Journal articles: 'Virus overexpression'

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Zou, Zhongcheng, John Misasi, Nancy Sullivan, and Peter D. Sun. "Overexpression of Ebola virus envelope GP1 protein." Protein Expression and Purification 135 (July 2017): 45–53. http://dx.doi.org/10.1016/j.pep.2017.04.010.

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Goila-Gaur, Ritu, Dimiter G. Demirov, Jan M. Orenstein, Akira Ono, and Eric O. Freed. "Defects in Human Immunodeficiency Virus Budding and Endosomal Sorting Induced by TSG101 Overexpression." Journal of Virology 77, no. 11 (June 1, 2003): 6507–19. http://dx.doi.org/10.1128/jvi.77.11.6507-6519.2003.

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ABSTRACT Retrovirus budding is greatly stimulated by the presence of Gag sequences known as late or L domains. The L domain of human immunodeficiency virus type 1 (HIV-1) maps to a highly conserved Pro-Thr-Ala-Pro (PTAP) sequence in the p6 domain of Gag. We and others recently observed that the p6 PTAP motif interacts with the cellular endosomal sorting protein TSG101. Consistent with a role for TSG101 in virus release, we demonstrated that overexpressing the N-terminal, Gag-binding domain of TSG101 (TSG-5′) suppresses HIV-1 budding by blocking L domain function. To elucidate the role of TSG101 in HIV-1 budding, we evaluated the significance of the binding between Gag and TSG-5′ on the inhibition of HIV-1 release. We observed that a mutation in TSG-5′ that disrupts the Gag/TSG101 interaction suppresses the ability of TSG-5′ to inhibit HIV-1 release. We also determined the effect of overexpressing a panel of truncated TSG101 derivatives and full-length TSG101 (TSG-F) on virus budding. Overexpressing TSG-F inhibits HIV-1 budding; however, the effect of TSG-F on virus release does not require Gag binding. Furthermore, overexpression of the C-terminal portion of TSG101 (TSG-3′) potently inhibits budding of not only HIV-1 but also murine leukemia virus. Confocal microscopy data indicate that TSG-F and TSG-3′ overexpression induces an aberrant endosome phenotype; this defect is dependent upon the C-terminal, Vps-28-binding domain of TSG101. We propose that TSG-5′ suppresses HIV-1 release by binding PTAP and blocking HIV-1 L domain function, whereas overexpressing TSG-F or TSG-3′ globally inhibits virus release by disrupting the cellular endosomal sorting machinery. These results highlight the importance of TSG101 and the endosomal sorting pathway in virus budding and suggest that inhibitors can be developed that, like TSG-5′, target HIV-1 without disrupting endosomal sorting.

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Seo, Young-Jin, Celeste Blake, Stephen Alexander, and Bumsuk Hahm. "Sphingosine 1-Phosphate-Metabolizing Enzymes Control Influenza Virus Propagation and Viral Cytopathogenicity." Journal of Virology 84, no. 16 (June 2, 2010): 8124–31. http://dx.doi.org/10.1128/jvi.00510-10.

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ABSTRACT Sphingosine 1-phosphate (S1P)-metabolizing enzymes regulate the level of sphingolipids and have important biological functions. However, the effects of S1P-metabolizing enzymes on host defense against invading viruses remain unknown. In this study, we investigated the role of S1P-metabolizing enzymes in modulating cellular responses to influenza virus infection. Overexpression of S1P lyase (SPL), which induces the degradation of S1P, interfered with the amplification of infectious influenza virus. Accordingly, SPL-overexpressing cells were much more resistant than control cells to the cytopathic effects caused by influenza virus infection. SPL-mediated inhibition of virus-induced cell death was supported by impairment of the upregulation of the proapoptotic protein Bax, a critical factor for influenza virus cytopathogenicity. Importantly, influenza virus infection of SPL-overexpressing cells induced rapid activation of extracellular signal-regulated kinase (ERK) and STAT1 but not of p38 mitogen-activated protein kinase (MAPK), Akt, or c-Jun N-terminal kinase (JNK). Blockade of STAT1 expression or inhibition of Janus kinase (JAK) activity elevated the level of influenza virus replication in the cells, indicating that SPL protects cells from influenza virus via the activation of JAK/STAT signaling. In contrast to that of SPL, the overexpression of S1P-producing sphingosine kinase 1 heightened the cells' susceptibility to influenza virus infection, an effect that was reversed by the inhibition of its kinase activity, representing opposed enzymatic activity. These findings indicate that the modulation of S1P-metabolizing enzymes is crucial for controlling the host defense against infection with influenza virus. Thus, S1P-metabolizing enzymes are novel potential targets for the treatment of diseases caused by influenza virus infection.

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Li, Shun, Shanwu Lyu, Yujuan Liu, Ming Luo, Suhua Shi, and Shulin Deng. "Cauliflower mosaic virus P6 Dysfunctions Histone Deacetylase HD2C to Promote Virus Infection." Cells 10, no. 9 (September 1, 2021): 2278. http://dx.doi.org/10.3390/cells10092278.

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Histone deacetylases (HDACs) are vital epigenetic modifiers not only in regulating plant development but also in abiotic- and biotic-stress responses. Though to date, the functions of HD2C—an HD2-type HDAC—In plant development and abiotic stress have been intensively explored, its function in biotic stress remains unknown. In this study, we have identified HD2C as an interaction partner of the Cauliflower mosaic virus (CaMV) P6 protein. It functions as a positive regulator in defending against CaMV infection. The hd2c mutants show enhanced susceptibility to CaMV infection. In support, the accumulation of viral DNA, viral transcripts, and the deposition of histone acetylation on the viral minichromosomes are increased in hd2c mutants. P6 interferes with the interaction between HD2C and HDA6, and P6 overexpression lines have similar phenotypes with hd2c mutants. In further investigations, P6 overexpression lines, together with CaMV infection plants, are more sensitive to ABA and NaCl with a concomitant increasing expression of ABA/NaCl-regulated genes. Moreover, the global levels of histone acetylation are increased in P6 overexpression lines and CaMV infection plants. Collectively, our results suggest that P6 dysfunctions histone deacetylase HD2C by physical interaction to promote CaMV infection.

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Barrera-Vázquez, Oscar Salvador, Clotilde Cancio-Lonches, Carlos Emilio Miguel-Rodríguez, Monica Margarita Valdes Pérez, and Ana Lorena Gutiérrez-Escolano. "Survivin Overexpression Has a Negative Effect on Feline Calicivirus Infection." Viruses 11, no. 11 (October 30, 2019): 996. http://dx.doi.org/10.3390/v11110996.

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It is known that levels of the anti-apoptotic protein survivin are reduced during Murine norovirus MNV-1 and Feline calicivirus (FCV) infection as part of the apoptosis establishment required for virus release and propagation in the host. Recently, our group has reported that overexpression of survivin causes a reduction of FCV protein synthesis and viral progeny production, suggesting that survivin may affect early steps of the replicative cycle. Using immunofluorescence assays, we observed that overexpression of survivin, resulted in the reduction of FCV infection not only in transfected but also in the neighboring nontransfected CrFK cells, thus suggesting autocrine and paracrine protective effects. Cells treated with the supernatants collected from CrFK cells overexpressing survivin showed a reduction in FCV but not MNV-1 protein production and viral yield, suggesting that FCV binding and/or entry were specifically altered. The reduced ability of FCV to bind to the surface of the cells overexpressing survivin, or treated with the supernatants collected from these cells, correlate with the reduction in the cell surface of the FCV receptor, the feline junctional adhesion molecule (fJAM) 1, while no effect was observed in the cells transfected with the pAm-Cyan vector or in cells treated with the corresponding supernatants. Moreover, the overexpression of survivin affects neither Vaccinia virus (VACV) production in CrFK cells nor MNV-1 virus production in RAW 267.4 cells, indicating that the effect is specific for FCV. All of these results taken together indicate that cells that overexpress survivin, or cell treatment with the conditioned medium from these cells, results in the reduction of the fJAM-1 molecule and, therefore, a specific reduction in FCV entry and infection.

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Sun, Lijun, Haiying Ren, Ruoxue Liu, Baoyan Li, Tingquan Wu, Feng Sun, Huimin Liu, Xiaomeng Wang, and Hansong Dong. "An h-Type Thioredoxin Functions in Tobacco Defense Responses to Two Species of Viruses and an Abiotic Oxidative Stress." Molecular Plant-Microbe Interactions® 23, no. 11 (November 2010): 1470–85. http://dx.doi.org/10.1094/mpmi-01-10-0029.

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Various thioredoxin (Trx) proteins have been identified in plants. However, many of the physiological roles played by these proteins remain to be elucidated. We cloned a TRXh-like gene predicted to encode an h-type Trx in tobacco (Nicotiana tabacum) and designated it NtTRXh3, based on the biochemical activity of the NtTRXh3 protein. Overexpression of NtTRXh3 conferred resistance to Tobacco mosaic virus and Cucumber mosaic virus, both of which showed reduced multiplication and pathogenicity in NtTRXh3-overexpressing plants compared with controls. NtTRXh3 overexpression also enhanced tobacco resistance to oxidative stress induced by paraquat, an herbicide that inhibits the production of reducing equivalents by chloroplasts. The NtTRXh3 protein localized exclusively to chloroplasts in coordination with the maintenance of cellular reducing conditions, which accompanied an elevation in the glutathione/glutathione disulfide couple ratio. NtTRXh3 gene expression and NtTRXh3 protein production were necessary for these defensive responses, because they were all arrested when NtTRXh3 was silenced and the production of NtTRXh3 protein was abrogated. These results suggest that NtTRXh3 is involved in the resistance of tobacco to virus infection and abiotic oxidative stress.

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Cooper, Andrew, Eric Johannsen, Seiji Maruo, Ellen Cahir-McFarland, Diego Illanes, David Davidson, and Elliott Kieff. "EBNA3A Association with RBP-Jκ Down-Regulates c-myc and Epstein-Barr Virus-Transformed Lymphoblast Growth." Journal of Virology 77, no. 2 (January 15, 2003): 999–1010. http://dx.doi.org/10.1128/jvi.77.2.999-1010.2003.

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ABSTRACT Epstein-Barr virus nuclear antigen protein 3A (EBNA3A) is one of four EBNAs (EBNA-2, EBNALP, EBNA3A, and EBNA3C) through the cellular DNA sequence-specific transcription factor RBP-Jκ/CBF-1/CSL and are essential for conversion of primary B lymphocytes to lymphoblastoid cell lines (LCLs). In the present study, we investigated the effects of EBNA3A on EBNA2 activation of transcription in the IB4 LCL by conditionally overexpressing EBNA3A three- to fivefold. EBNA3A overexpression increased EBNA3A association with RBP-Jκ, did not change EBNA3C association with RBP-Jκ or EBNA or LMP1 expression, decreased EBNA2 association with RBP-Jκ, decreased c-myc expression, and caused G0/G1 growth arrest with prolonged viability. Expression of the fusion protein MycERTM in cells with conditional EBNA3A overexpression restored cell cycle progression and caused apoptosis. In contrast, MycER in the same cells without EBNA3A overexpression enhanced cell proliferation and did not increase apoptosis. These data indicate that EBNA3A overexpression inhibits protection from c-myc-induced apoptosis. In assays of EBNA2- and RBP-Jκ-dependent transcription, EBNA3A amino acids 1 to 386 were sufficient for repression equivalent to that by wild-type EBNA3A, amino acids 1 to 124 were unimportant, amino acids 1 to 277 were insufficient, and a triple alanine substitution within the EBNA3A core RBP-Jκ binding domain was a null mutation. In reverse genetic experiments with IB4 LCLs, the effects of conditional EBNA3A overexpression on c-myc expression and proliferation did not require amino acids 524 to 944 but did require amino acids 278 to 524 as well as wild-type sequence in the core RBP-Jκ binding domain. The dependence of EBNA3A effects on the core RBP-Jκ interaction domain and on the more C-terminal amino acids (amino acids 278 to 524) required for efficient RBP-Jκ association strongly implicates RBP-Jκ in c-myc promoter regulation.

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Mathieu, Cyrille, Vanessa Guillaume, Amélie Sabine, Kien Chai Ong, Kum Thong Wong, Catherine Legras-Lachuer, and Branka Horvat. "Lethal Nipah Virus Infection Induces Rapid Overexpression of CXCL10." PLoS ONE 7, no. 2 (February 29, 2012): e32157. http://dx.doi.org/10.1371/journal.pone.0032157.

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Mcdonald, W. F., and P. Traktman. "Overexpression and Purification of the Vaccinia Virus DNA Polymerase." Protein Expression and Purification 5, no. 4 (August 1994): 409–21. http://dx.doi.org/10.1006/prep.1994.1059.

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Quinn, Kathrina, Melinda A. Brindley, Melodie L. Weller, Nikola Kaludov, Andrew Kondratowicz, Catherine L. Hunt, Patrick L. Sinn, et al. "Rho GTPases Modulate Entry of Ebola Virus and Vesicular Stomatitis Virus Pseudotyped Vectors." Journal of Virology 83, no. 19 (July 22, 2009): 10176–86. http://dx.doi.org/10.1128/jvi.00422-09.

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ABSTRACT To explore mechanisms of entry for Ebola virus (EBOV) glycoprotein (GP) pseudotyped virions, we used comparative gene analysis to identify genes whose expression correlated with viral transduction. Candidate genes were identified by using EBOV GP pseudotyped virions to transduce human tumor cell lines that had previously been characterized by cDNA microarray. Transduction profiles for each of these cell lines were generated, and a significant positive correlation was observed between RhoC expression and permissivity for EBOV vector transduction. This correlation was not specific for EBOV vector alone as RhoC also correlated highly with transduction of vesicular stomatitis virus GP (VSVG) pseudotyped vector. Levels of RhoC protein in EBOV and VSV permissive and nonpermissive cells were consistent with the cDNA gene array findings. Additionally, vector transduction was elevated in cells that expressed high levels of endogenous RhoC but not RhoA. RhoB and RhoC overexpression significantly increased EBOV GP and VSVG pseudotyped vector transduction but had minimal effect on human immunodeficiency virus (HIV) GP pseudotyped HIV or adeno-associated virus 2 vector entry, indicating that not all virus uptake was enhanced by expression of these molecules. RhoB and RhoC overexpression also significantly enhanced VSV infection. Similarly, overexpression of RhoC led to a significant increase in fusion of EBOV virus-like particles. Finally, ectopic expression of RhoC resulted in increased nonspecific endocytosis of fluorescent dextran and in formation of increased actin stress fibers compared to RhoA-transfected cells, suggesting that RhoC is enhancing macropinocytosis. In total, our studies implicate RhoB and RhoC in enhanced productive entry of some pseudovirions and suggest the involvement of actin-mediated macropinocytosis as a mechanism of uptake of EBOV GP and VSVG pseudotyped viral particles.

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Zhong, Yuchuan, Yan Li, Tao Song, and Dapeng Zhang. "MiR-718 mediates the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells." Physiological Genomics 51, no. 10 (October 1, 2019): 500–505. http://dx.doi.org/10.1152/physiolgenomics.00019.2019.

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It has been reported that SEMA3B-AS1 is a tumor-suppressive lncRNA in gastric cardia adenocarcinoma. We explored the possible involvement of SEMA3B-AS1 in hepatocellular carcinoma (HCC). We found that SEMA3B-AS1 was downregulated in HCC tissues compared with noncancer tissues and was not affected by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In addition, SEMA3B-AS1 expression was not affect by cancer development, and low SEMA3B-AS1 levels were closely correlated with poor survival. SEMA3B-AS1 in HCC tissues was inversely correlated with microRNA (miR)-718 and positively correlated with PTEN. In HCC cells, SEMA3B-AS1 overexpression resulted in upregulated, while miR-718 overexpression resulted in downregulated phosphatase and tensin homolog (PTEN) expression. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. SEMA3B-AS1 and PTEN overexpression resulted in a reduced proliferation rate of HCC cells, while miR-718 overexpression resulted in an increased rate. In addition, miR-718 overexpression attenuated the effects of SEMA3B-AS1 overexpression. Therefore, miR-718 may mediate the indirect interaction between lncRNA SEMA3B-AS1 and PTEN to regulate the proliferation of hepatocellular carcinoma cells.

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Fischer, J. E., J. E. Johnson, R. K. Kuli-Zade, T. R. Johnson, S. Aung, R. A. Parker, and B. S. Graham. "Overexpression of interleukin-4 delays virus clearance in mice infected with respiratory syncytial virus." Journal of virology 71, no. 11 (1997): 8672–77. http://dx.doi.org/10.1128/jvi.71.11.8672-8677.1997.

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Woo, Yanghee, Susanne G. Warner, Rula Geha, Marianne M. Stanford, Penelope Decarolis, Masmudur M. Rahman, Samuel Singer, Grant McFadden, and Yuman Fong. "The Oncolytic Activity of Myxoma Virus against Soft Tissue Sarcoma Is Mediated by the Overexpression of Ribonucleotide Reductase." Clinical Medicine Insights: Oncology 15 (January 2021): 117955492199306. http://dx.doi.org/10.1177/1179554921993069.

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Background: Myxoma virus (MYXV) is an oncolytic poxvirus that lacks the gene for 1 of the subunits of ribonucleotide reductase (RR), a crucial DNA synthesis and repair enzyme. The overexpression of RR has been implicated in the invasiveness of several cancers, including soft tissue sarcomas (STS). The purpose of the study was to investigate the oncolytic efficacy of MYXV in STS with different levels of RR expression. Methods: The oncolytic effect of recombinant MYXV was evaluated in 4 human STS cell lines, LS141 (a dedifferentiated liposarcoma), DDLS8817 (a dedifferentiated liposarcoma), RDD2213 (recurrent dedifferentiated liposarcoma), and HSSYII (a synovial sarcoma) using infectivity and cytotoxicity assays. Following the overexpression of RRM2 by cDNA transfection and silencing of RRM2 by siRRM2 in these STS cell lines, the RRM2 expression levels were analyzed by Western blot. Results: We observed a direct correlation between viral oncolysis and RRM2 mRNA levels ( R = 0.96) in STS. Higher RRM2 expression was associated with a more robust cell kill. Silencing the RRM2 gene led to significantly greater cell survival (80%) compared with the control group ( P = .003), whereas overexpression of the RRM2 increased viral oncolysis by 33% ( P < .001). Conclusions: Our results show that the oncolytic effects of MYXV correlate directly with RR expression levels and are enhanced in STS cell lines with naturally occurring or artificially induced high expression levels of RR. Myxoma virus holds promise in the treatment of advanced soft tissue cancer, especially in tumors overexpressing RR.

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Zhao, Ling, Harufusa Toriumi, Yi Kuang, Huanchun Chen, and Zhen F. Fu. "The Roles of Chemokines in Rabies Virus Infection: Overexpression May Not Always Be Beneficial." Journal of Virology 83, no. 22 (September 9, 2009): 11808–18. http://dx.doi.org/10.1128/jvi.01346-09.

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ABSTRACT It was found previously that induction of innate immunity, particularly chemokines, is an important mechanism of rabies virus (RABV) attenuation. To evaluate the effect of overexpression of chemokines on RABV infection, chemokines macrophage inflammatory protein 1α (MIP-1α), RANTES, and IP-10 were individually cloned into the genome of attenuated RABV strain HEP-Flury. These recombinant RABVs were characterized in vitro for growth properties and expression of chemokines. It was found that all the recombinant viruses grew as well as the parent virus, and each of the viruses expressed the intended chemokine in a dose-dependent manner. When these viruses were evaluated for pathogenicity in the mouse model, it was found that overexpression of MIP-1α further decreased RABV pathogenicity by inducing a transient innate immune response. In contrast, overexpression of RANTES or IP-10 increased RABV pathogenicity by causing neurological diseases, which is due to persistent and high-level expression of chemokines, excessive infiltration and accumulation of inflammatory cells in the central nervous system, and severe enhancement of blood-brain barrier permeability. These studies indicate that overexpression of chemokines, although important in controlling virus infection, may not always be beneficial to the host.

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Peng, Kah-Whye, Michael M. Timm, David Dingli, Angela Dispenzieri, Morie Gertz, Thomas E. Witzig, Philip R. Greipp, and Stephen J. Russell. "Oncolytic Measles Virus Selectively Targets CD46 Overexpression on Myeloma Cells." Blood 104, no. 11 (November 16, 2004): 2392. http://dx.doi.org/10.1182/blood.v104.11.2392.2392.

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Abstract Multiple myeloma remains incurable and novel therapeutics are urgently needed. We have shown that live attenuated Edmonston strain measles virus (MV-Edm) is potently oncolytic in multiple myeloma xenograft models and can efficiently infect CD138 sorted primary myeloma cells inducing extensive intercellular fusion which leads to cell death (Blood, 2001, v98, p2002). In contrast, the virus causes minimal damage to normal PHA-stimulated peripheral blood lymphocytes, fibroblasts and smooth muscle cells. To facilitate non-invasive imaging of sites of viral gene expression, we introduced the human thyroidal sodium iodide symporter (NIS) gene into the viral genome (MV-NIS). MV-NIS infected myeloma cells efficiently concentrate radioiodine which provides a basis for noninvasive imaging and destruction of infected tumors using beta emitters such as 131I (Blood, 2004, v103, p1641). Clinical translation of MV-NIS in patients with refractory myeloma is planned. However, the mechanism underlying the tumor selectivity of MV-Edm has not previously been defined. MV-Edm uses either of two cellular receptors for cell entry and cell fusion; CD46, a regulator of complement activation, is expressed on all nucleated cells, wheras SLAM (signaling lymphocyte activation molecule) is expressed only on activated B lymphocytes, T lymphocytes, and monocytes, and is not present on myeloma plasma cells. Using a panel of CHO cell transfectants, we demonstrated that MV-Edm -mediated cell killing increases exponentially above a threshold CD46 receptor density (Can Res, 2004, v64, p4919). We subsequently obtained bone marrow aspirates from 18 myeloma patients and performed multi-parameter flow cytometry to determine the relative expression levels of CD46 on the myeloma plasma cells versus the rest of the hematopoietic cells in the bone marrow. The myeloma cells expressed significantly higher levels (5-fold) of CD46 receptors (MFI=294.9 + 204.4, means ± SD) on their cell surfaces compared to hematopoietic cells of the erythroid, myeloid and lymphoid lineages (MFI=58.6 ± 9.0). Analysis of the myeloma array data generated by the Shaughnessy lab indicated that, in comparison to plasma cells from healthy volunteers (2997 ± 1053, n=30, means ± SD), primary myeloma cells express 2-fold elevated levels of CD46 mRNA (6592 ± 4029, n=72, p=0.001, Wilcoxon signed rank test). Taken together, these findings provide strong support for the hypothesis that selective destruction of myeloma cells by oncolytic measles viruses is a direct consequence of their overexpression of the cellular receptor CD46.

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Kheimar, Ahmed, Jakob Trimpert, Nicole Groenke, and Benedikt B. Kaufer. "Overexpression of cellular telomerase RNA enhances virus-induced cancer formation." Oncogene 38, no. 10 (October 19, 2018): 1778–86. http://dx.doi.org/10.1038/s41388-018-0544-1.

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Widmer, G. "Suppression of Leishmania RNA virus replication by capsid protein overexpression." Journal of virology 69, no. 7 (1995): 4122–26. http://dx.doi.org/10.1128/jvi.69.7.4122-4126.1995.

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Li, Q., Y. Li, C. Li, and X. Yu. "Enhanced ascorbic acid accumulation through overexpression of dehydroascorbate reductase confers tolerance to methyl viologen and salt stresses in tomato." Czech Journal of Genetics and Plant Breeding 48, No. 2 (May 30, 2012): 74–86. http://dx.doi.org/10.17221/100/2011-cjgpb.

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As an important antioxidant for plants and humans, L-ascorbic acid (AsA, vitamin C) can scavenge reactive oxygen species (ROS) and can be regenerated from its oxidized form in a reaction catalyzed by dehydroascorbate reductase (DHAR). To analyse the effect of overexpressing DHAR on tomato (Solanum lycopersicum), an expression vector containing potato cytosolic DHAR (DHAR1) or chloroplastic DHAR (DHAR2) cDNA driven by a cauliflower mosaic virus 35S promoter was transferred into tomato plants. Compared with the wild type (WT), DHAR1 overexpression increased DHAR activity and AsA content in both leaves and fruits, while DHAR2 overexpression increased DHAR activity and AsA content mainly in leaves. DHAR1 and DHAR2 overexpression increased the chlorophyll content and photosynthetic rate of transgenic lines, but had no effect on plant height and stem diameter. Furthermore, the germination rate, plant fresh weight, seedling length and chlorophyll content of transgenic DHAR1 and DHAR2 plants under salt stress were higher than those of WT plants. In addition, the transgenic plants also exhibited considerable tolerance to oxidative damage induced by methyl viologen (MV). Taken together, these results indicated that overexpressing potato DHAR1 and DHAR2 enhanced the level of AsA in tomato and, consequently, increased the tolerance of tomato to salt and MV stress.

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Kleist, Britta, Micaela Poetsch, and Juergen Schmoll. "Intranodal Palisaded Myofibroblastoma With Overexpression of Cyclin D1." Archives of Pathology & Laboratory Medicine 127, no. 8 (August 1, 2003): 1040–43. http://dx.doi.org/10.5858/2003-127-1040-ipmwoo.

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Abstract Intranodal palisaded myofibroblastoma (IPM) is a rare benign spindle-cell tumor of lymph nodes with myofibroblastic/smooth muscle differentiation. We present another case of IPM that confirms the myofibroblastic differentiation of the tumor cells and identifies the so-called amianthoid fibers as collagen deposits by immunohistochemical and ultrastructural techniques. Because IPM shares histomorphologic characteristics with an inflammatory myofibroblastic tumor that has been associated with a virus-induced alteration of cell cycle regulation, the diagnostic approach was extended in this case. We were able to demonstrate cyclin D1 overexpression but could detect neither amplification of the CCND1 gene nor allelic loss at chromosomes 9p22-21 and 13q (surrounding the genes p16 and Rb, respectively). Furthermore, no evidence of human herpesvirus-8 or Epstein-Barr virus infection could be found by polymerase chain reaction or immunostaining. Nevertheless, our results point to the cell cycle regulatory genes as a factor in the pathogenesis of IPM.

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Gill, Navkiran, and Ali A. Ashkar. "Overexpression of Interleukin-15 Compromises CD4-Dependent Adaptive Immune Responses against Herpes Simplex Virus 2." Journal of Virology 83, no. 2 (November 12, 2008): 918–26. http://dx.doi.org/10.1128/jvi.01282-08.

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ABSTRACT Interleukin-15 (IL-15) is necessary for the development and function of NK/NKT cells and the maintenance of naive and memory CD8+ T cells. In the absence of IL-15, protective innate immunity is not available; however, a functional adaptive immune response against vaginal herpes simplex virus 2 (HSV-2) is generated. Mice overexpressing IL-15 (IL-15tg mice) have higher numbers of NK cells, greater NK-derived gamma interferon, and more CD8+ T cells. Here we examined the consequences of IL-15 overexpression for innate and adaptive immunity against genital HSV-2. Surprisingly, IL-15tg mice immunized against HSV-2 were not protected against genital HSV-2 challenge compared to control immunized mice. IL-15tg mice had a higher frequency of NK cells in the genital mucosa than control mice. However, immunized IL-15tg mice had significantly lower numbers of HSV-2-specific CD4+ T cells than B6 mice. We then confirmed that CD4+ T cells, but not CD8+ T cells, are essential for protection against intravaginal HSV-2 challenge. Since we observed less protection in immunized IL-15tg mice, we then examined if the adaptive immune responses generated in an environment with overexpression of IL-15 could provide protection against HSV-2 in an environment with normal levels of IL-15 expression. We adoptively transferred immunized cells from IL-15tg and B6 mice into naive RAG-1−/− mice and found that the cells from immunized IL-15tg mice were able to provide protection in this IL-15-normal environment. Our data suggest that overexpression of IL-15 results in a reduced CD4+ T cell-mediated adaptive immune response against genital HSV-2.

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Rosas-Acosta, Germán, Sharon C. Braunagel, and Max D. Summers. "Effects of Deletion and Overexpression of the Autographa californica Nuclear Polyhedrosis Virus FP25KGene on Synthesis of Two Occlusion-Derived Virus Envelope Proteins and Their Transport into Virus-Induced Intranuclear Membranes." Journal of Virology 75, no. 22 (November 15, 2001): 10829–42. http://dx.doi.org/10.1128/jvi.75.22.10829-10842.2001.

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ABSTRACT Partial deletions within Autographa californica open reading frame 61 (FP25K) alter the expression and accumulation profile of several viral proteins and the transport of occlusion-derived virus (ODV)-E66 to intranuclear membranes during infection (S. C. Braunagel et al., J. Virol. 73:8559–8570, 1999). Here we show the effects of a full deletion and overexpression of FP25K on the transport and expression of two ODV envelope proteins, ODV-E66 (E66) and ODV-E25 (E25). Deletion and overexpression of FP25K substantially altered the levels of expression of E66 during infection. Compared with cells infected with wild-type (wt) virus, the levels of E66 were reduced fivefold in cells infected with a viral mutant lacking FP25K (ΔFP25K) and were slightly increased in cells infected with a viral mutant overexpressing FP25K (FP25Kpolh). In contrast, no significant changes were observed in the levels of E25 among wt-, ΔFP25K-, and FP25Kpolh-infected cells. The changes observed in the levels of E66 among the different viral mutants were not accompanied by changes in either the time of synthesis, membrane association, protein turnover, or steady-state transcript abundance. Deletion of FP25K also substantially altered the transport and localization of E66 during infection. In cells infected with the ΔFP25K mutant virus, E66 accumulated in localized regions at the nuclear periphery and the outer nuclear membrane and did not traffic to intranuclear membranes. In contrast, in cells infected with the FP25Kpolh mutant virus E66 trafficked to intranuclear membranes. For comparison, E25 was normally transported to intranuclear membranes in both ΔFP25K- and FP25Kpolh-infected cells. Altogether these studies suggest that FP25K affects the synthesis of E66 at a posttranscriptional level, probably by altering the translation of E66; additionally, the block in transport of E66 at the nuclear envelope in ΔFP25K-infected cells suggests that the pathway of E66 trafficking to the inner nuclear membrane and intranuclear microvesicles is specifically regulated and must be influenced by factors that do not control the traffic of E25.

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Burdick, Ryan, Jessica L. Smith, Chawaree Chaipan, Yeshitila Friew, Jianbo Chen, Narasimhan J. Venkatachari, Krista A. Delviks-Frankenberry, Wei-Shau Hu, and Vinay K. Pathak. "P Body-Associated Protein Mov10 Inhibits HIV-1 Replication at Multiple Stages." Journal of Virology 84, no. 19 (July 28, 2010): 10241–53. http://dx.doi.org/10.1128/jvi.00585-10.

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ABSTRACT Recent studies have shown that APOBEC3G (A3G), a potent inhibitor of human immunodeficiency virus type 1 (HIV-1) replication, is localized to cytoplasmic mRNA-processing bodies (P bodies). However, the functional relevance of A3G colocalization with P body marker proteins has not been established. To explore the relationship between HIV-1, A3G, and P bodies, we analyzed the effects of overexpression of P body marker proteins Mov10, DCP1a, and DCP2 on HIV-1 replication. Our results show that overexpression of Mov10, a putative RNA helicase that was previously reported to belong to the DExD superfamily and was recently reported to belong to the Upf1-like group of helicases, but not the decapping enzymes DCP1a and DCP2, leads to potent inhibition of HIV-1 replication at multiple stages. Mov10 overexpression in the virus producer cells resulted in reductions in the steady-state levels of the HIV-1 Gag protein and virus production; Mov10 was efficiently incorporated into virions and reduced virus infectivity, in part by inhibiting reverse transcription. In addition, A3G and Mov10 overexpression reduced proteolytic processing of HIV-1 Gag. The inhibitory effects of A3G and Mov10 were additive, implying a lack of functional interaction between the two inhibitors. Small interfering RNA (siRNA)-mediated knockdown of endogenous Mov10 by 80% resulted in a 2-fold reduction in virus production but no discernible impact on the infectivity of the viruses after normalization for the p24 input, suggesting that endogenous Mov10 was not required for viral infectivity. Overall, these results show that Mov10 can potently inhibit HIV-1 replication at multiple stages.

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Broussard, Dana R., Mary M. Lozano, and Jaquelin P. Dudley. "Rorγ (Rorc) Is a Common Integration Site in Type B Leukemogenic Virus-Induced T-Cell Lymphomas." Journal of Virology 78, no. 9 (May 1, 2004): 4943–46. http://dx.doi.org/10.1128/jvi.78.9.4943-4946.2004.

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ABSTRACT The retrovirus type B leukemogenic virus (TBLV) causes T-cell lymphomas in mice. We have identified the Rorγ locus as an integration site in 19% of TBLV-induced tumors. Overexpression of one or more Rorγ isoforms in >77% of the tumors tested may complement apoptotic effects of c-myc overexpression.

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Carsillo, Thomas, Mary Carsillo, Zachary Traylor, Päivi Rajala-Schultz, Phillip Popovich, Stefan Niewiesk, and Michael Oglesbee. "Major Histocompatibility Complex Haplotype Determines hsp70-Dependent Protection against Measles Virus Neurovirulence." Journal of Virology 83, no. 11 (March 25, 2009): 5544–55. http://dx.doi.org/10.1128/jvi.02673-08.

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ABSTRACT In vitro studies show that hsp70 promotes gene expression for multiple viral families, although there are few reports on the in vivo significance of virus-hsp70 interaction. Previously we showed that hsp70-dependent stimulation of Edmonston measles virus (Ed MeV) transcription caused an increased cytopathic effect and mortality in transgenic hsp70-overexpressing C57BL/6 mice (H-2 b ). The response to MeV infection is influenced by the major histocompatibility complex haplotype; H-2 d mice are resistant to brain infection due to robust antiviral immune responses, whereas H-2 b mice are susceptible due to deficiencies in this response. We therefore tested the hypothesis that the outcome of MeV-hsp70 interaction may be dependent upon the host H-2 haplotype. The impact of selective neuronal hsp70 overexpression on Ed MeV brain infection was tested with congenic C57BL/10 H-2 d neonatal mice. In this context, hsp70 overexpression conferred complete protection against virus-induced mortality, compared to >30% mortality in nontransgenic mice. Selective depletion of T-cell populations showed that transgenic mice exhibit a diminished reliance on T cells for protection. Brain transcript analysis indicated enhanced innate immune activation and signaling through Toll-like receptors 2 and 4 at early times postinfection for transgenic infected mice relative to those for nontransgenic infected mice. Collectively, results suggest that hsp70 can enhance innate antiviral immunity through Toll-like receptor signaling, supporting a protective role for physiological responses that enhance tissue levels of hsp70 (e.g., fever), and that the H-2 haplotype determines the effectiveness of this response.

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Malnoy, M., Q. Jin, E. E. Borejsza-Wysocka, S. Y. He, and H. S. Aldwinckle. "Overexpression of the Apple MpNPR1 Gene Confers Increased Disease Resistance in Malus × domestica." Molecular Plant-Microbe Interactions® 20, no. 12 (December 2007): 1568–80. http://dx.doi.org/10.1094/mpmi-20-12-1568.

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The NPR1 gene plays a pivotal role in systemic acquired resistance in plants. Its overexpression in Arabidopsis and rice results in increased disease resistance and elevated expression of pathogenesis-related (PR) genes. An NPR1 homolog, MpNPR1-1, was cloned from apple (Malus × domestica) and overexpressed in two important apple cultivars, Galaxy and M26. Apple leaf pieces were transformed with the MpNPR1 cDNA under the control of the inducible Pin2 or constitutive Cauliflower mosaic virus (CaMV)35S promoter using Agrobacterium tumefaciens. Overexpression of MpNPR1 mRNA was shown by reverse transcriptase-polymerase chain reaction. Activation of some PR genes (PR2, PR5, and PR8) was observed. Resistance to fire blight was evaluated in a growth chamber by inoculation of the shoot tips of our own rooted 30-cm-tall plants with virulent strain Ea273 of Erwinia amylovora. Transformed Galaxy lines overexpressing MpNPR1 had 32 to 40% of shoot length infected, compared with 80% in control Galaxy plants. Transformed M26 lines overexpressing MpNPR1 under the control of the CaMV35S promoter also showed a significant reduction of disease compared with control M26 plants. Some MpNPR-overexpressing Galaxy lines also exhibited increased resistance to two important fungal pathogens of apple, Venturia inaequalis and Gymnosporangium juniperi-virginianae. Selected transformed lines have been propagated for field trials for disease resistance and fruit quality.

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Yang, Ting, Long Qiu, Wanying Huang, Qianyi Xu, Jialing Zou, Qiding Peng, Honghui Lin, and Dehui Xi. "Chilli veinal mottle virus HCPro interacts with catalase to facilitate virus infection in Nicotiana tabacum." Journal of Experimental Botany 71, no. 18 (June 28, 2020): 5656–68. http://dx.doi.org/10.1093/jxb/eraa304.

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Abstract Plant symptoms are derived from specific interactions between virus and host components. However, little is known about viral or host factors that participate in the establishment of systemic necrosis. Here, we showed that helper component proteinase (HCPro), encoded by Chilli veinal mottle virus (ChiVMV), could directly interact with catalase 1 (CAT1) and catalase 3 (CAT3) in the cytoplasm of tobacco (Nicotiana tabacum) plants to facilitate viral infection. In vitro, the activities of CAT1 and CAT3 were inhibited by the interaction between HCPro and CATs. The C-terminus of HCPro was essential for their interaction and was also required for the decrease of enzyme activities. Interestingly, the mRNA and protein level of CATs were up-regulated in tobacco plants in response to ChiVMV infection. Nicotiana tabacum plants with HCPro overexpression or CAT1 knockout were more susceptible to ChiVMV infection, which was similar to the case of H2O2-pre-treated plants, and the overexpression of CAT1 inhibited ChiVMV accumulation. Also, neither CAT1 nor CAT3 could affect the RNA silencing suppression (RSS) activity of HCPro. Our results showed that the interaction between HCPro and CATs promoted the development of plant systemic necrosis, revealing a novel role for HCPro in virus infection and pathogenicity.

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Lee, Ying-Ray, Huan-Yao Lei, Shun-Hua Chen, Jen-Reng Wang, Yee-Shin Lin, Trai-Ming Yeh, Ching-Chuan Liu, and Hsiao-Sheng Liu. "Signaling Pathways Involved In Dengue-2 Virus Infection Induced RANTES Overexpression." American Journal of Infectious Diseases 4, no. 1 (January 1, 2008): 32–40. http://dx.doi.org/10.3844/ajidsp.2008.32.40.

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Lindbo, John A. "TRBO: A High-Efficiency Tobacco Mosaic Virus RNA-Based Overexpression Vector." Plant Physiology 145, no. 4 (August 24, 2007): 1232–40. http://dx.doi.org/10.1104/pp.107.106377.

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Zhou, Lian, Hongli He, Ruifang Liu, Qiang Han, Huixia Shou, and Bao Liu. "Overexpression of GmAKT2 potassium channel enhances resistance to soybean mosaic virus." BMC Plant Biology 14, no. 1 (2014): 154. http://dx.doi.org/10.1186/1471-2229-14-154.

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Pulmanausahakul, Rojjanaporn, Milosz Faber, Kinjiro Morimoto, Sergei Spitsin, Eberhard Weihe, D. Craig Hooper, Matthias J. Schnell, and Bernhard Dietzschold. "Overexpression of Cytochrome c by a Recombinant Rabies Virus Attenuates Pathogenicity and Enhances Antiviral Immunity." Journal of Virology 75, no. 22 (November 15, 2001): 10800–10807. http://dx.doi.org/10.1128/jvi.75.22.10800-10807.2001.

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ABSTRACT The pathogenicity of individual rabies virus strains appears to correlate inversely with the extent of apoptotic cell death they induce and with the expression of rabies virus glycoprotein, a major inducer of an antiviral immune response. To determine whether the induction of apoptosis by rabies virus contributes to a decreased pathogenicity by stimulating antiviral immunity, we have analyzed these parameters in tissue cultures and in mice infected with a recombinant rabies virus construct that expresses the proapoptotic protein cytochromec. The extent of apoptosis was strongly increased in primary neuron cultures infected with the recombinant virus carrying the active cytochrome c gene [SPBN-Cytoc(+)], compared with cells infected with the recombinant virus containing the inactive cytochrome c gene [SPBN-Cytoc(−)]. Mortality in mice infected intranasally with SPBN-Cyto c(+) was substantially lower than in SPBN-Cytoc(−)-infected mice. Furthermore, virus-neutralizing antibody (VNA) titers were significantly higher in mice immunized with SPBN-Cyto c(+) at the same dose. The VNA titers induced by these recombinant viruses paralleled their protective activities against a lethal rabies virus challenge infection, with SPBN-Cytoc(+) revealing an effective dose 20 times lower than that of SPBN-Cyto c(−). The strong increase in immunogenicity, coupled with the marked reduction in pathogenicity, identifies the SPBN-Cyto c(+) construct as a candidate for a live rabies virus vaccine.

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Pottinger, Sarah E., Aurelie Bak, Alexandra Margets, Matthew Helm, Lucas Tang, Clare Casteel, and Roger W. Innes. "Optimizing the PBS1 Decoy System to Confer Resistance to Potyvirus Infection in Arabidopsis and Soybean." Molecular Plant-Microbe Interactions® 33, no. 7 (July 2020): 932–44. http://dx.doi.org/10.1094/mpmi-07-19-0190-r.

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The Arabidopsis resistance protein RPS5 is activated by proteolytic cleavage of the protein kinase PBS1 by the Pseudomonas syringae effector protease AvrPphB. We have previously shown that replacing seven amino acids at the cleavage site of PBS1 with a motif cleaved by the NIa protease of turnip mosaic virus (TuMV) enables RPS5 activation upon TuMV infection. However, this engineered resistance conferred a trailing necrosis phenotype indicative of a cell-death response too slow to contain the virus. We theorized this could result from a positional mismatch within the cell between PBS1TuMV, RPS5, and the NIa protease. To test this, we relocalized PBS1TuMV and RPS5 to cellular sites of NIa accumulation. These experiments revealed that relocation of RPS5 away from the plasma membrane compromised RPS5-dependent cell death in Nicotiana benthamiana, even though PBS1 was efficiently cleaved. As an alternative approach, we tested whether overexpression of plasma membrane–localized PBS1TuMV could enhance RPS5 activation by TuMV. Significantly, overexpressing the PBS1TuMV decoy protein conferred complete resistance to TuMV when delivered by either agrobacterium or by aphid transmission, showing that RPS5-mediated defense responses are effective against bacterial and viral pathogens. Lastly, we have now extended this PBS1 decoy approach to soybean by modifying a soybean PBS1 ortholog to be cleaved by the NIa protease of soybean mosaic virus (SMV). Transgenic overexpression of this soybean PBS1 decoy conferred immunity to SMV, demonstrating that we can use endogenous PBS1 proteins in crop plants to engineer economically relevant disease resistant traits.

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Cheng, Xiaogang, Michael Belshan, and Lee Ratner. "Hsp40 Facilitates Nuclear Import of the Human Immunodeficiency Virus Type 2 Vpx-Mediated Preintegration Complex." Journal of Virology 82, no. 3 (November 21, 2007): 1229–37. http://dx.doi.org/10.1128/jvi.00540-07.

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ABSTRACT Human immunodeficiency virus type 2 (HIV-2) Vpx is required for nuclear translocation of the viral preintegration complex (PIC) in quiescent cells. In order to decipher the mechanism of action of Vpx, a cDNA library was screened with the yeast two-hybrid assay, resulting in the identification of heat shock protein 40, Hsp40/DnaJB6, as a Vpx-interactive protein. Interaction with Vpx was confirmed by glutathione S-transferase (GST) pull-down and coimmunoprecipitation assays. Overexpression of Hsp40/DnaJB6 enhanced Vpx nuclear import, whereas overexpression of a nuclear localization mutant of Hsp40/DnaJB6 (H31Q) or down-regulation of Hsp40/DnaJB6 by small interfering RNA (siRNA) reduced the nuclear import of Vpx. Hsp40/DnaJB6 competed with the Pr55Gag precursor protein for the binding of Vpx and incorporation into virus-like particles. Overexpression of Hsp40/DnaJB6 promoted viral PIC nuclear import, whereas siRNA down-regulation of Hsp40/DnaJB6 inhibited PIC nuclear import. These results demonstrate a role for Hsp40/DnaJB6 in the regulation of HIV-2 PIC nuclear transport.

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Bolisetty, Mohan T., George Dy, Wayne Tam, and Karen L. Beemon. "Reticuloendotheliosis Virus Strain T Induces miR-155, Which Targets JARID2 and Promotes Cell Survival." Journal of Virology 83, no. 23 (September 16, 2009): 12009–17. http://dx.doi.org/10.1128/jvi.01182-09.

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ABSTRACT The oncogenic microRNA miR-155 is upregulated by several oncogenic viruses. The precursor of miR-155, termed bic, was first observed to cooperate with myc in chicken B-cell lymphomas induced by avian leukosis proviral integrations. We identified another oncogenic retrovirus, reticuloendotheliosis virus strain T (REV-T), that upregulates miR-155 in chicken embryo fibroblasts. We also observed very high levels of miR-155 in REV-T-induced B-cell lymphomas. To study the role of miR-155 in these tumors, we identified JARID2/Jumonji, a cell cycle regulator and part of a histone methyltransferase complex, as a target of miR-155. The overexpression of miR-155 decreased levels of endogenous JARID2 mRNA. We confirmed that miR-155 directly targets both human and chicken JARID2 by assaying the repression of reporters containing the JARID2 3′-untranslated regions. Further, the overexpression of a sponge complementary to miR-155 in a tumor cell line increased endogenous JARID2 mRNA levels. The overexpression of JARID2 in chicken fibroblasts led to decreased cell numbers and an increase in apoptotic cells. The overexpression of miR-155 rescued cells undergoing cytopathic effect caused by infection with subgroup B avian retroviruses. Therefore, we propose that miR-155 has a prosurvival function that is mediated through the downregulation of targets including JARID2.

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Rajan, Lakshmi, Dana Broussard, Mary Lozano, Chun G. Lee, Christine A. Kozak, and Jaquelin P. Dudley. "The c-myc Locus Is a Common Integration Site in Type B Retrovirus-Induced T-Cell Lymphomas." Journal of Virology 74, no. 5 (March 1, 2000): 2466–71. http://dx.doi.org/10.1128/jvi.74.5.2466-2471.2000.

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ABSTRACT Type B leukemogenic virus (TBLV) induces rapidly appearing T-cell leukemias. TBLV insertions near the c-myc gene were detectable in 2 of 30 tumors tested, whereas 80% of the tumors showed c-myc overexpression. TBLV insertions on chromosome 15 (including a newly identified locus, Pad7) may cause c-myc overexpression by cis-acting effects at a distance.

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Abdullah, Sahibzada Waheed, Shichong Han, Jin’en Wu, Yun Zhang, Manyuan Bai, Ye Jin, Xiaoying Zhi, Junyong Guan, Shiqi Sun, and Huichen Guo. "The DDX23 Negatively Regulates Translation and Replication of Foot-and-Mouth Disease Virus and Is Degraded by 3C Proteinase." Viruses 12, no. 12 (November 25, 2020): 1348. http://dx.doi.org/10.3390/v12121348.

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DEAD-box helicase 23 (DDX23) is a host nuclear helicase, which is a part of the spliceosomal complex and involved in pre-mRNA splicing. To investigate whether DDX23, an internal ribosomal entry sites transacting factor (ITAF) affects foot-and-mouth disease virus (FMDV) replication and translation through internal ribosome entry site (IRES)-dependent manner. For this, we utilized a pull-down assay, Western blotting, quantitative real-time PCR, confocal microscopy, overexpression and small interfering RNA knockdown, as well as the median tissue culture infective dose. Our findings showed that FMDV infection inhibited DDX23 expression and the overexpression of DDX23 reduced viral replication, however, CRISPR Cas9 knockout/small interfering RNA knockdown increased FMDV replication. FMDV IRES domain III and IV interacted with DDX23, whereas DDX23 interacted with FMDV 3C proteinase and significantly degraded. The enzymatic activity of FMDV 3C proteinase degraded DDX23, whereas FMDV degraded DDX23 via the lysosomal pathway. Additionally, IRES-driven translation was suppressed in DDX23-overexpressing cells, and was enhanced in DDX23 knocked down. Collectively, our results demonstrated that DDX23 negatively affects FMDV IRES-dependent translation, which could be a useful target for the design of antiviral drugs.

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Peng, Chih-Wen, Bo Zhao, Hong-Chi Chen, Min-Luen Chou, Chiou-Yan Lai, Shinn-Zong Lin, Hsue-Yin Hsu, and Elliott Kieff. "Hsp72 up-regulates Epstein-Barr virus EBNALP coactivation with EBNA2." Blood 109, no. 12 (June 15, 2007): 5447–54. http://dx.doi.org/10.1182/blood-2006-08-040634.

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AbstractThe Epstein-Barr virus (EBV) transcriptional coactivator EBNALP specifically associates and colocalizes with Hsp72 in lymphoblastoid cell lines. We now find that overexpression of Hsp72 more than doubled EBNALP coactivation with EBNA2 of a transfected EBV LMP1 promoter in B lymphoblasts, did not affect EBNA2 or EBNALP protein levels, and strongly up-regulated EBNA2 and EBNALP coactivation of LMP1 protein expression from the endogenous EBV genome in latency I infected Akata cells. The Hsp72 ATP, protein binding, and the C-terminal regulatory domains were required for full activity. An EBNALP deletion mutant, EBNALPd45, which does not associate with Hsp72, coactivated with EBNA2, but was not affected by Hsp72 overexpression, despite Hsp72 up-regulation of wild-type EBNALP coactivation with EBNA2 at all levels of EBNALP expression, indicating the importance of Hsp72 association with EBNALP for Hsp72 up-regulation of coactivation. Of importance, a 90% RNAi knockdown of Hsp72 reduced EBNALP coactivation with EBNA2 of transfected EBV LMP1 and Cp promoters by approximately 50%. Overexpression of the Hsp72 C-terminal interacting and regulatory protein, CHIP, strongly down-regulated EBNALP coactivation, independently of CHIP ubiquitin ligase activity. CHIP effects were Hsp72 dependent, indicating a background downmodulating role for CHIP in Hsp72 augmentation of EBNA2 and EBNALP coactivation. Based on these and other cited data, we favor a model in which Hsp72 chaperones EBNALP shuttling of repressors from EBNA2-enhanced promoters.

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Jain, Surbhi, Lori W. McGinnes, and Trudy G. Morrison. "Overexpression of Thiol/Disulfide Isomerases Enhances Membrane Fusion Directed by the Newcastle Disease Virus Fusion Protein." Journal of Virology 82, no. 24 (October 1, 2008): 12039–48. http://dx.doi.org/10.1128/jvi.01406-08.

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ABSTRACT Newcastle disease virus (NDV) fusion (F) protein directs membrane fusion, which is required for virus entry and cell-cell fusion. We have previously shown that free thiols are present in cell surface-expressed NDV F protein and that blocking the production of free thiols by thiol-disulfide exchange inhibitors inhibited the membrane fusion mediated by F protein (J Virol. 81:2328-2339, 2007). Extending these observations, we evaluated the role of the overexpression of two disulfide bond isomerases, protein disulfide isomerase (PDI) and ERdj5, in cell-cell fusion mediated by NDV glycoproteins. The overexpression of these isomerases resulted in significantly increased membrane fusion, as measured by syncytium formation and content mixing. The overexpression of these isomerases enhanced the production of free thiols in F protein when expressed without hemagglutination-neuraminidase (HN) protein but decreased free thiols in F protein expressed with HN protein. By evaluating the binding of conformation-sensitive antibodies, we found that the overexpression of these isomerases favored a postfusion conformation of surface-expressed F protein in the presence of HN protein. These results suggest that isomerases belonging to the PDI family catalyze the production of free thiols in F protein, and free thiols in F protein facilitate membrane fusion mediated by F protein.

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Bluhm, Wolfgang F., Jody L. Martin, Ruben Mestril, and Wolfgang H. Dillmann. "Specific heat shock proteins protect microtubules during simulated ischemia in cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 6 (December 1, 1998): H2243—H2249. http://dx.doi.org/10.1152/ajpheart.1998.275.6.h2243.

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The protective effects of heat shock proteins (HSPs) during myocardial ischemia are now well documented, but little is known about the mechanisms of protection and the specificity of different HSPs. Because cytoskeletal injury plays a crucial role in the pathogenesis of irreversible ischemic damage, we tested whether overexpression of specific HSPs protects the integrity of microtubules during simulated ischemia in rat neonatal cardiac myocytes. Overexpression of specific HSPs was achieved by adenovirus-mediated transgene expression. Damage was assessed by comparing control cells to cells that were subjected to a simulated ischemia protocol. Microtubular integrity was measured by indirect immunofluorescence, confocal microscopy, and image analysis. Within 14 h of simulated ischemia, microtubular integrity decreased significantly in uninfected myocytes (from 24.6 ± 1.2 to 13.2 ± 0.4) and in myocytes infected with a control virus that expressed no transgene (from 25.9 ± 1.8 to 13.1 ± 1.4). Microtubular integrity after ischemia was significantly better preserved in cells overexpressing constitutive Hsp70 (21.7 ± 1.6) or αB-crystallin (18.0 ± 2.7) but not in cells overexpressing inducible Hsp70 (11.5 ± 0.8) or Hsp27 (14.0 ± 2.2). We conclude that specific HSPs protect the microtubules during simulated cardiac ischemia.

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PASMANIK-CHOR, Metsada, Orna ELROY-STEIN, Hans AERTS, Vered AGMON, Shimon GATT, and Mia HOROWITZ. "Overexpression of human glucocerebrosidase containing different-sized leaders." Biochemical Journal 317, no. 1 (July 1, 1996): 81–88. http://dx.doi.org/10.1042/bj3170081.

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Gaucher disease results from impaired activity of the lysosomal enzyme glucocerebrosidase. Aiming at overexpressing the human glucocerebrosidase and testing the efficiency of the two in-frame ATGs of its gene in directing synthesis of an active enzyme, it was coupled to the T7 RNA polymerase promoter in a vaccinia virus-derived expression vector (pTM-1). cDNAs containing either one or both ATGs of the glucocerebrosidase mRNA were linked to the T7 polymerase promoter. Recombinant viruses were produced and used for infecting human cells in tissue culture. The results demonstrated that both ATGs directed translation of active glucocerebrosidase, resulting in a 10-fold increase in enzymic activity. Most of the protein remained sensitive to endoglycosidase H. The active enzyme represented a small fraction of the expressed glucocerebrosidase. The recombinant enzyme had the same Km and optimal pH towards the artificial substrate 4-methylumbelliferyl glucopyranoside as the authentic endogenous human enzyme. Measurements of intracellular enzymic activity directed by the cDNAs with either one or both ATGs in cells loaded with a fluorescent glucosylceramide demonstrated a 30% increase in activity directed by the cDNAs containing the first ATG over that containing the second ATG. This indicates that the protein synthesized from the first ATG, with a 38 amino acid leader, is translocated through the endoplasmic reticulum more readily than its counterpart directed by the second ATG, with a 19 amino acid leader. The elevation in glucocerebrosidase activity and the reproducibility of the data leads us to propose the use of the vaccinia virus-derived expression system as a tool for studying glucocerebrosidase mutants in Gaucher disease.

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de Sá, Patricia B., Hua Li, Wendy M. Havens, Mark L. Farman, and Said A. Ghabrial. "Overexpression of the Victoriocin Gene in Helminthosporium (Cochliobolus) victoriae Enhances the Antifungal Activity of Culture Filtrates." Phytopathology® 100, no. 9 (September 2010): 890–96. http://dx.doi.org/10.1094/phyto-100-9-0890.

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We have previously reported the isolation and characterization of the broad-spectrum antifungal protein, victoriocin, from culture filtrates of a virus-infected isolate of the plant-pathogenic fungus Helminthosporium (teleomorph: Cochliobolus) victoriae. We predicted that the 10-kDa mature victoriocin is derived in vivo from a preprotoxin precursor that is processed by a signal peptidase and kexin-like endopeptidase. We also presented evidence that the victoriocin precursor is encoded by a host gene, designated the victoriocin (vin) gene. In the present study, an H. victoriae genomic DNA library was constructed in the cosmid vector pMLF-2, and a cosmid clone carrying the vin gene and flanking sequences was isolated and used to generate constructs for transformation of virus-free and virus-infected H. victoriae isolates with the vin gene. Culture filtrates of the virus-free vin transformants exhibited high levels of antifungal activity compared with that revealed by the nontransformed virus-free wild-type strain, which exhibited little or no antifungal activity. Moreover, transformation of the wild-type virus-infected H. victoriae strain with the vin gene resulted in still higher production of victoriocin and higher antifungal activity in the culture filtrates of the vin transformants compared with the virus-infected wild-type strain. As previously predicted, the presence in the vin transformants of the preprovictoriocin and its post-translationally generated products, the provictoriocin and the mature victoriocin, was clearly demonstrated. Processing of the victoriocin preprotoxin requires eukaryotic host factors because no processing occurred in an in vitro translation system or in bacteria. It is of interest that some of the virus-free isolates transformed with the vin gene exhibited some features of the virus-induced disease phenotype, including moderate stunting and sectoring. Present data suggests that victoriocin may play an indirect role in disease development. Taken together, these results indicate that victoriocin is the primary protein responsible for the antifungal activity in culture filtrates of virus-infected H. victoriae isolates and that virus infection upregulates the expression of victoriocin. Overproduction of victoriocin may give the slower-growing virus-infected fungal strains some competitive advantage by inhibiting the growth of other fungi.

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Tischer, B. Karsten, Daniel Schumacher, Danièlle Chabanne-Vautherot, Vladimir Zelnik, Jean-François Vautherot, and Nikolaus Osterrieder. "High-Level Expression of Marek's Disease Virus Glycoprotein C Is Detrimental to Virus Growth In Vitro." Journal of Virology 79, no. 10 (May 15, 2005): 5889–99. http://dx.doi.org/10.1128/jvi.79.10.5889-5899.2005.

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ABSTRACT Expression levels of Marek's disease virus (MDV) glycoprotein C (gC) are significantly reduced after serial virus passage in cell culture. Reduced gC expression coincides with enhanced MDV growth in vitro and attenuation. To analyze this phenomenon in detail, a full-length infectious MDV clone was modified by Red-based and shuttle mutagenesis in Escherichia coli. Besides a gC-negative deletion mutant harboring a kanamycin resistance gene, a markerless mutant with the UL 44 gene deleted was constructed. On the basis of this deletion mutant, the original or a modified UL 44 gene with a mutated start codon (AUG→ACG) was reinserted into the authentic locus. Similarly, mutants expressing authentic gC or the start codon mutation under the control of a strong constitutive promoter were generated. In vitro studies demonstrated that gC deletion mutants induced twofold-larger plaques than the parental virus did, whereas constitutive overexpression of the glycoprotein resulted in a more than twofold reduction in plaque size. In addition, plaque sizes of the gC deletion mutant were reduced when virus was grown using supernatants from cells infected with parental virus, but supernatants obtained from cells infected with the gC deletion mutant had no measurable effect on plaque size. The results indicated that (i) expression of MDV gC, albeit at low levels in a highly passaged virus, had a significant negative impact on the cell-to-cell spread capabilities of the virus, which was alleviated in its absence and exacerbated by its overexpression, and that (ii) this activity was mediated by the secreted form of MDV gC.

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LESLIE, J., F. J. RIXON, and J. MCLAUCHLAN. "Overexpression of the Herpes Simplex Virus Type 1 Tegument Protein VP22 Increases Its Incorporation into Virus Particles." Virology 220, no. 1 (June 1996): 60–68. http://dx.doi.org/10.1006/viro.1996.0286.

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Luukkonen, B. G. Mattias, Eva Maria Fenyö, and Stefan Schwartz. "Overexpression of Human Immunodeficiency Virus Type 1 Protease Increases Intracellular Cleavage of Gag and Reduces Virus Infectivity." Virology 206, no. 2 (February 1995): 854–65. http://dx.doi.org/10.1006/viro.1995.1008.

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Sinha, Kumari Veena, Abdul Kader Jailani, Bikash Mandal, Sunil K. Mukherjee, and Neeti Sanan-Mishra. "Overexpression of an insect virus encoded silencing suppressor does not enhance plants’ susceptibility to its natural virus." VirusDisease 32, no. 2 (March 30, 2021): 338–42. http://dx.doi.org/10.1007/s13337-020-00644-5.

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Carsillo, Mary, Dhohyung Kim, and Stefan Niewiesk. "Role of AKT Kinase in Measles Virus Replication." Journal of Virology 84, no. 4 (November 25, 2009): 2180–83. http://dx.doi.org/10.1128/jvi.01316-09.

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ABSTRACT Many RNA and DNA viruses activate serine-threonine kinase AKT to increase virus replication. In contrast, measles virus (MV) infection leads to downregulation of AKT. This is thought to be beneficial for the virus because it correlates with immune suppression. To determine whether this is a sacrifice for the virus, we used a recombinant virus and transfected cells expressing constitutively active AKT and evaluated its effect on virus replication. In vitro, overexpression of AKT did not influence virus replication but did affect (cell-type dependent) virus release. In vivo, the recombinant virus did not abrogate inhibition of proliferation of spleen cells from MV-infected cotton rats.

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Kelly, James T., Stacey Human, Joseph Alderman, Fatoumatta Jobe, Leanne Logan, Thomas Rix, Daniel Gonçalves-Carneiro, et al. "BST2/Tetherin Overexpression Modulates Morbillivirus Glycoprotein Production to Inhibit Cell–Cell Fusion." Viruses 11, no. 8 (July 30, 2019): 692. http://dx.doi.org/10.3390/v11080692.

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The measles virus (MeV), a member of the genus Morbillivirus, is an established pathogen of humans. A key feature of morbilliviruses is their ability to spread by virus–cell and cell–cell fusion. The latter process, which leads to syncytia formation in vitro and in vivo, is driven by the viral fusion (F) and haemagglutinin (H) glycoproteins. In this study, we demonstrate that MeV glycoproteins are sensitive to inhibition by bone marrow stromal antigen 2 (BST2/Tetherin/CD317) proteins. BST2 overexpression causes a large reduction in MeV syncytia expansion. Using quantitative cell–cell fusion assays, immunolabeling, and biochemistry we further demonstrate that ectopically expressed BST2 directly inhibits MeV cell–cell fusion. This restriction is mediated by the targeting of the MeV H glycoprotein, but not other MeV proteins. Using truncation mutants, we further establish that the C-terminal glycosyl-phosphatidylinositol (GPI) anchor of BST2 is required for the restriction of MeV replication in vitro and cell–cell fusion. By extending our study to the ruminant morbillivirus peste des petits ruminants virus (PPRV) and its natural host, sheep, we also confirm this is a broad and cross-species specific phenotype.

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Guo, Qi, Liang Zhao, Xinqi Fan, Peng Xu, Zhenzhen Xu, Xianggui Zhang, Shan Meng, and Xinlian Shen. "Transcription Factor GarWRKY5 Is Involved in Salt Stress Response in Diploid Cotton Species (Gossypium aridum L.)." International Journal of Molecular Sciences 20, no. 21 (October 23, 2019): 5244. http://dx.doi.org/10.3390/ijms20215244.

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Cotton is one of the most economically important crops in the world, and it is exposed to various abiotic stresses during its lifecycle, especially salt stress. However, the molecular mechanisms underlying cotton tolerance to salt stress are still not fully understood due to the complex nature of salt response. Therefore, identification of salt stress tolerance-related functional genes will help us understand key components involved in stress response and provide valuable genes for improving salt stress tolerance via genetic engineering in cotton. In the present study, virus-induced gene silencing of GhWRKY5 in cotton showed enhanced salt sensitivity compared to wild-type plants under salt stress. Overexpression of GarWRKY5 in Arabidopsis positively regulated salt tolerance at the stages of seed germination and vegetative growth. Additionally, GarWRKY5-overexpressing plants exhibited higher activities of superoxide dismutase (SOD) and peroxidase (POD) under salt stress. The transcriptome sequencing analysis of transgenic Arabidopsis plants and wild-type plants revealed that there was enriched coexpression of genes involved in reactive oxygen species (ROS) scavenging (including glutamine S-transferases (GSTs) and SODs) and altered response to jasmonic acid and salicylic acid in the GarWRKY5-OE lines. GarWRKY5 is involved in salt stress response by the jasmonic acid- or salicylic acid-mediated signaling pathway based on overexpression of GarWRKY5 in Arabidopsis and virus-induced gene silencing of GarWRKY5 in cotton.

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Algarté, Michèle, Hannah Nguyen, Christophe Heylbroeck, Rongtuan Lin, and John Hiscott. "IκB-Mediated Inhibition of Virus-Induced Beta Interferon Transcription." Journal of Virology 73, no. 4 (April 1, 1999): 2694–702. http://dx.doi.org/10.1128/jvi.73.4.2694-2702.1999.

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ABSTRACT We have examined the consequences of overexpression of the IκBα and IκBβ inhibitory proteins on the regulation of NF-κB-dependent beta interferon (IFN-β) gene transcription in human cells after Sendai virus infection. In transient coexpression studies or in cell lines engineered to express different forms of IκB under tetracycline-inducible control, the IFN-β promoter (−281 to +19) linked to the chloramphenicol acetyltransferase reporter gene was differentially inhibited in response to virus infection. IκBα exhibited a strong inhibitory effect on virus-induced IFN-β expression, whereas IκBβ exerted an inhibitory effect only at a high concentration. Despite activation of the IκB kinase complex by Sendai virus infection, overexpression of the double-point-mutated (S32A/S36A) dominant repressors of IκBα (TD-IκBα) completely blocked IFN-β gene activation by Sendai virus. Endogenous IFN-β RNA production was also inhibited in Tet-inducible TD-IκBα-expressing cells. Inhibition of IFN-β expression directly correlated with a reduction in the binding of NF-κB (p50-RelA) complex to PRDII after Sendai virus infection in IκBα-expressing cells, whereas IFN-β expression and NF-κB binding were only slightly reduced in IκBβ-expressing cells. These experiments demonstrate a major role for IκBα in the regulation of NF-κB-induced IFN-β gene activation and a minor role for IκBβ in the activation process.

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Li, Weike, Ravi Chakra Turaga, Xin Li, Malvika Sharma, Zahra Enadi, Sydney Nicole Dunham Tompkins, Kyle Christian Hardy, et al. "Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance." Molecular Therapy - Oncolytics 14 (September 2019): 188–95. http://dx.doi.org/10.1016/j.omto.2019.05.006.

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Ojima, Hitoshi, Toshio Fukuda, Takashi Nakajima, and Yukio Nagamachi. "Infrequent Overexpression of p53 Protein in Epstein-Barr Virus-associated Gastric Carcinomas." Japanese Journal of Cancer Research 88, no. 3 (March 1997): 262–66. http://dx.doi.org/10.1111/j.1349-7006.1997.tb00376.x.

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Journal articles on the topic 'Virus overexpression'

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