Transactivation of the Rous sarcoma virus long terminal repeat promoter by Marek's disease virus

Tieber, Virginia L.; Zalinskis, Lelda L.; Silva, Robert F.; Finkelstein, Ann; Coussens, Paul M.

doi:10.1016/0042-6822(90)90139-i

Cited by 33 publications

(15 citation statements)

References 43 publications

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“…It is also of interest that production of ALV in CEF has been shown to increase when accompanied by infection with the avian herpesvirus Marek's disease virus (MDV) (Pulaski et al, 1992). This increase was correlated with a concomitant increase in the level of RNA initiated from the ALV LTR promoter, suggesting that MDV may also encode or induce factors that act to increase transcription from the ALV LTR (Tieber et al, 1990).…”

Section: Discussionmentioning

confidence: 97%

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

1993

Journal of General Virology

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The level of RNA transcripts in human foreskin fibroblast (HFF) cells initiated from the avian sarcoma virus (ASV) long terminal repeat (LTR) promoter was stimulated more than 10-fold when the cells were also infected with human cytomegalovirus (HCMV). HCMV was able to stimulate transcription from the ASV LTR promoter even when all the LTR sequence upstream of the TATA box was deleted, suggesting that only the basal LTR promoter is required for the effect. There were no significant changes in the ASV RNA splicing pattern in stimulated and unstimulated HFF cells. The mRNAs showing an increase during HCMV stimulation included aberrantly spliced ASV RNA species as well as unspliced gag-pol, single-spliced env and single-spliced src mRNAs. This pattern was quite different from ASV splicing in chicken embryo fibroblasts (CEF) but typical of that seen in other mammalian cells. A dramatic increase in infectious ASV production from the normally non-permissive HFF was correlated with the increase in amount of ASV RNA in response to HCMV. Thus, there is not an absolute block to ASV production in human cells. However, infectious ASV production was inefficent in HCMV-stimulated HFF compared to that in CEF cells.

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Section: Discussionmentioning

confidence: 97%

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

1993

Journal of General Virology

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“…Based on the similarities of MDV to HSV and the cascade pattern of MDV gene expression (55), it seems likely that the MDV genome and the related HVT genome encode proteins capable of activating MDV and HVT promoters. Tieber et al (62) showed that MDV and HVT can transactivate the promoter region in the long terminal repeat (LTR) of Rous sarcoma virus. Furthermore, they reported that HVT can efficiently transactivate the ICP4 and beta-thymidine kinase gene promoters of HSV as well as the promoter of the IE gene of human cytomegalovirus.…”

Section: Marek's Disease (Md) Is a Highly Contagious Lymphoproliferatmentioning

confidence: 99%

Transactivation of Latent Marek's Disease Herpesvirus Genes in QT35, a Quail Fibroblast Cell Line, by Herpesvirus of Turkeys

Yamaguchi

Kaplan

Wakenell

et al. 2000

J Virol

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(62) showed that MDV and HVT can transactivate the promoter region in the long terminal repeat (LTR) of Rous sarcoma virus. Furthermore, they reported that HVT can efficiently transactivate the ICP4 and beta-thymidine kinase gene promoters of HSV as well as the promoter of the IE gene of human cytomegalovirus.More than 200 lymphoblastoid cell lines have been established from MD tumors (1, 7-9, 32, 35, 39). Most of these cell lines are CD4 ϩ CD8 Ϫ T cells (56). These lymphoblastoid cell lines are often considered the equivalent of latently infected cells, based on the limited expression of viral genes. In addition to the lymphoblastoid cell lines, an MDV-transformed chicken embryo fibroblast (CEF) cell line has been established, but this cell line also expresses late MDV genes, such as that for glycoprotein B (gB) (5).Three groups of transcripts located in the repeat regions of MDV in MD lymphoblastoid cell lines have been described. The first group consists of the latency-associated transcripts (LATs), which are antisense to ICP4 (see Fig. 1). Several groups have reported the presence of LATs in MD lymphomas and MD-derived lymphoblastoid cell lines (10,11,21,22,27,33); some of these (the MD small RNAs [MSRs]) are poly(A) negative and are retained in the nuclei (11), similar to the 1.5-and 2.0-kb LATs described for HSV (64). Interestingly, the MSRs are also found in nuclei of CEF productively infected with MDV.The second and third group of transcripts described for MD lymphomas and lymphoblastoid cell lines are located in the I 2 ,

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“…Recently, it was shown that Marek disease virus (MDV), a chicken herpesvirus, can augment lymphoid leukosis induced by avian leukosis virus (ALV) (1). Infection of duck embryo fibroblasts (DEFs) with MDV has also been shown to transactivate the Rous sarcoma virus long terminal repeat (LTR) (2). The expression and replication of human immunodeficiency virus (HIV) can be accelerated by herpes simplex virus and human herpesvirus 6 (3-8).…”

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confidence: 99%

Retrovirus insertion into herpesvirus in vitro and in vivo.

Isfort

Jones

Kost

et al. 1992

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

139

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Retroviruses and herpesviruses are naturally occurring pathogens of humans and animals. Coinfection of the same host with both these viruses is common. We report here that a retrovirus can integrate directly into a herpesvirus genome. Specifically, we demonstrate insertion of a nonacute retrovirus, reticuloendotheliosis virus (REV), into a herpesvirus, Marek disease virus (MDV). Both viruses are capable of inducing T lymphomas in chickens and often coexist in the same animal. REV DNA integration into MDV occurred in a recently attenuated strain of MDV and in a short-term coinfection experiment in vitro. We also provide suggestive evidence that REV has inserted into pathogenic strains of MDV in the past. Sequences homologous to the REV long terminal repeat are found in oncogenic MDV but not in nononcogenic strains. These results raise the possibility that retroviral information may be transmitted by herpesvirus and that herpesvirus expression can be modulated by retroviral elements. In addition, retrovirus may provide a useful tool to characterize herpesviral function by insertional mutagenesis.

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Transactivation of the Rous sarcoma virus long terminal repeat promoter by Marek's disease virus

Cited by 33 publications

References 43 publications

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

Avian sarcoma virus RNA synthesis, RNA splicing and virus production in human foreskin fibroblasts: effect of co-infection with human cytomegalovirus

Transactivation of Latent Marek's Disease Herpesvirus Genes in QT35, a Quail Fibroblast Cell Line, by Herpesvirus of Turkeys

Retrovirus insertion into herpesvirus in vitro and in vivo.

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