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

Hunt, John; Marcus, Philip I.

doi:10.1128/jvi.14.1.99-109.1974

Cited by 18 publications

(5 citation statements)

References 27 publications

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“…If one increases the multiplicity of infection to 10 or more with EMC and reovirus, the cells do not form colonies. The fact that the cells are resistant to a wide range of viruses suggests that we are observing an interference similar to the intrinsic interference described by Marcus and co-workers (9).…”

Section: Characteristics Of the Persistent Infectionsupporting

confidence: 75%

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Persistent reovirus infection of CHO cells resulting in virus resistance

Taber¹,

Alexander²,

Whitford³

1976

J Virol

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We obtained a persistently infected line of Chinese hamster ovary cells by selection for resistance to reovirus infection. The cells were persistently infected by a population of viruses that were (i) cytopathic for parental chinese hamster ovary cells and (ii) similar to wild-type reovirus in molecular characteristics. The growth rate, plating efficiency, and morphology of the cells were altered. A large majority of the cells in the population were infected. There was no detectable interferon present in the medium. The cells were relatively resistant to a wide range of viruses. Cells can acquire resistance to virus infection by a number of mechanisms. The least understood of these are mechanisms that do not involve extracellular factors such as interferon and humoral antibodies (15, 24). To study mechanisms of intracellular resistance we have selected Chinese hamster ovary (CHO) cells that are resistant to reovirus. In this communication, we describe one such cell line (VRR) that is characterized by the constant presence of infectious reovirus in the media. Such persistent infections are well known in virology, primarily with viruses that are weakly cytopathic such as certain enveloped viruses (2, 5, 14, 17, 19, 22-24). The molecular nature of such infections is poorly understood. We believe that this cell line is a unique manifestation of a reovirus infection and that the further study of such an infection with a virus whose molecular biology is extremely well characterized (11) should yield important information regarding the general phenomena of persistence. MATERIALS AND METHODS Cells. The parental cell line was CHO-KI (CCL 61) obtained from the American Type Culture Collection and periodically cloned (10). The cells are routinely maintained in Ham F-12 medium (6) buffered with 25 mM N-2-hydroxymethylpiperazine-N'2-ethanesulfonic acid (with a consequent reduction in NaH2CO, to maintain isotonicity) (Grand Island Biological Co.). This medium was supplemented with 10% fetal calf serum (Microbiological Associates). The cells are grown at 37 C in Forma water-jacketed incubators. Both CHO and VRR cells were periodically assayed for mycoplasma contamination by L. Hayflick.

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Section: Characteristics Of the Persistent Infectionsupporting

confidence: 75%

“…It is therefore unlikely that the resistance of the cells is due to a surface effect. A more likely explanation is that the resistance is due to an effect similar to the "intrinsic interference" described by Marcus and co-workers (9). This interference is characterized by a cellular state of refractoriness to heterologous virus.…”

Section: Discussionmentioning

confidence: 86%

Persistent reovirus infection of CHO cells resulting in virus resistance

Taber¹,

Alexander²,

Whitford³

1976

J Virol

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“…Titer (pfu/ml) was calculated according to the formula pfu/ml = 10 n −0.7 , where n = logTCID 50 /ml as originally described for vesicular stomatitis virus. 48 Assays were performed twice, in triplicate.…”

Section: Methodsmentioning

confidence: 99%

Vaccinia Virus Induces Programmed Necrosis in Ovarian Cancer Cells

et al. 2013

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The mechanisms by which oncolytic vaccinia virus induces tumor cell death are poorly understood. We have evaluated cell death pathways following infection of ovarian cancer cells with both wild-type and thymidine kinase-deleted (dTK) Lister strain vaccinia. We show that death does not rely upon classical apoptosis despite the appearances of some limited apoptotic features, including phosphatidylserine externalization and appearance of sub-G1 DNA populations. Vaccinia infection induces marked lipidation of LC3 proteins, but there is no general activation of the autophagic process and cell death does not rely upon autophagy induction. We show that vaccinia induces necrotic morphology on transmission electron microscopy, accompanied by marked by reductions in intracellular adenosine triphosphate, altered mitochondrial metabolism, and release of high mobility group box 1 (HMGB1) protein. This necrotic cell death appears regulated, as infection induces formation of a receptor interacting protein (RIP1)/caspase-8 complex. In addition, pharmacological inhibition of both RIP1 and substrates downstream of RIP1, including MLKL, significantly attenuate cell death. Blockade of TNF-α, however, does not alter virus efficacy, suggesting that necrosis does not result from autocrine cytokine release. Overall, these results show that, in ovarian cancer cells, vaccinia virus causes necrotic cell death that is mediated through a programmed series of events.

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“…The capacity to induce intrinsic interference was demonstrated with some other viruses (3, 7-9, 12, 13, 16), and the plaque test of this type has been applied to some noncytopathic viruses (1,13,16). In addition to NDV, VSV was also added to a virus group blocked by intrinsic interference (3,12). In this experiment, aimed at the development of a new plaque technique for the assay of HCV inducing heterologous interference, the RPF method represents a very simple, reliable, and sensitive procedure for determination of virus infectivity.…”

Section: Resultsmentioning

confidence: 99%

Reverse plaque formation by hog cholera virus of the GPE-strain inducing heterologous interference

Fukusho¹,

Ogawa²,

Yamamoto³

et al. 1976

Infect Immun

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A simple and rapid plaque procedure was developed for the assay of hog cholera virus (HCV) of a particular strain, GPE-, based on its intrinsic interference with vesicular stomatitis virus (VSV) on the primary swine testicle cells and on an established swine kidney cell line; the procedure is called the reverse plaque formation (RPF) method. The plaques were produced as colonies of HCV-infected cells which were VSV-sensitive, disintegrated cell sheet. These plaques became visible after 15 to 20 h of superinfection with VSV done 2 days after an initial inoculation of the GPE- strain. The plaque formation was inhibited by a specific antiserum against HCV. All cells within the plaque had HCV antigen detectable by fluorescent-antibody staining. The variations of reverse plaque count were low enough to permit virus titration. The relationship between virus concentration and the number of plaques was essentially linear. The titer measured by the RPF method was a little higher than that of the tube culture interference method.

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

Cited by 18 publications

References 27 publications

Persistent reovirus infection of CHO cells resulting in virus resistance

Persistent reovirus infection of CHO cells resulting in virus resistance

Vaccinia Virus Induces Programmed Necrosis in Ovarian Cancer Cells

Reverse plaque formation by hog cholera virus of the GPE-strain inducing heterologous interference

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