Role of Interferon in Six Cell Lines Persistently Infected with Rubella Virus

Stanwick, Trevor L.; Hallum, Jules V.

doi:10.1128/iai.10.4.810-815.1974

Cited by 30 publications

(8 citation statements)

References 26 publications

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“…Thus, the IFN response counteracts, but does not eliminate, virus in the infected culture. Similar conclusions were drawn in previous studies of RUB infection in several IFN-competent anddeficient cell lines (Mifune et al, 1970;Stanwick and Hallum, 1974;Wong et al, 1967).…”

Section: Discussionsupporting

confidence: 91%

Analysis of gene expression in fetal and adult cells infected with rubella virus

2008

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Congenital infection with rubella virus (RUB) leads to persistent infection and congenital defects and we showed previously that primary human fetal fibroblasts did not undergo apoptosis when infected with RUB, which could promote fetal virus persistence [Adamo, P., Asís, L., Silveyra, P., Cuffini, C., Pedranti, M., Zapata, M., 2004. Rubella virus does not induce apoptosis in primary human embryo fibroblasts cultures: a possible way of viral persistence in congenital infection. Viral Immunol. 17, 87-100]. To extend this observation, gene chip analysis was performed on a line of primary human fetal fibroblasts (10 weeks gestation) and a line of human adult lung fibroblasts (which underwent apoptosis in response to RUB infection) to compare gene expression in infected and uninfected cells. A total of 632 and 516 genes were upregulated or downregulated in the infected fetal and adult cells respectively in comparison to uninfected cells, however only 52 genes were regulated in both cell types. Although the regulated genes were different, across functional gene categories the patterns of gene regulation were similar. In general, regulation of pro- and anti-apoptotic genes following infection appeared to favor apoptosis in the adult cells and lack of apoptosis in the fetal cells, however there was a greater relative expression of anti-apoptotic genes and reduced expression of pro-apoptotic genes in uninfected fetal cells versus uninfected adult cells and thus the lack of apoptosis in fetal cells following RUB infection was also due to the prevailing background of gene expression that is antagonistic to apoptosis. In support of this hypothesis, it was found that of a battery of five chemicals known to induce apoptosis, two induced apoptosis in the adult cells, but not in fetal cells, and two induced apoptosis more rapidly in the adult cells than in fetal cells (the fifth did not induce apoptosis in either). A robust interferon-stimulated gene response was induced following infection of both fetal and adult cells and many of the genes upregulated in both cell types were those involved in establishment of an antiviral state; this is the first demonstration of an interferon response at this early stage of human embryonic development. In both fetal and adult cells, interferon controlled but did not eliminate virus spread and apoptosis was not induced in infected fetal cells in the absence of interferon. In addition to the interferon response, chemokines were induced in both infected fetal and adult cells. Thus, it is possible that fetal damage following congenital RUB infection, which involves cell proliferation and differentiation, could be due to induction of the innate immune response as well as frank virus infection.

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Section: Discussionsupporting

confidence: 91%

Analysis of gene expression in fetal and adult cells infected with rubella virus

2008

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“…However, it is difficult to invoke the interferon mechanism in the case of cell lines which are defective IF producers. Despite this deficiency, these cell lines (Vero or BHK-21) have been persistently infected with a variety of viruses (14,15,17). It seems likely that a multiplicity of factors acting in concert or individually may be responsible for the establishment and maintenance of persistent infections with a variety of viruses in different cell lines.…”

Section: Discussionmentioning

confidence: 99%

Persistent Infection of L Cells with Vesicular Stomatitis Virus: Evolution of Virus Populations

Youngner

Preble

Jones

1978

J Virol

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A previous report (Youngner et al., J. Virol. 19:90-101, 1976) documented that noncytocidal persistent infection can be established with wild-type vesicular stomatitis virus (VSV) in mouse L cells at 37°C and that a rapid selection of RNA-, group I temperature-sensitive (ts) mutants consistently occurs in this system. To assess the selective advantage of the RNAts phenotype, evolution of the virus population was studied in persistent infections initiated in L cells by use of VSV ts 0 23 and ts 0 45, RNA' mutants belonging to complementation groups III and V. In L cells persistently infected with ts 0 23, the ts RNA' virus population was replaced gradually by viruses which had a ts RNAphenotype. VSV ts 0 45 (V) has another marker in addition to reduced virus yield at 39.5°C: a defective protein (G) which renders virion infectivity heat labile at 50°C. Persistent infections initiated with this virus (ts, heat labile, RNA') evolved into

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“…Unlike alphaviruses however, RV infection in cultured cells is characterized by relatively long latency periods, slow replication, and limited cytopathology. As well as being able to establish persistent infections in all cell lines tested (Cunningham and Fraser, 1985;Norval, 1979;Stanwick and Hallum, 1974), RV is known to persist in viva in humans after congenital and postnatal infections (Cooper and Buimovici-Kein, 1985). Moreover initiation of a persistent infection in cultured cells by RV is not dependent upon the presence of defective-interfering particles (Frey and Hemphill.…”

Section: Introductionmentioning

confidence: 99%

Processing and intracellular transport of rubella virus structural proteins in COS cells

1990

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Plasmids encoding rubella virus (RV) structural proteins C-E2-E1, E2-E1, E2, and E1 have been constructed in the eukaryotic expression vector pCMV5. The processing and intracellular transport of these proteins have been examined by transient expression of the cDNAs in COS cells. Compared to alphaviruses, processing of RV glycoprotein moieties occurred relatively slowly and the transport of glycoproteins E2 and E1 to the plasma membrane was inefficient. Indirect immunofluorescence revealed that the majority of RV antigen in transfected and infected COS cells was localized to the Golgi region, including the capsid protein. Accumulation of capsid protein in the juxtanuclear region was determined to be RV glycoprotein dependent. Unlike alphaviruses, RV E1 did not require E2 for targeting to the Golgi where it was retained. E2 was however necessary for cell surface expression of E1. This study revealed that the processing and transport of RV structural proteins is quite different from alphaviruses and that the accumulation of antigens in the Golgi region may be significant in light of previous reports which suggest that RV buds from the internal membranes in some cell types.

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Role of Interferon in Six Cell Lines Persistently Infected with Rubella Virus

Cited by 30 publications

References 26 publications

Analysis of gene expression in fetal and adult cells infected with rubella virus

Analysis of gene expression in fetal and adult cells infected with rubella virus

Persistent Infection of L Cells with Vesicular Stomatitis Virus: Evolution of Virus Populations

Processing and intracellular transport of rubella virus structural proteins in COS cells

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