RNA synthesis in poliovirus-infected cells

Zimmerman, Ernest F.; Heeter, Margaret; Darnell, James

doi:10.1016/0042-6822(63)90080-1

Cited by 166 publications

(46 citation statements)

References 19 publications

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“…Influenza viruses are an obvious exception, since they replicate in the nucleus of the host cell and require newly synthesized host transcripts for generation of the capped oligonucleotides used as primers for viral mRNA synthesis. For many members of other RNA virus families, such as picornaviruses and rhabdoviruses, the inhibition of host RNA synthesis is a prominent feature of virus infection that has been recognized for many years (6,61,132,139,148). For poliovirus, the prototype picornavirus, and vesicular stomatitis virus (VSV), the prototype rhabdovirus, substantial progress has been made in identifying the viral gene products responsible for the inhibition of host transcription and their molecular targets in the host cell.…”

Section: Inhibition Of Host Transcriptonmentioning

confidence: 99%

Cytopathogenesis and Inhibition of Host Gene Expression by RNA Viruses

Lyles

2000

Microbiol Mol Biol Rev

163

139

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SUMMARY Many viruses interfere with host cell function in ways that are harmful or pathological. This often results in changes in cell morphology referred to as cytopathic effects. However, pathogenesis of virus infections also involves inhibition of host cell gene expression. Thus the term “cytopathogenesis,” or pathogenesis at the cellular level, is meant to be broader than the term “cytopathic effects” and includes other cellular changes that contribute to viral pathogenesis in addition to those changes that are visible at the microscopic level. The goal of this review is to place recent work on the inhibition of host gene expression by RNA viruses in the context of the pathogenesis of virus infections. Three different RNA virus families, picornaviruses, influenza viruses, and rhabdoviruses, are used to illustrate common principles involved in cytopathogenesis. These examples were chosen because viral gene products responsible for inhibiting host gene expression have been identified, as have some of the molecular targets of the host. The argument is made that the role of the virus-induced inhibition of host gene expression is to inhibit the host antiviral response, such as the response to double-stranded RNA. Viral cytopathogenesis is presented as a balance between the host antiviral response and the ability of viruses to inhibit that response through the overall inhibition of host gene expression. This balance is a major determinant of viral tissue tropism in infections of intact animals.

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Section: Inhibition Of Host Transcriptonmentioning

confidence: 99%

Cytopathogenesis and Inhibition of Host Gene Expression by RNA Viruses

Lyles

2000

Microbiol Mol Biol Rev

163

139

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“…Pol III transcription of transiently transfected tRNA genes is increased in cells infected with adenovirus (19,20) and in cells expressing the pseudorabies virus immediate early protein (20). In contrast, poliovirus infection substantially decreases pol III transcription of cellular genes (21). The activities of extracts prepared from virus-infected cells reflect these types of regulation when assayed in vitro.…”

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confidence: 99%

Human transcription factor IIIC box B bindingsubunit.

L’Étoile

Fahnestock

Shen

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Transcription factor HIC (TFIC) is a multisubut basic TF for RNA polymerase m. It initiates transcriptin complex assembly on tRNA and related genes by binding to the internal box B promoter element and is also required for transcription ofSS rRNA In contrast to the yeast system, activities in a partially purified human TFIIIC fraction required for tRNA transcription separate into two components called TFIIIC1 and TF-IIIC2 (11). RNA pol III TFs from Bombxy mori also resolve into several components including two activities separated from a partially purified TFIIIC fraction called TFIIIC and TRIIID (12). The human TFIIIC2 fraction most closely resembles yeast TFIIIC in that it also binds to the box B promoter element with high affinity (11,13,14), can stably sequester a template (15), and is a multisubunit protein composed of five copurifying polypeptides of 230, 110, 100, 80, and 60 kDa (14,16,17). In both the yeast and human systems, the largest polypeptide can be specifically crosslinked to box B DNA (13,(16)(17)(18). Because the protein we have referred to as TFIIIC2 (16) 1652The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…Infection of HeLa cells with poliovirus, for example, causes a dramatic decrease in total cellular transcription within 3 h of infection (7,16,29). Transcription mediated by each of the three polymerase systems (RNA polymerases [pol] I, II, and III) is affected.…”

mentioning

confidence: 99%

An RNA polymerase II transcription factor inactivated in poliovirus-infected cells copurifies with transcription factor TFIID.

Kliewer

Dasgupta

1988

Mol. Cell. Biol.

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Inhibition of host cell RNA polymerase II-mediated transcription by poliovirus infection was studied in vitro. Whole-cell extracts prepared from poliovirus-infected HeLa cells at 3 h postinfection were shown to be deficient in a factor required for specific transcription from the adenovirus major late promoter. Three lines of evidence suggest that transcription factor TFIID is deficient in poliovirus-infected cells. First, the activity required to specifically restore transcription in poliovirus-infected cell extracts was shown to copurify with TFIID through three chromatographic steps. Second, transcription reactions reconstituted with phosphocellulose-derived chromatographic fractions revealed a fourfold decrease in the specific activity of the TFIID-containing fraction prepared from poliovirus-infected cells compared with that of the same fraction prepared from mock-infected cells. Finally, TFIID and the activity required to specifically restore transcription in virus-infected cell extracts were shown to have the same kinetics of heat inactivation. Together, these results suggest that inactivation of TFIID is an early event in the inhibition of host cell RNA polymerase II transcription by poliovirus.Infection of mammalian cells with picornaviruses results in the inhibition of host cell RNA synthesis (2,3,17). Infection of HeLa cells with poliovirus, for example, causes a dramatic decrease in total cellular transcription within 3 h of infection (7,16,29). Transcription mediated by each of the three polymerase systems (RNA polymerases [pol] I, II, and III) is affected.Early attempts to elucidate the mechanism of picornavirus-induced inhibition of host cell transcription focused on the polymerases. RNA pol I, II, and III solubilized from infected-cell extracts, however, were shown to be fully active when assayed under conditions requiring only nonspecific initiation (27). Furthermore, no differences were observed in the chromatographic properties of partially purified RNA polymerases prepared from infected and uninfected cells (1, 27). Finally, two-dimensional gel electrophoresis revealed no differences in the subunit structure of RNA pol II isolated from infected and uninfected cells (1). These results suggested that a transcriptional component other than the elongating polymerase was inactivated by picornavirus infection.Crawford et al. first showed that the poliovirus-induced inhibition of transcription observed in vivo could be studied in vitro (7). In contrast to mock-infected cell extracts, poliovirus-infected cell extracts prepared 3 h postinfection were unable to support RNA pol II-mediated transcription from the adenovirus type 2 (Ad2) major late promoter (MLP). Addition of purified RNA pol II to poliovirusinfected cell extracts failed to restore transcription. However, pol II transcription in infected-cell extracts was restored by the addition of an S100 extract containing transcription factors. When the S100 extract was fractionated by chromatography on phosphocellulose, the restoring activity eluted ...

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RNA synthesis in poliovirus-infected cells

Cited by 166 publications

References 19 publications

Cytopathogenesis and Inhibition of Host Gene Expression by RNA Viruses

Cytopathogenesis and Inhibition of Host Gene Expression by RNA Viruses

Human transcription factor IIIC box B bindingsubunit.

An RNA polymerase II transcription factor inactivated in poliovirus-infected cells copurifies with transcription factor TFIID.

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