scholarly journals Potential of Genetically- Modified Measles Virus as A Treatment Modality For Carcinoma: A Review

2018 ◽  
Vol 11 (2) ◽  
pp. 917-922
Author(s):  
Anirudha kabilan ◽  
Lakshmi Lakshmi ◽  
Pavithra Priyadarshoni S
Keyword(s):  
Measles Virus ◽  
Genetically Modified ◽  
Leukemia Virus ◽  
Mumps Virus ◽  
Moloney Leukemia Virus ◽  
Advanced Stages ◽  
Vesicular Stomatitis ◽  
Simplex Virus ◽  
Methods Of Treatment ◽  
Natural Preference

Malignancy is a disease in which cell division is uncontrolled and prognosis is often poor. Despite recent advances in the felid of medicine the life expectancy after the diagnosis of advanced stages of cancers has high mortality rates . The traditional methods of treatment have low curative effects and high risk of side effects. Further the possibility of re-occurrence is not completely eliminated by any of the conventional methods of treatment. Thus, a technique that affects only the tumour cells without leaving behind any cancer initiator cells must be deviced. Recently genetically modified variants of measles virus were used to cure multiple myeloma .The idea to use of measles virus dates back to 1950’s.Constant research has lead the advent of a branch known as oncolytic virotheraphy . Precise targeting of cancer cells is one of the dominant advantages of cancer therapy through virus and it can be achieved in multiple manners. A few viruses such as exclusively replicating mumps virus, moloney leukemia virus, parvoviruses, reovirus, newcastle disease virus have a natural preference for malignant cells, whereas vesicular stomatitis adenovirus, virus, measles, vaccinia and herpes simplex virus can be adapted or engineered to make them cancer-specific.

scholarly journals IFN-stimulated P2Y13 protects mice from viral infection by suppressing the cAMP/EPAC1 signaling pathway

2018 ◽  
Vol 11 (5) ◽  
pp. 395-407 ◽  
Author(s):  
Chengfei Zhang ◽  
Yan Yan ◽  
Hongwang He ◽  
Li Wang ◽  
Na Zhang ◽  
...  
Keyword(s):  
Viral Infection ◽  
Viral Infections ◽  
Leukemia Virus ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Herpes Simplex Virus 1 ◽  
Antiviral Activities ◽  
Vesicular Stomatitis ◽  
Simplex Virus ◽  
Antiviral Targets

Abstract Among the most important sensors of extracellular danger signals, purinergic receptors have been demonstrated to play crucial roles in host defense against infection. However, the function of P2 receptors in viral infection has been little explored. Here we demonstrated that P2Y13 and its ligand ADP play an important role in protecting hosts from viral infections. First, we demonstrate that P2Y13, as a typical interferon-stimulated gene, is induced together with extracellular ADP during viral infection. Most importantly, extracellular ADP restricts the replication of different kinds of viruses, including vesicular stomatitis virus, Newcastle disease virus, herpes simplex virus 1, and murine leukemia virus. This kind of protection is dependent on P2Y13 but not P2Y1 or P2Y12, which are also considered as receptors for ADP. Furthermore, cyclic adenosine monophosphate and EPAC1 are downregulated by extracellular ADP through the P2Y13-coupled Gi alpha subunit. Accordingly, inhibition or deletion of EPAC1 significantly eliminates ADP/P2Y13-mediated antiviral activities. Taken together, our results show that P2Y13 and ADP play pivotal roles in the clearance of invaded virus and have the potential as antiviral targets.

Altered thymic epithelial cells may be decisive for Moloney virus-induced lymphoma development

1983 ◽  
Vol 41 ◽  
pp. 784-785
Author(s):  
U.I. Heine ◽  
G.R.F. Krueger ◽  
E. Munoz ◽  
A. Karpinski
Keyword(s):  
Epithelial Cells ◽  
Leukemia Virus ◽  
Light And Electron Microscopy ◽  
Tumor Development ◽  
Current Evidence ◽  
Thymic Epithelial Cells ◽  
Thymic Tissue ◽  
Newborn Mice ◽  
Moloney Leukemia Virus ◽  
Differentiation Block

Infection of newborn mice with Moloney leukemia virus (M-MuLV) causes a T-cell differentiation block in the thymic cortex accompanied by proliferation and accumulation of prethymic lymphoblasts in the thymus and subsequent spreading of these cells to generate systemic lymphoma. Current evidence shows that thymic reticular epithelial cells (REC) provide a microenvironment necessary for the maturation of prethymic lymphoblasts to mature T-lymphocytes by secretion of various thymic factors. A change in that environment due to infection of REC by virus could be decisive for the failure of lymphoblasts to mature and thus contribute to lymphoma development.We have studied the morphology and distribution of the major thymic cell populations at different stages of tumorigenesis in Balb/c mice infected when newborn with 0.2ml M-MuLV suspension, 6.8 log FFU/ml. Thymic tissue taken at 1-2 weekly intervals up to tumor development was processed for light and electron microscopy, using glutaraldehyde-OsO4fixation and Epon-Araldite embedding.

Aberrant Type C Virus Production in a Cell Line Derived from Balb/3T3

1972 ◽  
Vol 30 ◽  
pp. 286-287
Author(s):  
N. Savage ◽  
A. Hackett
Keyword(s):  
Electron Microscopy ◽  
Cell Line ◽  
Leukemia Virus ◽  
Morphological Characteristics ◽  
Virus Production ◽  
Oncogenic Viruses ◽  
Endogenous Virus ◽  
Virus Particles ◽  
Moloney Leukemia Virus ◽  
A Cell

A cell line, UC1-B, which was derived from Balb/3T3 cells, maintains the same morphological characteristics of the non-transformed parental culture, and shows no evidence of spontaneous virus production. Survey by electron microscopy shows that the cell line consists of spindle-shaped cells with no unusual features and no endogenous virus particles.UC1-B cells respond to Moloney leukemia virus (MLV) infection by a change in morphology and growth pattern which is typical of cells transformed by sarcoma virus. Electron microscopy shows that the cells are now variable in shape (rounded, rhomboid, and spindle), and each cell type has some microvilli. Virtually all (90%) of the cells show virus particles developing at the cell surface and within the cytoplasm. Maturing viruses, typical of the oncogenic viruses, are found along with atypical tubular forms in the same cell.

scholarly journals Structure and assembly of double-headed Sendai virus nucleocapsids

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Na Zhang ◽  
Hong Shan ◽  
Mingdong Liu ◽  
Tianhao Li ◽  
Rui Luo ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Measles Virus ◽  
Sendai Virus ◽  
Nipah Virus ◽  
Mumps Virus ◽  
Genome Replication ◽  
Direct Visualization ◽  
Closed State ◽  
Cryo Electron Microscopy ◽  
Negative Sense

AbstractParamyxoviruses, including the mumps virus, measles virus, Nipah virus and Sendai virus (SeV), have non-segmented single-stranded negative-sense RNA genomes which are encapsidated by nucleoproteins into helical nucleocapsids. Here, we reported a double-headed SeV nucleocapsid assembled in a tail-to-tail manner, and resolved its helical stems and clam-shaped joint at the respective resolutions of 2.9 and 3.9 Å, via cryo-electron microscopy. Our structures offer important insights into the mechanism of the helical polymerization, in particular via an unnoticed exchange of a N-terminal hole formed by three loops of nucleoproteins, and unveil the clam-shaped joint in a hyper-closed state for nucleocapsid dimerization. Direct visualization of the loop from the disordered C-terminal tail provides structural evidence that C-terminal tail is correlated to the curvature of nucleocapsid and links nucleocapsid condensation and genome replication and transcription with different assembly forms.

scholarly journals Adaptation of a retrovirus as a eucaryotic vector transmitting the herpes simplex virus thymidine kinase gene.

1982 ◽  
Vol 2 (4) ◽  
pp. 426-436 ◽  
Author(s):  
C J Tabin ◽  
J W Hoffmann ◽  
S P Goff ◽  
R A Weinberg
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Thymidine Kinase ◽  
Dna Sequences ◽  
Leukemia Virus ◽  
Chimeric Virus ◽  
Animal Cells ◽  
Kinase Gene ◽  
General Applicability ◽  
Simplex Virus

We investigated the feasibility of using retroviruses as vectors for transferring DNA sequences into animal cells. The thymidine kinase (tk) gene of herpes simplex virus was chosen as a convenient model. The internal BamHI fragments of a DNA clone of Moloney leukemia virus (MLV) were replaced with a purified BamHI DNA segment containing the tk gene. Chimeric genomes were created carrying the tk insert in both orientations relative to the MLV sequence. Each was transfected into TK- cells along with MLV helper virus, and TK+ colonies were obtained by selection in the presence of hypoxanthine, aminopterin, and thymidine (HAT). Virus collected from TK+-transformed, MLV producer cells passed the TK+ phenotype to TK- cells. Nonproducer cells were isolated, and TK+ transducing virus was subsequently rescued from them. The chimeric virus showed single-hit kinetics in infections. Virion and cellular RNA and cellular DNA from infected cells were all shown to contain sequences which hybridized to both MLV- and tk-specific probes. The sizes of these sequences were consistent with those predicted for the chimeric virus. In all respects studied, the chimeric MLV-tk virus behaved like known replication-defective retroviruses. These experiments suggest great general applicability of retroviruses as eucaryotic vectors.

A novel myoblast enhancer element mediates MyoD transcription

1992 ◽  
Vol 12 (11) ◽  
pp. 4994-5003
Author(s):  
S J Tapscott ◽  
A B Lassar ◽  
H Weintraub
Keyword(s):  
Skeletal Muscle ◽  
Specific Activity ◽  
Leukemia Virus ◽  
Regulatory Region ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Enhancer Element ◽  
Distal Regulatory Region ◽  
Avian Muscle ◽  
Moloney Leukemia Virus

The MyoD gene can orchestrate the expression of the skeletal muscle differentiation program. We have identified the regions of the gene necessary to reproduce transcription specific to skeletal myoblasts and myotubes. A proximal regulatory region (PRR) contains a conserved TATA box, a CCAAT box, and a GC-rich region that includes a consensus SP1 binding site. The PRR is sufficient for high levels of skeletal muscle-specific activity in avian muscle cells. In murine cells the PRR alone has only low levels of activity and requires an additional distal regulatory region to achieve high levels of muscle-specific activity. The distal regulatory region differs from a conventional enhancer in that chromosomal integration appears necessary for productive interactions with the PRR. While the Moloney leukemia virus long terminal repeat can enhance transcription from the MyoD PRR in both transient and stable assays, the simian virus 40 enhancer cannot, suggesting that specific enhancer-promoter interactions are necessary for PRR function.

scholarly journals Identification of Homeodomain Proteins, PBX1 and PREP1, Involved in the Transcription of Murine Leukemia Virus

2003 ◽  
Vol 23 (3) ◽  
pp. 831-841 ◽  
Author(s):  
Sheng-Hao Chao ◽  
John R. Walker ◽  
Sumit K. Chanda ◽  
Nathanael S. Gray ◽  
Jeremy S. Caldwell
Keyword(s):  
Murine Leukemia Virus ◽  
Kinase Inhibitors ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Viral Transcription ◽  
Long Terminal Repeats ◽  
Homeodomain Proteins ◽  
Cellular Genes ◽  
Simplex Virus ◽  
Murine Leukemia

ABSTRACT Cyclin-dependent kinase inhibitors (CDKIs) have been shown to block human immunodeficiency virus and herpes simplex virus. It is hypothesized that CDKIs block viral replication by inhibiting transcription of specific cellular genes. Here we find that three CDKIs, flavopiridol, purvalanol A, and methoxy-roscovitine, block Moloney murine leukemia virus (MLV) transcription events. Using gene expression microarray technology to examine the inhibitory effects of CDKIs, we observed a cellular gene, the pre-B-cell leukemia transcription factor 1 (Pbx1) gene, down-regulated by CDKI treatment. The PBX consensus element (PCE), TGATTGAC, is conserved in the long terminal repeats of several murine retroviruses, including Moloney MLV. Mutations in the PCE completely inhibited viral transcription whereas overexpression of PBX1 and a PBX1-associated protein, PREP1, enhanced viral transcription. The interaction between the PCE and PBX1-PREP1 proteins was confirmed by gel shift experiments. Blocking PBX1 protein synthesis resulted in a significant decrease in viral transcription. Collectively, our results represent the first work demonstrating that the homeodomain proteins PBX1 and PREP1 are cellular factors involved in Moloney MLV transcription regulation.

scholarly journals Many Nonmammalian Cells Exhibit Postentry Blocks to Transduction by Gammaretroviruses Pseudotyped with Various Viral Envelopes, Including Vesicular Stomatitis Virus G Glycoprotein

2001 ◽  
Vol 75 (14) ◽  
pp. 6375-6383 ◽  
Author(s):  
Clarissa Dirks ◽  
A. Dusty Miller
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Reverse Transcription ◽  
Leukemia Virus ◽  
Culture Conditions ◽  
Viral Envelope ◽  
Division Rate ◽  
Retroviral Transduction ◽  
Vesicular Stomatitis ◽  
Viral Envelopes ◽  
Vector Transduction

ABSTRACT Previous studies have suggested that Moloney murine leukemia virus (MoMLV)-based vectors pseudotyped with the vesicular stomatitis virus G glycoprotein (VSV-G) have extensive ability to transduce nonmammalian cells. However, we have identified multiple cell lines from fish (FHM), mosquitoes (Mos-55), moths (Sf9 and High-5), flies (S2), and frogs (XPK2) that are not efficiently transduced by MoMLV-based vectors pseudotyped with many different viral envelope proteins, including VSV-G, while the same vectors are functional in these cells following transfection. A comparison of MoMLV-based vector transduction in mammalian and nonmammalian cells shows that the nonmammalian cells exhibit blocks at either entry, reverse transcription, or integration. Additionally, VSV-G-pseudotyped MoMLV-based vector transduction is attenuated in the zebrafish cell line ZF4 at entry and/or reverse transcription, whereas other transduction processes are unaffected. We show that the variation of transduction by MoMLV-based vectors in mammalian and nonmammalian cells is not due to differences in culture conditions or cell division rate but is likely the result of divergence in cellular factors required for retroviral transduction.

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