild-type strain as well as that of heterologous wild-type strains.…”

Section: Viral Interference (Competitive Suppression)mentioning

confidence: 88%

Virological and Immunological Outcomes of Coinfections

et al. 2018

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SUMMARYCoinfections involving viruses are being recognized to influence the disease pattern that occurs relative to that with single infection. Classically, we usually think of a clinical syndrome as the consequence of infection by a single virus that is isolated from clinical specimens. However, this biased laboratory approach omits detection of additional agents that could be contributing to the clinical outcome, including novel agents not usually considered pathogens. The presence of an additional agent may also interfere with the targeted isolation of a known virus. Viral interference, a phenomenon where one virus competitively suppresses replication of other coinfecting viruses, is the most common outcome of viral coinfections. In addition, coinfections can modulate virus virulence and cell death, thereby altering disease severity and epidemiology. Immunity to primary virus infection can also modulate immune responses to subsequent secondary infections. In this review, various virological mechanisms that determine viral persistence/exclusion during coinfections are discussed, and insights into the isolation/detection of multiple viruses are provided. We also discuss features of heterologous infections that impact the pattern of immune responsiveness that develops.

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“…RubeUa.--Rubefla virus, strain F-8, was obtained from Dr. P. I. Marcus (6). It was passaged three times in the Veto line of Mrican green monkey kidney cells (Microbiological Associates, Inc., Bethesda, Md.)…”

Section: Methodsmentioning

confidence: 99%

“…before it was used to infect synovial cultures. Rubella virus was detected and titered by means of the hemadsorption-negative particle assay of Marcus and Carver (6,7), using a strain of human fibroblasts grown from pleura. The input multiplicity of infection was 1-3 hemadsorption-negative microplaque-forming units per cell, unless otherwise stated.…”

Section: Methodsmentioning

confidence: 99%

Rubella Infection of Synovial Cells and the Resistance of Cells Derived From Patients With Rheumatoid Arthritis

Grayzel¹,

Beck²

1970

The Journal of Experimental Medicine

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The mechanism of growth stimulation in allogeneic lymphocytes mixed in vitro was studied at the cell level by means of cytophotometric techniques. A pronounced increase in fluorescence intensity of fixed and acridine orange (AO) stained lymphocytes was observed as soon as after 1–3 hr in mixed culture. No increase in the amount of DNA took place during this time. The higher fluorescence intensity was due to an increased accessibility of AO binding sites in the deoxyribonucleoprotein (DNP) complex, most probably as a result of weakened bonds between the DNA and the protein moiety in the DNP complex. Similar DNP changes have been found in other systems of growth stimulation and may be one prerequisite for later induction of cellular synthetic processes. Increased AO binding only occurred when the lymphocyte donors were incompatible at the major histocompatibility locus (HL-A); there was no change in AO binding in cases of HL-A identity. The AO binding reaction probably reflects a specific recognition of HL-A antigens, whereas other antigenic discrepancies between the individuals do not seem to cause an analogous response.

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Intrinsic Interference: a New Type of Viral Interference

Cited by 64 publications

References 18 publications

Mechanism of Sindbis Virus-Induced Intrinsic Interference with Vesicular Stomatitis Virus Replication

Mechanism of Sindbis Virus-Induced Intrinsic Interference with Vesicular Stomatitis Virus Replication

Virological and Immunological Outcomes of Coinfections

Rubella Infection of Synovial Cells and the Resistance of Cells Derived From Patients With Rheumatoid Arthritis

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