Decreased interferon sensitivity and production in cells transformed by sv40 and other oncogenic agents

Brailovsky, Carlos; Berman, Leonard D.; Chany, C

doi:10.1002/ijc.2910040209

Cited by 18 publications

(11 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…As part of these studies, we also examined another HEL-TERT derivative cell line that expresses SV40 large Tag (hereafter named HEL-TERT-T). SV40 large Tag is known to alter the IFN-response [63]. From this experiment, HEL-TERT-T cells appeared to have an altered cellular morphology, with the cells decreasing in length and broadening in width.…”

Section: Resultsmentioning

confidence: 77%

hTERT Extends the Life of Human Fibroblasts without Compromising Type I Interferon Signaling

et al. 2013

View full text Add to dashboard Cite

Primary cells are often used to study viral replication and host-virus interactions as their antiviral pathways have not been altered or inactivated; however, their use is restricted by their short lifespan. Conventional methods to extend the life of primary cultures typically utilize viral oncogenes. Many of these oncogenes, however, perturb or inactivate cellular antiviral pathways, including the interferon (IFN) response. It has been previously shown that expression of the telomerase reverse transcriptase (TERT) gene extends the life of certain cell types. The effect that TERT expression has on the innate antiviral response to RNA- and DNA-containing viruses has not been examined. In the current study, we introduced the human TERT (hTERT) gene into a primary human embryonic lung (HEL-299) cell strain, which is known to respond to the type I IFN, IFN-β. We show that the resulting HEL-TERT cell line is capable of replicating beyond 100 population doublings without exhibiting signs of senescence. Treatment with IFN-β resulted in the upregulation of four model IFN stimulated genes (ISGs) in HEL-299 and HEL-TERT cells. Both cell lines supported the replication of herpes simplex virus type 1 (HSV-1) and vesicular stomatitis virus (VSV) and impaired the replication of both viruses upon IFN-β pretreatment. Introduction of the viral oncoprotein, simian virus 40 (SV40) large T-antigen, which is frequently used to immortalize cells, largely negated this effect. Taken together, our data indicate that expression of hTERT does not alter type 1 IFN signaling and/or the growth of two viruses, making this cell line a useful reagent for studying viral replication and virus-cell interactions.

show abstract

Section: Resultsmentioning

confidence: 77%

hTERT Extends the Life of Human Fibroblasts without Compromising Type I Interferon Signaling

et al. 2013

View full text Add to dashboard Cite

show abstract

“…However, it is apparent that high multiplicities of infection are required. In a previous study, cells rendered neoplastic were shown to exhibit decreased sensitivity to and production of interferon (1). It is known that adenovirus 12 enhances the growth of the Kilham (K) rat virus (26).…”

Section: Discussionmentioning

confidence: 99%

“…The VSV plaque assay is described in a previous report (1). Titrations with EMC and vaeeinia were carried out in a similar manner, except that EMC plaques were routinely read 24--30 hours after infection, and vaccinia plaques 70--80 hours post infection.…”

Section: Viral Assaysmentioning

confidence: 99%

See 1 more Smart Citation

Stimulatory and inhibitory effects of adenovirus and SV 40 on various virus-cell systems

Berman

Chany

1970

Archiv f Virusforschung

Self Cite

View full text Add to dashboard Cite

Infection of mouse, rat, hamster, or chicken cells with adenovirus types 5 and 12, or SV40, caused inhibition of subsequent challenge with VSV, EMC and vaccinia viruses. This effect was most marked with adenovirus on mouse cells, where a transitory phase of stimulation was frequently demonstrated immediately after adenovirus infection. The inhibitory phase usually commenced 2--6 hours after infection and depended on infection with intact virions, although the intact adenovirus genome was not necessary. Binding of virus by antiserum did not prevent the inhibition, and inhibition could not be explained by differences in adsorption, interferon production, chromosome breakage, or the effect of soluble capsid antigens. After transformation with SV40, mouse ceils showed increased VSV sensitivity in distinction to acutely infected cells in which the challenge virus was inhibited. The implications of these studies in the evolution of the transformation process are discussed.

show abstract

“…On peut donc definir dans notre systkme I'interaction stinlulante entre deux virus de la f a~o n suivante: I'infection simultanCe ou successive d'une cellule par deux virus antigkniquement distincts conduit A la stimulation de la multiplication du virus rCvClateur par le virus inducteur. De plus, on a note que des cellules de rat infectkes par le virus SV40, perdaient progressivement pendant le cours de la transformation leur sensibilitt ii l'interferon et parallt5lement leur capacitt productrice d'interferon (5). A partir des extraits de ces cellules transformees et aussi de cellules de hamster transformees par le virus SV40, nous avons pu mettre en evidence un facteur que nous avons appele "stimulon" (4) capable de stimuler la replication du virus K du rat.…”

Section: Introductionunclassified

Etudes sur l'action anti-interféron des extraits de cellules transformées par le virus SV40

Brodeur¹,

Légaré²,

Brailovsky³

1973

Can. J. Microbiol.

Self Cite

View full text Add to dashboard Cite

From extracts of a hamster cell line transformed by the Simian virus 40, we have shown the presence of a factor that stimulates the replication of K virus and also counteracts the mechanism of action of interferon. The sensitivity of this factor to a proteolytic enzyme is a possible indication that we are dealing with a protein. This "stimulon" is unrelated to the T antigen as shown by chromatography on Sephadex G-100 and by complement fixation test. Furthermore, at 56 °C, all direct effects on virus K replication are lost but the anti-interferon activity is preserved.

show abstract

Decreased interferon sensitivity and production in cells transformed by sv40 and other oncogenic agents

Abstract: From a pool of primary rat embryo fibroblast cells, three lines-two

Cited by 18 publications

References 23 publications

hTERT Extends the Life of Human Fibroblasts without Compromising Type I Interferon Signaling

hTERT Extends the Life of Human Fibroblasts without Compromising Type I Interferon Signaling

Stimulatory and inhibitory effects of adenovirus and SV 40 on various virus-cell systems

Etudes sur l'action anti-interféron des extraits de cellules transformées par le virus SV40

Contact Info

Product

Resources

About