Journal articles: 'Virus sarcome murin'

1

van der Hoorn, F. A., and V. Müller. "Differential transformation of C3H10T1/2 cells by v-mos: sequential expression of transformation parameters." Molecular and Cellular Biology 5, no. 9 (September 1985): 2204–11. http://dx.doi.org/10.1128/mcb.5.9.2204.

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Extremely small quantities of the product of the transforming gene v-mos of Moloney murine sarcoma virus are able to efficiently transform cells. Recent data indicate the existence of a threshold level for v-mos transformation of NIH3T3 cells. Using mouse mammary tumor virus long terminal repeat sequences or hybrid promoters consisting of mouse mammary tumor virus and Moloney murine sarcoma virus long terminal repeat elements to express v-mos in C3H10T1/2 cells, we established cell lines representing different stages of morphological transformation in vitro. The threshold level for v-mos transformation was considerably lower than that for NIH3T3 cells, because no treatment with dexamethasone or primary selection other than transformation was necessary during standard transfection procedures. Using the cell lines mentioned we established an association of the level of v-mos expression with the transformation parameters examined, but not with p53 levels. Furthermore, the characterization of the different promoters showed (i) that the distal binding site confers hormone responsiveness to Moloney murine sarcoma virus promoter elements and (ii) that artifactual transcription initiation sites can be detected in mouse mammary tumor virus-Moloney murine sarcoma virus hybrid promoters which are, however, not regulated by the hormone.

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2

van der Hoorn, F. A., and V. Müller. "Differential transformation of C3H10T1/2 cells by v-mos: sequential expression of transformation parameters." Molecular and Cellular Biology 5, no. 9 (September 1985): 2204–11. http://dx.doi.org/10.1128/mcb.5.9.2204-2211.1985.

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Extremely small quantities of the product of the transforming gene v-mos of Moloney murine sarcoma virus are able to efficiently transform cells. Recent data indicate the existence of a threshold level for v-mos transformation of NIH3T3 cells. Using mouse mammary tumor virus long terminal repeat sequences or hybrid promoters consisting of mouse mammary tumor virus and Moloney murine sarcoma virus long terminal repeat elements to express v-mos in C3H10T1/2 cells, we established cell lines representing different stages of morphological transformation in vitro. The threshold level for v-mos transformation was considerably lower than that for NIH3T3 cells, because no treatment with dexamethasone or primary selection other than transformation was necessary during standard transfection procedures. Using the cell lines mentioned we established an association of the level of v-mos expression with the transformation parameters examined, but not with p53 levels. Furthermore, the characterization of the different promoters showed (i) that the distal binding site confers hormone responsiveness to Moloney murine sarcoma virus promoter elements and (ii) that artifactual transcription initiation sites can be detected in mouse mammary tumor virus-Moloney murine sarcoma virus hybrid promoters which are, however, not regulated by the hormone.

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3

Graves, B. J., S. P. Eisenberg, D. M. Coen, and S. L. McKnight. "Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat." Molecular and Cellular Biology 5, no. 8 (August 1985): 1959–68. http://dx.doi.org/10.1128/mcb.5.8.1959.

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The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

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4

Graves, B. J., S. P. Eisenberg, D. M. Coen, and S. L. McKnight. "Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat." Molecular and Cellular Biology 5, no. 8 (August 1985): 1959–68. http://dx.doi.org/10.1128/mcb.5.8.1959-1968.1985.

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The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

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5

Armando, Federico, Adnan Fayyad, Stefanie Arms, Yvonne Barthel, Dirk Schaudien, Karl Rohn, Matteo Gambini, et al. "Intratumoral Canine Distemper Virus Infection Inhibits Tumor Growth by Modulation of the Tumor Microenvironment in a Murine Xenograft Model of Canine Histiocytic Sarcoma." International Journal of Molecular Sciences 22, no. 7 (March 30, 2021): 3578. http://dx.doi.org/10.3390/ijms22073578.

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Histiocytic sarcomas refer to highly aggressive tumors with a poor prognosis that respond poorly to conventional treatment approaches. Oncolytic viruses, which have gained significant traction as a cancer therapy in recent decades, represent a promising option for treating histiocytic sarcomas through their replication and/or by modulating the tumor microenvironment. The live attenuated canine distemper virus (CDV) vaccine strain Onderstepoort represents an attractive candidate for oncolytic viral therapy. In the present study, oncolytic virotherapy with CDV was used to investigate the impact of this virus infection on tumor cell growth through direct oncolytic effects or by virus-mediated modulation of the tumor microenvironment with special emphasis on angiogenesis, expression of selected MMPs and TIMP-1 and tumor-associated macrophages in a murine xenograft model of canine histiocytic sarcoma. Treatment of mice with xenotransplanted canine histiocytic sarcomas using CDV induced overt retardation in tumor progression accompanied by necrosis of neoplastic cells, increased numbers of intratumoral macrophages, reduced angiogenesis and modulation of the expression of MMPs and TIMP-1. The present data suggest that CDV inhibits tumor growth in a multifactorial way, including direct cell lysis and reduction of angiogenesis and modulation of MMPs and their inhibitor TIMP-1, providing further support for the concept of its role in oncolytic therapies.

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Inayoshi, Yujin, Yuuki Okino, Katsuhide Miyake, Akifumi Mizutani, Junko Yamamoto-Kishikawa, Yuya Kinoshita, Yusuke Morimoto, et al. "Transcription Factor YY1 Interacts with Retroviral Integrases and Facilitates Integration of Moloney Murine Leukemia Virus cDNA into the Host Chromosomes." Journal of Virology 84, no. 16 (June 2, 2010): 8250–61. http://dx.doi.org/10.1128/jvi.02681-09.

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ABSTRACT Retroviral integrases associate during the early viral life cycle with preintegration complexes that catalyze the integration of reverse-transcribed viral cDNA into the host chromosomes. Several cellular and viral proteins have been reported to be incorporated in the preintegration complex. This study demonstrates that transcription factor Yin Yang 1 binds to Moloney murine leukemia virus, human immunodeficiency virus type 1, and avian sarcoma virus integrases. The results of coimmunoprecipitation and in vitro pulldown assays revealed that Yin Yang 1 interacted with the catalytic core and C-terminal domains of Moloney murine leukemia virus and human immunodeficiency virus type 1 integrases, while the transcriptional repression and DNA-binding domains of the Yin Yang 1 molecule interacted with Moloney murine leukemia virus integrase. Immunoprecipitation of the cytoplasmic fraction of virus-infected cells followed by Southern blotting and chromatin immunoprecipitation demonstrated that Yin Yang 1 associated with Moloney murine leukemia virus cDNA in virus-infected cells. Yin Yang 1 enhanced the in vitro integrase activity of Moloney murine leukemia virus, human immunodeficiency virus type 1, and avian sarcoma virus integrases. Furthermore, knockdown of Yin Yang 1 in host cells by small interfering RNA reduced Moloney murine leukemia virus cDNA integration in vivo, although viral cDNA synthesis was increased, suggesting that Yin Yang 1 facilitates integration events in vivo. Taking these results together, Yin Yang 1 appears to be involved in integration events during the early viral life cycle, possibly as an enhancer of integration.

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7

Graves, B. J., R. N. Eisenman, and S. L. McKnight. "Delineation of transcriptional control signals within the Moloney murine sarcoma virus long terminal repeat." Molecular and Cellular Biology 5, no. 8 (August 1985): 1948–58. http://dx.doi.org/10.1128/mcb.5.8.1948.

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We identified three distinct elements within the Moloney murine sarcoma virus long terminal repeat that control transcription. The phenotypes of unidirectional deletion mutants of the long terminal repeat were assayed in microinjected frog oocytes and in transfected mouse fibroblasts. Steady-state levels of RNA bearing the same 5' terminus as the authentic Moloney murine sarcoma viral transcripts were measured by primer extension in assays that included a pseudo-wild-type internal reference. Mutant phenotypes define the boundaries of three functional elements. A region between 21 and 31 base pairs upstream from the mRNA cap site contains AT-rich sequences that function to establish the transcription start site. A second control element, termed the distal signal, lies between 31 and 84 base pairs upstream of the mRNA cap site. A CAT box consensus sequence is located at the 5' boundary of the distal signal. Additional components of the distal signal include a hexanucleotide sequence that is repeated four times. The distal signal augments transcription efficiency in oocytes but contributes only weakly to long terminal repeat-mediated expression in mouse fibroblasts. A third transcriptional control element lies between 156 and 364 base pairs upstream of the mRNA cap site. This element includes the 75-base-pair repeats previously identified as the Moloney murine sarcoma virus enhancer. In contrast to the distal signal, the Moloney murine sarcoma virus enhancer is crucial for significant expression in mouse fibroblasts but does not contribute to transcriptional expression in frog oocytes.

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8

Graves, B. J., R. N. Eisenman, and S. L. McKnight. "Delineation of transcriptional control signals within the Moloney murine sarcoma virus long terminal repeat." Molecular and Cellular Biology 5, no. 8 (August 1985): 1948–58. http://dx.doi.org/10.1128/mcb.5.8.1948-1958.1985.

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Abstract:

We identified three distinct elements within the Moloney murine sarcoma virus long terminal repeat that control transcription. The phenotypes of unidirectional deletion mutants of the long terminal repeat were assayed in microinjected frog oocytes and in transfected mouse fibroblasts. Steady-state levels of RNA bearing the same 5' terminus as the authentic Moloney murine sarcoma viral transcripts were measured by primer extension in assays that included a pseudo-wild-type internal reference. Mutant phenotypes define the boundaries of three functional elements. A region between 21 and 31 base pairs upstream from the mRNA cap site contains AT-rich sequences that function to establish the transcription start site. A second control element, termed the distal signal, lies between 31 and 84 base pairs upstream of the mRNA cap site. A CAT box consensus sequence is located at the 5' boundary of the distal signal. Additional components of the distal signal include a hexanucleotide sequence that is repeated four times. The distal signal augments transcription efficiency in oocytes but contributes only weakly to long terminal repeat-mediated expression in mouse fibroblasts. A third transcriptional control element lies between 156 and 364 base pairs upstream of the mRNA cap site. This element includes the 75-base-pair repeats previously identified as the Moloney murine sarcoma virus enhancer. In contrast to the distal signal, the Moloney murine sarcoma virus enhancer is crucial for significant expression in mouse fibroblasts but does not contribute to transcriptional expression in frog oocytes.

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9

Braoudaki, Maria, and Fotini Tzortzatou-Stathopoulou. "Tumorigenesis related to retroviral infections." Journal of Infection in Developing Countries 5, no. 11 (November 10, 2011): 751–58. http://dx.doi.org/10.3855/jidc.1773.

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Retroviral infections are considered important risk factors for cancer development in humans since approximately 15-20% of cancer worldwide is caused by an infectious agent. This report discusses the most established oncogenic retroviruses, including human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV-1 and -2), Rous sarcoma virus (RSV), Abelson murine leukemia virus (A-MuLV), Moloney murine leukemia virus (M-MuLV), murine mammary tumor virus (MMTV), bovine leukemia virus, (BLV), Jaagsiekte sheep retrovirus (JSRV), and Friend spleen focus-forming virus (SFFV). The role of retroviruses as inducers of carcinogenesis, the mechanisms underlying oncogenic transformation, and the routes of transmission of several cancer-related retroviral infections are also described. Finally, the impact of cancer-related retroviral infections in the developing world is addressed. This review is an update of carcinogenesis caused by retroviral infections.

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10

Ashton, Laura V., Sandra L. Quackenbush, Jake Castle, Garin Wilson, Jasmine McCoy, Mariah Jordan, and Amy L. MacNeill. "Recombinant Myxoma Virus Expressing Walleye Dermal Sarcoma Virus orfC Is Attenuated in Rabbits." Viruses 12, no. 5 (May 8, 2020): 517. http://dx.doi.org/10.3390/v12050517.

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The poxvirus, myxoma virus (MYXV) has shown efficacy as an oncolytic virus (OV) in some cancer models. However, MYXV replication within murine cancer models and spontaneous canine sarcomas is short-lived. In mice, successful treatment of tumors requires frequent injections with MYXV. We hypothesize that treatment of cancer with a recombinant MYXV that promotes apoptosis could improve the efficacy of MYXV. The orfC gene of walleye dermal sarcoma virus (WDSV), which induces apoptosis, was recombined into the MYXV genome (MYXVorfC). A marked increase in apoptosis was observed in cells infected with MYXVorfC. To ensure that expression of WDSV orfC by MYXV does not potentiate the pathogenesis of MYXV, we evaluated the effects of MYXVorfC inoculation in the only known host of MYXV, New Zealand white rabbits. Virus dissemination in rabbit tissues was similar for MYXVorfC and MYXV. Virus titers recovered from tissues were lower in MYXVorfC-infected rabbits as compared to MYXV-infected rabbits. Importantly, rabbits infected with MYXVorfC had a delayed onset of clinical signs and a longer median survival time than rabbits infected with MYXV. This study indicates that MYXVorfC is attenuated and suggests that MYXVorfC will be safe to use as an OV therapy in future studies.

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11

STEFF, Ann-Muriel, Serge CARILLO, Magali PARIAT, and Marc PIECHACZYK. "Decreased susceptibility to calpains of v-FosFBR but not of v-FosFBJ or v-JunASV17 retroviral proteins compared with their cellular counterparts." Biochemical Journal 323, no. 3 (May 1, 1997): 685–92. http://dx.doi.org/10.1042/bj3230685.

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The c-Fos and c-Jun transcription factors are rapidly turned over in vivo. One of the multiple pathways responsible for their breakdown is probably initiated by calpains, which are cytoplasmic calcium-dependent cysteine proteases. The c-fos gene has been transduced by two murine oncogenic retroviruses called Finkel-Biskis-Jenkins murine sarcoma virus (FBJ-MSV) and Finkel-Biskis-Reilly murine sarcoma virus (FBR-MSV); c-jun has been transduced by the chicken avian sarcoma virus 17 (ASV17) retrovirus. Using an in vitro degradation assay, we show that the mutated v-FosFBR, but not v-FosFBJ or v-JunASV17, is resistant to calpains. This property raises the interesting possibility that decreased sensitivity to calpains might contribute to the tumorigenic potential of FBR-MSV by allowing greater accumulation of the protein that it encodes in infected cells. It has also been demonstrated that resistance to cleavage by calpains does not result from mutations that have accumulated in the Fos moiety of the viral protein but rather from the addition of atypical peptide motifs at its both ends. This observation raises the interesting possibility that homologous regions in viral and cellular Fos either display slightly different conformations or are differentially accessible to interacting proteins.

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Hatziioannou, Theodora, and Stephen P. Goff. "Infection of Nondividing Cells by Rous Sarcoma Virus." Journal of Virology 75, no. 19 (October 1, 2001): 9526–31. http://dx.doi.org/10.1128/jvi.75.19.9526-9531.2001.

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ABSTRACT A direct comparison demonstrates that Rous sarcoma virus is capable of infecting aphidicolin-arrested cells 10-fold more efficiently than murine leukemia virus but less efficiently than human immunodeficiency virus. The efficiency of infection of nondividing cells by the three viruses correlates with the respective ability of each viral DNA to enter the nucleus.

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13

Eckert, HG, M. Stockschlader, U. Just, S. Hegewisch-Becker, M. Grez, A. Uhde, A. Zander, W. Ostertag, and C. Baum. "High-dose multidrug resistance in primary human hematopoietic progenitor cells transduced with optimized retroviral vectors." Blood 88, no. 9 (November 1, 1996): 3407–15. http://dx.doi.org/10.1182/blood.v88.9.3407.bloodjournal8893407.

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Retroviral transfer of the multidrug-resistance 1 (mdr1) cDNA into primary human hematopoietic progenitor cells (HPC) of cancer patients undergoing high-dose chemotherapy has been proposed to protect the bone marrow from the dose-limiting cytotoxicity of cytostatic agents. Preclinical studies performed with vectors derived from the Moloney murine leukemia virus (MoMuLV) or the related Harvey murine sarcoma virus have established that chemoprotection of HPC is feasible. The efficacy of vector-mediated multidrug-resistance under high doses of cytostatic agents, however, remained unclear. We report here that this goal can only be achieved with improved vector design. Novel vectors termed SF-MDR and MP-MDR, which are based on the spleen focus-forming virus or the myeloproliferative sarcoma virus for the enhancer and the murine embryonic stem cell virus for the leader, significantly elevate survival of transduced primary human HPC under moderate doses of colchicine and paclitaxel in vitro when compared with a conventional MoMuLV-based vector. Importantly, SF-MDR and also MP-MDR confer an absolute advantage at high doses of paclitaxel in vitro corresponding to peak plasma levels achieved in patients during chemotherapy. This observation has important consequences for a variety of ongoing and planned gene therapy trials.

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Buss, J. E., and B. M. Sefton. "Direct identification of palmitic acid as the lipid attached to p21ras." Molecular and Cellular Biology 6, no. 1 (January 1986): 116–22. http://dx.doi.org/10.1128/mcb.6.1.116.

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p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.

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Buss, J. E., and B. M. Sefton. "Direct identification of palmitic acid as the lipid attached to p21ras." Molecular and Cellular Biology 6, no. 1 (January 1986): 116–22. http://dx.doi.org/10.1128/mcb.6.1.116-122.1986.

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p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.

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Ryden, T. A., and K. Beemon. "Avian retroviral long terminal repeats bind CCAAT/enhancer-binding protein." Molecular and Cellular Biology 9, no. 3 (March 1989): 1155–64. http://dx.doi.org/10.1128/mcb.9.3.1155.

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DNA-protein interactions involving enhancer and promoter sequences within the U3 regions of several avian retroviral long terminal repeats (LTRs) were studied by DNase I footprinting. The rat CCAAT/enhancer-binding protein, C/EBP, bound to all four viral LTRs examined. The Rous sarcoma virus binding site corresponded closely to the 5' limit of the LTR enhancer; nucleotides -225 to -188 were protected as a pair of adjacent binding domains. The Fujinami sarcoma virus LTR bound C/EBP at a single site at nucleotides -213 to -195. C/EBP also bound to the promoter region of the enhancerless Rous-associated virus-0 LTR at nucleotides -77 to -57. The avian myeloblastosis virus LTR bound C/EBP at three sites: nucleotides -262 to -246, -154 to -134, and -55 to -39. We have previously observed binding of C/EBP to an enhancer in the gag gene of avian retroviruses. A heat-treated nuclear extract from chicken liver bound to all of the same retroviral sequences as did C/EBP. Alignment of the avian retroviral binding sequences with the published binding sites for C/EBP in two CCAAT boxes and in the simian virus 40, polyoma, and murine sarcoma virus enhancers suggested TTGNNGCTAATG as a consensus sequence for binding of C/EBP. When two bases of this consensus sequence were altered by site-specific mutagenesis of the Rous sarcoma virus LTR, binding of the heat-stable chicken protein was eliminated.

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Ryden, T. A., and K. Beemon. "Avian retroviral long terminal repeats bind CCAAT/enhancer-binding protein." Molecular and Cellular Biology 9, no. 3 (March 1989): 1155–64. http://dx.doi.org/10.1128/mcb.9.3.1155-1164.1989.

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DNA-protein interactions involving enhancer and promoter sequences within the U3 regions of several avian retroviral long terminal repeats (LTRs) were studied by DNase I footprinting. The rat CCAAT/enhancer-binding protein, C/EBP, bound to all four viral LTRs examined. The Rous sarcoma virus binding site corresponded closely to the 5' limit of the LTR enhancer; nucleotides -225 to -188 were protected as a pair of adjacent binding domains. The Fujinami sarcoma virus LTR bound C/EBP at a single site at nucleotides -213 to -195. C/EBP also bound to the promoter region of the enhancerless Rous-associated virus-0 LTR at nucleotides -77 to -57. The avian myeloblastosis virus LTR bound C/EBP at three sites: nucleotides -262 to -246, -154 to -134, and -55 to -39. We have previously observed binding of C/EBP to an enhancer in the gag gene of avian retroviruses. A heat-treated nuclear extract from chicken liver bound to all of the same retroviral sequences as did C/EBP. Alignment of the avian retroviral binding sequences with the published binding sites for C/EBP in two CCAAT boxes and in the simian virus 40, polyoma, and murine sarcoma virus enhancers suggested TTGNNGCTAATG as a consensus sequence for binding of C/EBP. When two bases of this consensus sequence were altered by site-specific mutagenesis of the Rous sarcoma virus LTR, binding of the heat-stable chicken protein was eliminated.

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Lichtman, A. H., D. S. Reynolds, D. V. Faller, and A. K. Abbas. "Mature murine B lymphocytes immortalized by Kirsten sarcoma virus." Nature 324, no. 6096 (December 1986): 489–91. http://dx.doi.org/10.1038/324489a0.

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SCHULZE, FRANK, ERNST BOEHNLEIN, and PETER GRUSS. "Mutational Analyses of the Moloney Murine Sarcoma Virus Enhancer." DNA 4, no. 3 (June 1985): 193–202. http://dx.doi.org/10.1089/dna.1985.4.193.

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Escobedo, Jaime, Balraj Singh, Dino Dina, and Ralph B. Arlinghaus. "Temperature-dependent cytocidal effects of Moloney murine sarcoma virus." Virus Research 6, no. 1 (October 1986): 75–84. http://dx.doi.org/10.1016/0168-1702(86)90058-4.

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Wu, Xiaolin, Yuan Li, Bruce Crise, Shawn M. Burgess, and David J. Munroe. "Weak Palindromic Consensus Sequences Are a Common Feature Found at the Integration Target Sites of Many Retroviruses." Journal of Virology 79, no. 8 (April 15, 2005): 5211–14. http://dx.doi.org/10.1128/jvi.79.8.5211-5214.2005.

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ABSTRACT Integration into the host genome is one of the hallmarks of the retroviral life cycle and is catalyzed by virus-encoded integrases. While integrase has strict sequence requirements for the viral DNA ends, target site sequences have been shown to be very diverse. We carefully examined a large number of integration target site sequences from several retroviruses, including human immunodeficiency virus type 1, simian immunodeficiency virus, murine leukemia virus, and avian sarcoma-leukosis virus, and found that a statistical palindromic consensus, centered on the virus-specific duplicated target site sequence, was a common feature at integration target sites for these retroviruses.

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López-Lastra, Marcelo, Sandrine Ulrici, Caroline Gabus, and Jean-Luc Darlix. "Identification of an Internal Ribosome Entry Segment in the 5′ Region of the Mouse VL30 Retrotransposon and Its Use in the Development of Retroviral Vectors." Journal of Virology 73, no. 10 (October 1, 1999): 8393–402. http://dx.doi.org/10.1128/jvi.73.10.8393-8402.1999.

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ABSTRACT Mouse virus-like 30S RNAs (VL30m) constitute a family of retrotransposons, present at 100 to 200 copies, dispersed in the mouse genome. They display little sequence homology to Moloney murine leukemia virus (MoMLV), do not encode virus-like proteins, and have not been implicated in retroviral carcinogenesis. However, VL30 RNAs are efficiently packaged into MLV particles that are propagated in cell culture. In this study, we addressed whether the 5′ region of VL30m could replace the 5′ leader of MoMLV functionally in a recombinant vector construct. Our data confirm that the putative packaging sequence of VL30 is located within the 5′ region (nucleotides 362 to 1149 with respect to the cap structure) and that it can replace the packaging sequence of MoMLV. We also show that VL30m contains an internal ribosome entry segment (IRES) in the 5′ region, as do MoMLV, Friend murine leukemia virus, Harvey murine sarcoma virus, and avian reticuloendotheliosis virus type A. Our data show that both the packaging and IRES functions of the 5′ region of VL30m RNA can be efficiently used to develop retrotransposon-based vectors.

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Pierce, J. H., and S. A. Aaronson. "Myeloid cell transformation by ras-containing murine sarcoma viruses." Molecular and Cellular Biology 5, no. 4 (April 1985): 667–74. http://dx.doi.org/10.1128/mcb.5.4.667.

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BALB and Harvey murine sarcoma viruses contain ras transforming genes capable of altering the proliferation and differentiation of cells within the erythroid and lymphoid lineages (W. D. Hankins and E. M. Scolnick, Cell 26:91-97, 1981; J. H. Pierce and S. A. Aaronson, J. Exp. Med. 156:873-887, 1982; E. M. Scolnick et al., Mol. Cell. Biol. 1:68-74). The present studies demonstrate hematopoietic targets of ras-containing viruses within the myeloid lineage. Diffuse colonies were induced by BALB or Harvey marine sarcoma virus infection of murine bone marrow cells. Generally, these colonies were made up of relatively mature macrophages which exhibited increased self-renewal capacity but eventually underwent terminal differentiation in culture. Cells from one BALB murine sarcoma virus-induced colony displayed phenotypic markers of more immature myelomonocytic cells. This colony, designated BAMC1, readily established as a continuous cell line and was highly malignant in vivo. Exposure of these cells to 12-O-tetradecanoylphorbol-13-acetate led to the induction of a more mature myeloid phenotype, which was associated with decreased growth potential in vitro and in vivo. The effects of the inducing agent were not mediated by an alteration in the level of expression of the ras-coded p21 transforming protein. Our present findings extend the spectrum of targets whose growth is altered by ras-containing retroviruses to cells at several stages of differentiation within each of the major hematopoietic lineages.

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Pierce, J. H., and S. A. Aaronson. "Myeloid cell transformation by ras-containing murine sarcoma viruses." Molecular and Cellular Biology 5, no. 4 (April 1985): 667–74. http://dx.doi.org/10.1128/mcb.5.4.667-674.1985.

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BALB and Harvey murine sarcoma viruses contain ras transforming genes capable of altering the proliferation and differentiation of cells within the erythroid and lymphoid lineages (W. D. Hankins and E. M. Scolnick, Cell 26:91-97, 1981; J. H. Pierce and S. A. Aaronson, J. Exp. Med. 156:873-887, 1982; E. M. Scolnick et al., Mol. Cell. Biol. 1:68-74). The present studies demonstrate hematopoietic targets of ras-containing viruses within the myeloid lineage. Diffuse colonies were induced by BALB or Harvey marine sarcoma virus infection of murine bone marrow cells. Generally, these colonies were made up of relatively mature macrophages which exhibited increased self-renewal capacity but eventually underwent terminal differentiation in culture. Cells from one BALB murine sarcoma virus-induced colony displayed phenotypic markers of more immature myelomonocytic cells. This colony, designated BAMC1, readily established as a continuous cell line and was highly malignant in vivo. Exposure of these cells to 12-O-tetradecanoylphorbol-13-acetate led to the induction of a more mature myeloid phenotype, which was associated with decreased growth potential in vitro and in vivo. The effects of the inducing agent were not mediated by an alteration in the level of expression of the ras-coded p21 transforming protein. Our present findings extend the spectrum of targets whose growth is altered by ras-containing retroviruses to cells at several stages of differentiation within each of the major hematopoietic lineages.

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Atkinson, M. M., and J. D. Sheridan. "Altered junctional permeability between cells transformed by v-ras, v-mos, or v-src." American Journal of Physiology-Cell Physiology 255, no. 5 (November 1, 1988): C674—C683. http://dx.doi.org/10.1152/ajpcell.1988.255.5.c674.

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Junctional permeability in normal and transformed NRK cells was quantitatively assessed by microinjecting fluorescent dye into one cell of a pair, digitizing the changes of fluorescence intensity using video analysis techniques, and applying the digital values to a solution of Fick's diffusion equation. We show that this approach reliably estimates the junctional permeance of a cell pair. Cells that are temperature sensitive for transformation were shown to also be temperature sensitive vis-a-vis junctional permeance. Thus permeance values were reduced approximately 80-90% on transformation by either a mutant Rous sarcoma virus or a mutant Moloney murine sarcoma virus. Cells transformed by wild-type Kirsten sarcoma virus were also shown to possess levels of junctional permeance significantly lower than nontransformed controls. The transformed junctional phenotype could be observed as early as 15 min after shifting to transformation-permissive conditions. Our results suggest that the oncogenes src, ras, and mos exert their effects on NRK cell junctions via converging pathways, of which one may be phosphorylation of junctional proteins.

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Hamelin, R., K. Kabat, D. Blair, and R. B. Arlinghaus. "Temperature-sensitive splicing defect of ts110 Moloney murine sarcoma virus is virus encoded." Journal of Virology 57, no. 1 (1986): 301–9. http://dx.doi.org/10.1128/jvi.57.1.301-309.1986.

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Greger, James G., Richard A. Katz, Konstantin Taganov, Glenn F. Rall, and Anna Marie Skalka. "Transduction of Terminally Differentiated Neurons by Avian Sarcoma Virus." Journal of Virology 78, no. 9 (May 1, 2004): 4902–6. http://dx.doi.org/10.1128/jvi.78.9.4902-4906.2004.

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ABSTRACT Recent studies have demonstrated that avian sarcoma virus (ASV) can transduce cycle-arrested cells. Here, we have assessed quantitatively the transduction efficiency of an ASV vector in naturally arrested mouse hippocampal neurons. This efficiency was determined by comparing the number of transduced cells after infection of differentiated neurons versus dividing progenitor cells. The results indicate that ASV is able to transduce these differentiated neurons efficiently and that this activity is not the result of infection of residual dividing cells. The transduction efficiency of the ASV vector was found to be intermediate between the relatively high and low efficiencies obtained with human immunodeficiency virus type 1 and murine leukemia virus vectors, respectively.

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28

Fodor, Sharon K., and Volker M. Vogt. "Walleye dermal sarcoma virus reverse transcriptase is temperature sensitive." Journal of General Virology 83, no. 6 (June 1, 2002): 1361–65. http://dx.doi.org/10.1099/0022-1317-83-6-1361.

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Walleye dermal sarcoma virus (WDSV) is a piscine retrovirus that replicates naturally in fish at temperatures near 4 °C. The reverse transcriptase (RT) protein from virus particles isolated from walleye tumours was purified and biochemically characterized. Like the RT of the distantly related murine leukaemia virus, WDSV RT sediments as a monomer in the absence of template. It exhibits a K m of 22 μM for TTP in an assay with poly(rA) as a template and oligo(dT) as a primer. The enzyme is rapidly inactivated at temperatures greater than 15 °C. The ratio of RT activity at 15 °C to that at 4 °C is similar for WDSV and recombinant human immunodeficiency virus type 1, suggesting that, at least with this template, the fish enzyme is not specially adapted to function more efficiently in the cold.

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29

Sealey, L., and R. Chalkley. "At least two nuclear proteins bind specifically to the Rous sarcoma virus long terminal repeat enhancer." Molecular and Cellular Biology 7, no. 2 (February 1987): 787–98. http://dx.doi.org/10.1128/mcb.7.2.787.

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We used the sensitive gel electrophoresis DNA-binding assay and DNase I footprinting to detect at least two protein factors (EFI and EFII) that bound specifically to the Rous sarcoma virus (RSV) enhancer in vitro. These factors were differentially extracted from quail cell nuclei, recognized different nucleotide sequences in the U3 region of the RSV long terminal repeat, and appeared to bind preferentially to opposite DNA strands as monitored by the DNase I protection assay. The EFI- and EFII-protected regions within U3 corresponded closely to sequences previously demonstrated by deletion mutagenesis to be required for enhancer activity, strongly suggesting a functional significance for these proteins. Only weak homologies between other enhancer consensus sequence motifs and the EFI and EFII recognition sites were observed, and other viral enhancers from simian virus 40 and Moloney murine sarcoma virus did not compete effectively with the RSV enhancer for binding either factor.

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30

Sealey, L., and R. Chalkley. "At least two nuclear proteins bind specifically to the Rous sarcoma virus long terminal repeat enhancer." Molecular and Cellular Biology 7, no. 2 (February 1987): 787–98. http://dx.doi.org/10.1128/mcb.7.2.787-798.1987.

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We used the sensitive gel electrophoresis DNA-binding assay and DNase I footprinting to detect at least two protein factors (EFI and EFII) that bound specifically to the Rous sarcoma virus (RSV) enhancer in vitro. These factors were differentially extracted from quail cell nuclei, recognized different nucleotide sequences in the U3 region of the RSV long terminal repeat, and appeared to bind preferentially to opposite DNA strands as monitored by the DNase I protection assay. The EFI- and EFII-protected regions within U3 corresponded closely to sequences previously demonstrated by deletion mutagenesis to be required for enhancer activity, strongly suggesting a functional significance for these proteins. Only weak homologies between other enhancer consensus sequence motifs and the EFI and EFII recognition sites were observed, and other viral enhancers from simian virus 40 and Moloney murine sarcoma virus did not compete effectively with the RSV enhancer for binding either factor.

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31

Izmailova, Elena, and Anna Aldovini. "Functional Analysis of the Murine Sarcoma Virus RNA Packaging Sequence." Journal of Virology 76, no. 9 (May 1, 2002): 4643–48. http://dx.doi.org/10.1128/jvi.76.9.4643-4648.2002.

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ABSTRACT We investigated the features of the Moloney murine sarcoma virus leader sequence necessary for RNA packaging function by using a deletion analysis approach. We found that sequences that extend beyond those characterized genetically in previous reports are important for optimal packaging efficiency. A fragment covering a minimum of four potential stem-loop structures is required for the shortest packaging element compatible with gene transfer. Our results reveal the extent to which each of the segments of the packaging sequence contribute to packaging efficiency.

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32

Kang, Yubin, Christopher J. Moressi, Todd E. Scheetz, Litao Xie, Diane Thi Tran, Thomas L. Casavant, Prashanth Ak, Craig J. Benham, Beverly L. Davidson, and Paul B. McCray. "Integration Site Choice of a Feline Immunodeficiency Virus Vector." Journal of Virology 80, no. 17 (September 1, 2006): 8820–23. http://dx.doi.org/10.1128/jvi.00719-06.

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ABSTRACT We mapped 226 unique integration sites in human hepatoma cells following gene transfer with a feline immunodeficiency virus (FIV)-based lentivirus vector. FIV integrated across the entire length of the transcriptional units. Microarray data indicated that FIV integration favored actively transcribed genes. Approximately 21% of FIV integrations within transcriptional units occurred in genes regulated by the LEDGF/p75 transcriptional coactivator. DNA in regions of FIV insertion sites exhibited a “bendable” structure and a pattern of duplex destabilization favoring strand separation. FIV integration preferences are more similar to those of primate lentiviruses and distinct from those of Moloney murine leukemia virus, avian sarcoma leukosis virus, and foamy virus.

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33

van der Hoorn, F. A., T. Lahaye, V. Müller, M. A. Ogle, and H. D. Engers. "Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo." Journal of Experimental Medicine 162, no. 1 (July 1, 1985): 128–44. http://dx.doi.org/10.1084/jem.162.1.128.

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The gag membrane protein gP85gag, encoded by Moloney murine leukemia virus (M-MLV), was identified as a target molecule recognized by Moloney murine sarcoma virus--M-MLV (M-MSV--M-MLV)-specific cytolytic T lymphocyte (CTL) clones. Target cells infected with Ab-X-MLV, an M-MLV-derived mutant virus not encoding gP85gag, were not lysed by the CTL clones. The same CTL clones were shown previously to induce the destruction of M-MLV-induced tumor cells in the peritoneal cavity. We have now characterized CTL-resistant antigen-loss tumor cell variants that have lost the surface antigen, but which retain transcriptionally silent M-MLV genomes. A cloned antigen-loss variant that reverted in vitro to the CTL-susceptible phenotype reexpressed M-MLV genomes that had undergone an insertion event in the region of the viral DNA coding for the gag membrane protein. Intravenous injection of virus-specific CTL clones inhibited tumor formation in mice injected subcutaneously with M-MSV--M-MLV.

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Marques, Sofia, Stacey Efstathiou, K. G. Smith, Matthias Haury, and J. Pedro Simas. "Selective Gene Expression of Latent Murine Gammaherpesvirus 68 in B Lymphocytes." Journal of Virology 77, no. 13 (July 1, 2003): 7308–18. http://dx.doi.org/10.1128/jvi.77.13.7308-7318.2003.

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ABSTRACT Intranasal infection of mice with murine gammaherpesvirus 68 (MHV-68), a virus genetically related to the human pathogen Kaposi's sarcoma-associated herpesvirus, results in a persistent, latent infection in the spleen and other lymphoid organs. Here, we have determined the frequency of virus infection in splenic dendritic cells, macrophages, and several B-cell subpopulations, and we quantified cell type-dependent virus transcription patterns. The frequencies of virus genome positive cells were maximal at 14 days postinfection in all splenic cell populations analyzed. Marginal zone and germinal center B cells harbored the highest frequency of infection and the former population accounted for approximately half the total number of infected B cells. Analysis of virus transcription during the establishment of latency revealed that virus gene expression in B cells was restricted and dependent on the differentiation stage of the B cell. Notably, transcription of ORF73 was detected in germinal center B cells, a finding in agreement with the predicted latent genome maintenance function of ORF73 in dividing cells. At late times after infection, virus DNA could only be detected in newly formed and germinal center B cells, which suggests that B cells play a critical role in facilitating life-long latency.

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35

Kamata, N., R. M. Jotte, and J. T. Holt. "Myristylation alters DNA-binding activity and transactivation of FBR (gag-fos) protein." Molecular and Cellular Biology 11, no. 2 (February 1991): 765–72. http://dx.doi.org/10.1128/mcb.11.2.765.

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FBR murine sarcoma virus (gag-fos) protein, a virally transduced Fos protein, exhibits decreased gene transactivation in comparison with the cellular Fos protein. Biochemical analysis suggests that myristylation of the virally encoded N-terminal gag region results in decreased DNA binding and transcriptional activation without affecting heterodimerization with Jun protein. These findings demonstrate that protein myristylation can modulate gene regulation by a DNA-binding protein.

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36

Kamata, N., R. M. Jotte, and J. T. Holt. "Myristylation alters DNA-binding activity and transactivation of FBR (gag-fos) protein." Molecular and Cellular Biology 11, no. 2 (February 1991): 765–72. http://dx.doi.org/10.1128/mcb.11.2.765-772.1991.

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FBR murine sarcoma virus (gag-fos) protein, a virally transduced Fos protein, exhibits decreased gene transactivation in comparison with the cellular Fos protein. Biochemical analysis suggests that myristylation of the virally encoded N-terminal gag region results in decreased DNA binding and transcriptional activation without affecting heterodimerization with Jun protein. These findings demonstrate that protein myristylation can modulate gene regulation by a DNA-binding protein.

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37

de Mars, M., P. E. Cizdziel, and E. C. Murphy. "Activation of cryptic splice sites in murine sarcoma virus-124 mutants." Journal of Virology 64, no. 11 (1990): 5260–69. http://dx.doi.org/10.1128/jvi.64.11.5260-5269.1990.

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38

Cizdziel, P. E., M. A. Nash, D. G. Blair, and E. C. Murphy. "Molecular basis underlying phenotypic revertants of Moloney murine sarcoma virus MuSVts110." Journal of Virology 57, no. 1 (1986): 310–17. http://dx.doi.org/10.1128/jvi.57.1.310-317.1986.

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39

Miksicek, Richard, Angelika Heber, Wolfgang Schmid, Ulrich Danesch, Gerhard Posseckert, Miguel Beato, and Günther Schütz. "Glucocorticoid responsiveness of the transcriptional enhancer of Moloney Murine Sarcoma Virus." Cell 46, no. 2 (July 1986): 283–90. http://dx.doi.org/10.1016/0092-8674(86)90745-2.

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40

Bennett, Robert P., and John W. Wills. "Conditions for Copackaging Rous Sarcoma Virus and Murine Leukemia Virus Gag Proteins during Retroviral Budding." Journal of Virology 73, no. 3 (March 1, 1999): 2045–51. http://dx.doi.org/10.1128/jvi.73.3.2045-2051.1999.

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ABSTRACT Rous sarcoma virus (RSV) and murine leukemia virus (MLV) are examples of distantly related retroviruses that normally do not encounter one another in nature. Their Gag proteins direct particle assembly at the plasma membrane but possess very little sequence similarity. As expected, coexpression of these two Gag proteins did not result in particles that contain both. However, when the N-terminal membrane-binding domain of each molecule was replaced with that of the Src oncoprotein, which is also targeted to the cytoplasmic face of the plasma membrane, efficient copackaging was observed in genetic complementation and coimmunoprecipitation assays. We hypothesize that the RSV and MLV Gag proteins normally use distinct locations on the plasma membrane for particle assembly but otherwise have assembly domains that are sufficiently similar in function (but not sequence) to allow heterologous interactions when these proteins are redirected to a common membrane location.

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41

MacAuley, A., N. Auersperg, and T. Pawson. "Expression of viral p21ras during acquisition of a transformed phenotype by rat adrenal cortex cells infected with Kirsten murine sarcoma virus." Molecular and Cellular Biology 6, no. 1 (January 1986): 342–46. http://dx.doi.org/10.1128/mcb.6.1.342.

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Rat adrenal cortex cells infected with Kirsten murine sarcoma virus acquire a transformed phenotype in a progressive fashion. The expression of the viral p21ras does not appear to correlate with the degree of transformation of the adrenocortical cells but rather is produced at similar levels as the culture becomes transformed. This indicates that the expression of an oncogenic form of p21ras is not of itself sufficient to completely transform rat adrenal cortex cells.

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42

MacAuley, A., N. Auersperg, and T. Pawson. "Expression of viral p21ras during acquisition of a transformed phenotype by rat adrenal cortex cells infected with Kirsten murine sarcoma virus." Molecular and Cellular Biology 6, no. 1 (January 1986): 342–46. http://dx.doi.org/10.1128/mcb.6.1.342-346.1986.

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Rat adrenal cortex cells infected with Kirsten murine sarcoma virus acquire a transformed phenotype in a progressive fashion. The expression of the viral p21ras does not appear to correlate with the degree of transformation of the adrenocortical cells but rather is produced at similar levels as the culture becomes transformed. This indicates that the expression of an oncogenic form of p21ras is not of itself sufficient to completely transform rat adrenal cortex cells.

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43

Narezkina, Anna, Konstantin D. Taganov, Samuel Litwin, Radka Stoyanova, Junpei Hayashi, Christoph Seeger, Anna Marie Skalka, and Richard A. Katz. "Genome-Wide Analyses of Avian Sarcoma Virus Integration Sites." Journal of Virology 78, no. 21 (November 1, 2004): 11656–63. http://dx.doi.org/10.1128/jvi.78.21.11656-11663.2004.

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ABSTRACT The chromosomal features that influence retroviral integration site selection are not well understood. Here, we report the mapping of 226 avian sarcoma virus (ASV) integration sites in the human genome. The results show that the sites are distributed over all chromosomes, and no global bias for integration site selection was detected. However, RNA polymerase II transcription units (protein-encoding genes) appear to be favored targets of ASV integration. The integration frequency within genes is similar to that previously described for murine leukemia virus but distinct from the higher frequency observed with human immunodeficiency virus type 1. We found no evidence for preferred ASV integration sites over the length of genes and immediate flanking regions. Microarray analysis of uninfected HeLa cells revealed that the expression levels of ASV target genes were similar to the median level for all genes represented in the array. Although expressed genes were targets for integration, we found no preference for integration into highly expressed genes. Our results provide a more detailed description of the chromosomal features that may influence ASV integration and support the idea that distinct, virus-specific mechanisms mediate integration site selection. Such differences may be relevant to viral pathogenesis and provide utility in retroviral vector design.

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44

Katz, Richard A., James G. Greger, Kristen Darby, Pamela Boimel, Glenn F. Rall, and Anna Marie Skalka. "Transduction of Interphase Cells by Avian Sarcoma Virus." Journal of Virology 76, no. 11 (June 1, 2002): 5422–34. http://dx.doi.org/10.1128/jvi.76.11.5422-5434.2002.

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ABSTRACT It has been generally believed that oncoretroviruses are dependent on mitosis for efficient nuclear entry of viral DNA. We previously identified a nuclear localization signal in the integrase protein of an oncoretrovirus, avian sarcoma virus (ASV), suggesting an active import mechanism for the integrase-DNA complex (G. Kukolj, R. A. Katz, and A. M. Skalka, Gene 223:157-163, 1998). Here, we have evaluated the requirement for mitosis in nuclear import and integration of ASV DNA. Using a modified ASV encoding a murine leukemia virus amphotropic env gene and a green fluorescent protein (GFP) reporter gene, DNA nuclear import was measured in cell cycle-arrested avian (DF-1) as well as human (HeLa) and mouse cells. The results showed efficient accumulation of nuclear forms of ASV DNA in γ-irradiation-arrested cells. Efficient transduction of a GFP reporter gene was also observed after infection of cells that were arrested with γ-irradiation, mitomycin C, nocodazole, or aphidicolin, confirming that nuclear import and integration of ASV DNA can occur in the absence of mitosis. By monitoring GFP expression in individual cells, we also obtained evidence for nuclear import of viral DNA during interphase in cycling cells. Lastly, we observed that ASV can transduce postmitotic mouse neurons. These results support an active nuclear import mechanism for the oncoretrovirus ASV and suggest that this mechanism can operate in both nondividing and dividing cells.

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45

Hikita, Shin-ichi, Yusuke Yanagi, and Shinji Ohno. "Murine gammaherpesvirus 68 ORF35 is required for efficient lytic replication and latency." Journal of General Virology 96, no. 12 (December 1, 2015): 3624–34. http://dx.doi.org/10.1099/jgv.0.000310.

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Murine gammaherpesvirus (MHV) 68, a natural pathogen of field mice, is related to human gammaherpesviruses, Epstein–Barr virus (EBV; human herpesvirus 4) and Kaposi's sarcoma-associated herpesvirus (KSHV; human herpesvirus 8). The ORF35 of MHV-68 and its homologues of EBV and KSHV are located in the gene cluster composed of ORF34–ORF38 in which each gene overlaps with adjacent genes. Although MHV-68 ORF35 was reported to be an essential gene, its function during infection is presently unknown. In this study, we show, by analysing ORF35-transfected cells, that three serine residues in the C terminus are responsible for the phosphorylation and that the ORF35 protein forms homo-oligomers via a predicted coiled-coil motif. The ORF35 protein expressed by transfection was preferentially located in the cytoplasm of cells uninfected or infected with MHV-68. The recombinant virus lacking ORF35 (35S virus) exhibited genome replication and expression of lytic proteins comparable to those of the WT virus, but reduced levels of virus production, suggesting that the ORF35 protein acts at the virion assembly and/or egress step. Lytic replication in the lung after intranasal infection and the frequency of ex vivo reactivation from latency after intraperitoneal infection were lower in 35S virus-infected mice than in mice infected with the WT or marker-reverted virus. Our results indicate that ORF35 is not essential for MHV-68 lytic replication, but plays an important role in efficient viral replication and reactivation from latency.

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46

Johnston, Elizabeth R., and Kathryn Radke. "The SU and TM Envelope Protein Subunits of Bovine Leukemia Virus Are Linked by Disulfide Bonds, both in Cells and in Virions." Journal of Virology 74, no. 6 (March 15, 2000): 2930–35. http://dx.doi.org/10.1128/jvi.74.6.2930-2935.2000.

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ABSTRACT After the polyprotein precursor of retroviral envelope proteins is proteolytically cleaved, the surface (SU) and transmembrane (TM) subunits remain associated with each other by noncovalent interactions or by disulfide bonds. Disulfide linkages confer a relatively stable association between the SU and TM envelope protein subunits of Rous sarcoma virus and murine leukemia virus. In contrast, the noncovalent association between SU and TM of human immunodeficiency virus leads to significant shedding of SU from the surface of infected cells. The SU and TM proteins of bovine leukemia virus (BLV) initially were reported to be disulfide linked but later were concluded not to be, since TM is often lost during purification of SU protein. Here, we show that SU and TM of BLV do, indeed, associate through disulfide bonds, whether the envelope proteins are overexpressed in transfected cells, are produced in virus-infected cells, or are present in newly produced virions.

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47

Martinez-Guzman, DeeAnn, Tammy Rickabaugh, Ting-Ting Wu, Helen Brown, Steven Cole, Moon Jung Song, Leming Tong, and Ren Sun. "Transcription Program of Murine Gammaherpesvirus 68." Journal of Virology 77, no. 19 (October 1, 2003): 10488–503. http://dx.doi.org/10.1128/jvi.77.19.10488-10503.2003.

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ABSTRACT Murine gammaherpesvirus 68 (MHV-68 [also referred to as γHV68]) is phylogenetically related to Kaposi's sarcoma-associated herpesvirus (KSHV [also referred to as HHV-8]) and Epstein-Barr virus (EBV). However, unlike KSHV or EBV, MHV-68 readily infects fibroblast and epithelial cell lines derived from several mammalian species, providing a system to study productive and latent infections as well as reactivation of gammaherpesviruses in vivo and in vitro. To carry out rapid genome-wide analysis of MHV-68 gene expression, we made DNA arrays containing nearly all of the known and predicted open reading frames (ORFs) of the virus. RNA obtained from an MHV-68 latently infected cell line, from cells lytically infected with MHV-68 in culture, and from the lung tissue of infected mice was used to probe the MHV-68 arrays. Using a tightly latent B-cell line (S11E), the MHV-68 latent transcription program was quantitatively described. Using BHK-21 cells and infected mice, we demonstrated that latent genes are transcribed during lytic replication and are relatively independent of de novo protein synthesis. We determined that the transcription profiles at the peak of lytic gene expression are similar in cultured fibroblast and in the lung of infected mice. Finally, the MHV-68 DNA arrays were used to examine the gene expression profile of a recombinant virus that overexpresses replication and transcription activator (RTA), C-RTA/MHV-68, during lytic replication in cell culture. The recombinant virus replicates faster then the parental strain and the DNA arrays revealed that nearly every MHV-68 ORF examined was activated by RTA overexpression. Examination of the gene expression patterns of C-RTA/MHV-68 over a time course led to the finding that the M3 promoter is RTA responsive in the absence of other viral factors.

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48

Fowler, Polly, Sofia Marques, J. Pedro Simas, and Stacey Efstathiou. "ORF73 of murine herpesvirus-68 is critical for the establishment and maintenance of latency." Journal of General Virology 84, no. 12 (December 1, 2003): 3405–16. http://dx.doi.org/10.1099/vir.0.19594-0.

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In vitro studies have established that the latency-associated nuclear antigen encoded by human Kaposi's sarcoma-associated herpesvirus and the related ORF73 gene product of herpesvirus saimiri interact with virus origins of replication to facilitate maintenance of episomal DNA. Such a function implies a critical role for ORF73 in the establishment and maintenance of latency in vivo. To determine the role of ORF73 in virus pathogenesis, the ORF73 gene product encoded by murine herpesvirus-68 (MHV-68) was disrupted by making an ORF73 deletion mutant, Δ73, and an independent ORF73 frameshift mutant, FS73. The effect of the mutations introduced in ORF73 on MHV-68 pathogenesis was analysed in vivo using a well-characterized murine model system. These studies have revealed that ORF73 is not required for efficient lytic replication either in vitro or in vivo. In contrast, a severe latency deficit is observed in splenocytes of animals infected with an ORF73 mutant, as assessed by infectious centre reactivation assay or by in situ hybridization detection of latent virus. Assessment of viral genome-positive cells in sorted splenocyte populations confirmed the absence of ORF73 mutant virus from splenic latency reservoirs, including germinal centre B cells. These data indicate a crucial role for ORF73 in the establishment of latency and for virus persistence in the host.

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49

Huai, L., S. M. Chiocca, M. A. Gilbreth, J. R. Ainsworth, L. A. Bishop, and E. C. Murphy. "Moloney murine sarcoma virus MuSVts110 DNA: cloning, nucleotide sequence, and gene expression." Journal of Virology 66, no. 9 (1992): 5329–37. http://dx.doi.org/10.1128/jvi.66.9.5329-5337.1992.

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50

Reddy, E. P., D. Lipman, P. R. Andersen, S. R. Tronick, and S. A. Aaronson. "Nucleotide sequence analysis of the BALB/c murine sarcoma virus transforming gene." Journal of Virology 53, no. 3 (1985): 984–87. http://dx.doi.org/10.1128/jvi.53.3.984-987.1985.

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Journal articles on the topic 'Virus sarcome murin'

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