scholarly journals Tamoxifen Protects from Vesicular Stomatitis Virus Infection

2019 ◽  
Vol 12 (4) ◽  
pp. 142 ◽  
Author(s):  
Lamin B. Cham ◽  
Sarah-Kim Friedrich ◽  
Tom Adomati ◽  
Hilal Bhat ◽  
Maximilian Schiller ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Vesicular Stomatitis Virus ◽  
Early Stage ◽  
Vero Cells ◽  
Inhibitory Effect ◽  
Virus Infections ◽  
Biological Targets ◽  
Vesicular Stomatitis

Background: Tamoxifen (TAM) is an estrogen-receptor antagonist, widely used in the adjuvant treatment of early stage estrogen-sensitive breast cancer. Several studies have revealed new biological targets of TAM that mediate the estrogen receptor independent activities of the drug. Recently, the antiviral activity of TAM on replication of human immunodeficiency virus (HIV), hepatitis C virus (HCV) and Herpes simplex virus (HSV-1) in vitro was described. In the current study, we aimed to investigate the effect of TAM on infection with vesicular stomatitis virus (VSV). Methods: Vero cells were treated with different concentrations of TAM for 24 h and then infected with VSV. Additionally, C57BL/6 mice were pretreated with 4 mg TAM, one day and three days before infection with VSV. Results: Treatment of Vero cells with TAM suppressed the viral replication of VSV in vitro and in vivo. The inhibitory effect of TAM on VSV replication correlated with an enhanced interferon-I response and stimulation of macrophages. Conclusions: TAM was identified as being capable to protect from VSV infection in vitro and in vivo. Consequently, this antiviral function (as an advantageous side-effect of TAM) might give rise to new clinical applications, such as treatment of resistant virus infections, or serve as an add-on to standard antiviral therapy.

Further studies on the relative antiviral efficacies of interferons induced by polyI:C and Mengo virus

1976 ◽  
Vol 22 (5) ◽  
pp. 712-718 ◽  
Author(s):  
J. B. Campbell
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Reduction Method ◽  
Mouse Serum ◽  
Antiviral Action ◽  
Virus Infections ◽  
Lethal Infection ◽  
Vesicular Stomatitis ◽  
Mengo Virus

Mouse serum interferons induced by polyI:C, vesicular stomatitis virus (VSV), reovirus, and Mengo virus were assayed in monolayers of mouse L-929 cells by the plaque-reduction method using both VSV and Mengo as challenge viruses. Titers obtained with Mengo virus as challenge were all lower than with VSV. With the interferons induced by VSV, reovirus, and polyI:C, the reductions were of the order of two- to three-fold. With Mengo virus-induced interferon the reduction was much greater (about 17-fold). This offers an explanation for the observation that, unit for unit (measured by the plaque reduction of VSV), Mengo virus-induced interferon is only about [Formula: see text] as effective as polyI:C-induced interferon in protecting mice against lethal infection with Mengo virus. The data are consistent with the hypothesis that an interferon antagonist is produced in the serum of mice infected with Mengo virus. This antagonist, which is not produced in mice inoculated with polyI:C, or reovirus, effectively blocks the antiviral action of interferon during Mengo virus infections, both in vivo and in vitro.

scholarly journals A Potential Nutraceutical Candidate Lactucin Inhibits Adipogenesis through Downregulation of JAK2/STAT3 Signaling Pathway-Mediated Mitotic Clonal Expansion

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 331 ◽  
Author(s):  
Xin Wang ◽  
Min Liu ◽  
Guo He Cai ◽  
Yan Chen ◽  
Xiao Chen Shi ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Early Stage ◽  
Lipid Synthesis ◽  
Clonal Expansion ◽  
Inhibitory Effect ◽  
Limiting Factor ◽  
Stat3 Signaling Pathway ◽  
Mitotic Clonal Expansion

The prevalence of obesity has increased dramatically worldwide in the past ~50 years. Searching for safe and effective anti-obesity strategies are urgently needed. Lactucin, a plant-derived natural small molecule, is known for anti-malaria and anti-hyperalgesia. The study is to investigate whether lactucin plays a key role in adipogenesis. To this end, in vivo male C57BL/6 mice fed a high-fat diet (HFD) were treated with 20 mg/kg/day of lactucin or vehicle by gavage for seven weeks. Compared with vehicle-treated controls, Lactucin-treated mice showed lower body mass and mass of adipose tissue. Consistently, in vitro 3T3-L1 cells were treated with 20 μM of lactucin. Compared to controls, lactucin-treated cells showed significantly less lipid accumulation during adipocyte differentiation and lower levels of lipid synthesis markers. Mechanistically, we showed the anti-adipogenic property of lactucin was largely limited to the early stage of adipogenesis. Lactucin-treated cells fail to undergo mitotic clonal expansion (MCE). Further studies demonstrate that lactucin-induced MCE arrests might result from reduced phosphorylation of JAK2 and STAT3. We then asked whether activation of JAK2/STAT3 would restore the inhibitory effect of lactucin on adipogenesis with pharmacological STAT3 activator colivelin. Our results revealed similar levels of lipid accumulation between lactucin-treated cells and controls in the presence of colivelin, indicating that inactivation of STAT3 is the limiting factor for the anti-adipogenesis of lactucin in these cells. Together, our results provide the indication that lactucin exerts an anti-adipogenesis effect, which may open new therapeutic options for obesity.

scholarly journals Studies on the mechanism for entry of vesicular stomatitis virus glycoprotein g mRNA into membrane-bound polyribosome complexes

1977 ◽  
Vol 74 (1) ◽  
pp. 43-57 ◽  
Author(s):  
MJ Grubman ◽  
JA Weinstein ◽  
DA Shafritz
Keyword(s):  
Protein Synthesis ◽  
Vesicular Stomatitis Virus ◽  
Cytosol Fraction ◽  
Initial Event ◽  
Glycoprotein G ◽  
Nonspecific Effects ◽  
Membrane Bound ◽  
Vesicular Stomatitis

Glycoprotein mRNA (G mRNA) of vesicular stomatitis virus is synthesized in the cytosol fraction of infected HeLa cells. Shortly after synthesis, this mRNA associates with 40S ribosomal subunits and subsequently forms 80S monosomes in the cytosol fraction. The bulk of labeled G mRNA is then found in polysomes associated with the membrane, without first appearing in the subunit or monomer pool of the membrane-bound fraction. Inhibition of the initiation of protein synthesis by pactamycin or muconomycin A blocks entry of newly synthesized G m RNA into membrane-bound polysomes. Under these circumstances, labeled G mRNA accumulates into the cytosol. Inhibition of the elongation of protein synthesis by cucloheximide, however, allows entry of 60 percent of newly synthesized G mRNA into membrane-bound polysomes. Furthermore, prelabeled G mRNA associated with membrane-bound polysomes is released from the membrane fraction in vivo by pactamycin or mucomycon A and in vitro by 1mM puromycin - 0.5 M KCI. This release is not due to nonspecific effects of the drugs. These results demonstrate that association of G mRNA with membrane-bound polysomes is dependent upon polysome formation and initiation of protein synthesis. Therefore, direct association of the 3' end of G mRNA with the membrane does not appear to be the initial event in the formation of membrane-bound polysomes.

scholarly journals Inhibitory Effect of Dihydroartemisinin on the Proliferation and Migration of Melanoma Cells and Experimental Lung Metastasis From Melanoma in Mice

2021 ◽  
Vol 12 ◽  
Author(s):  
Qi Zhang ◽  
Linbo Jin ◽  
Quanxin Jin ◽  
Qiang Wei ◽  
Mingyuan Sun ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Early Stage ◽  
Metastatic Tumor ◽  
Treg Cells ◽  
Inhibitory Effect ◽  
B16f10 Cells ◽  
And Migration ◽  
Migration Capacity

Melanoma is aggressive and can metastasize in the early stage of tumor. It has been proved that dihydroartemisinin (DHA) positively affects the treatment of tumors and has no apparent toxic and side effects. Our previous research has shown that DHA can suppress the formation of melanoma. However, it remains poorly established how DHA impacts the invasion and metastasis of melanoma. In this study, B16F10 and A375 cell lines and metastatic tumor models will be used to investigate the effects of DHA. The present results demonstrated that DHA inhibited the proliferative capacity in A375 and B16F10 cells. As expected, the migration capacity of A375 and B16F10 cells was also reduced after DHA administration. DHA alleviated the severity and histopathological changes of melanoma in mice. DHA induced expansion of CD8+CTL in the tumor microenvironment. By contrast, DHA inhibited Treg cells infiltration into the tumor microenvironment. DHA enhanced apoptosis of melanoma by regulating FasL expression and Granzyme B secretion in CD8+CTLs. Moreover, DHA impacts STAT3-induced EMT and MMPS in tumor tissue. Furthermore, Metabolomics analysis indicated that PGD2 and EPA significantly increased after DHA administration. In conclusion, DHA inhibited the proliferation, migration and metastasis of melanoma in vitro and in vivo. These results have important implications for the potential use of DHA in the treatment of melanoma in humans.

The natural compound Cirsitakaoside enhances antiviral innate responses against vesicular stomatitis virus in vitro and in vivo

2020 ◽  
Vol 86 ◽  
pp. 106783
Author(s):  
Qianqian Di ◽  
Huihui Zhu ◽  
Debing Pu ◽  
Xibao Zhao ◽  
Xiaoli Li ◽  
...  
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Natural Compound ◽  
Vesicular Stomatitis

scholarly journals RUBELLA VIRUS CARRIER CULTURES DERIVED FROM CONGENITALLY INFECTED INFANTS

1966 ◽  
Vol 123 (5) ◽  
pp. 795-816 ◽  
Author(s):  
William E. Rawls ◽  
Joseph L. Melnick
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Viral Persistence ◽  
Carrier State ◽  
Congenital Rubella ◽  
Infected Cells ◽  
Eclipse Phase ◽  
Vesicular Stomatitis ◽  
Simplex Virus

Spontaneous rubella carrier cultures derived from tissues of infants with congenital rubella were studied in an attempt to elucidate a possible mechanism for viral persistence observed in these infants. Chronically infected cells were found to have a reduced growth rate and the cultures appeared to have a shortened life span. The rubella carrier state was not dependent on serum inhibitors or rubella antibodies. Virtually every cell in the carrier population was found to be producing virus. The carrier cultures could not be cured by rubella antibodies. The rubella-infected cells were resistant to superinfection with vesicular stomatitis virus and herpes simplex virus but were susceptible to infection with echovirus 11. The replication of vesicular stomatitis virus was apparently blocked at an intracellular site, for the virus readily adsorbed to the chronically infected cells and entered into an eclipse phase; however no infectious virus developed. No evidence of interferon production by these cells could be obtained. It is postulated that clones of rubella-infected cells in vivo, with properties similar to those in carrier cultures developed in vitro from tissues of in utero infected infants, might explain the observed viral persistence noted in congenital rubella.

scholarly journals Identification of a Novel Tripartite Complex Involved in Replication of Vesicular Stomatitis Virus Genome RNA

2003 ◽  
Vol 77 (1) ◽  
pp. 732-738 ◽  
Author(s):  
Ashim K. Gupta ◽  
Daniel Shaji ◽  
Amiya K. Banerjee
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Reverse Genetics ◽  
Insect Cells ◽  
Recombinant Baculovirus ◽  
Wild Type ◽  
Bhk Cells ◽  
P Protein ◽  
Vesicular Stomatitis

ABSTRACT Our laboratory's recent observations that transcriptionally inactive phosphoprotein (P) mutants can efficiently function in replicating vesicular stomatitis virus (VSV) defective interfering particle in a three-plasmid-based (L, P, and N) reverse genetics system in vivo (A. K. Pattnaik, L. Hwang, T. Li, N. Englund, M. Mathur, T. Das, and A. K. Banerjee, J. Virol. 71:8167-8175, 1997) led us to propose that a tripartite complex consisting of L-(N-P) protein may represent the putative replicase for synthesis of the full-length genome RNA. In this communication we demonstrate that such a complex is indeed detectable in VSV-infected BHK cells. Furthermore, coexpression of L, N, and P proteins in Sf21 insect cells by recombinant baculovirus containing the respective genes also resulted in the formation of a tripartite complex, as shown by immunoprecipitation with specific antibodies. A basic amino acid mutant of P protein, P260A, previously shown to be inactive in transcription but active in replication (T. Das, A. K. Pattnaik, A. M. Takacs, T. Li, L. N. Hwang, and A. K. Banerjee, Virology 238:103-114, 1997) was also capable of forming the mutant [L-(N-Pmut)] complex in both insect cells and BHK cells. Sf21 extract containing either the wild-type P protein or the mutant P protein along with the L and N proteins was capable of synthesizing 42S genome-sense RNA in an in vitro replication reconstitution reaction. Addition of N-Pmut or wild-type N-P complex further stimulated the synthesis of the genome-length RNA. These results indicate that the transcriptase and replicase complexes of VSV are possibly two distinct entities involved in carrying out capped mRNAs and uncapped genome and antigenome RNAs, respectively.

scholarly journals Enhanced Gene Transfer with Fusogenic Liposomes Containing Vesicular Stomatitis Virus G Glycoprotein

1998 ◽  
Vol 72 (7) ◽  
pp. 6159-6163 ◽  
Author(s):  
Akihiro Abe ◽  
Atsushi Miyanohara ◽  
Theodore Friedmann
Keyword(s):  
Gene Transfer ◽  
Vesicular Stomatitis Virus ◽  
Sucrose Density Gradient ◽  
Virus Envelope ◽  
Lipid Complex ◽  
Targeted Gene Delivery ◽  
Vesicular Stomatitis ◽  
Sucrose Density Gradient Sedimentation

ABSTRACT Exposure of Lipofectin-DNA complexes to the partially purified G glycoprotein of the vesicular stomatitis virus envelope (VSV-G) results in loss of serum-mediated inhibition and in enhanced efficiency of gene transfer. Sucrose density gradient sedimentation analysis indicated that the VSV-G associates physically with the DNA-lipid complex to produce a VSV-G liposome. The ability to incorporate surrogate viral or cellular envelope components such as VSV-G into liposomes may allow more-efficient and possibly targeted gene delivery by lipofection, both in vitro and in vivo.

Curcumin and Boswellia serrata gum resin extract inhibit chikungunya and vesicular stomatitis virus infections in vitro

2016 ◽  
Vol 125 ◽  
pp. 51-57 ◽  
Author(s):  
Christine von Rhein ◽  
Tatjana Weidner ◽  
Lisa Henß ◽  
Judith Martin ◽  
Christopher Weber ◽  
...  
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Virus Infections ◽  
Boswellia Serrata ◽  
Vesicular Stomatitis ◽  
Resin Extract

scholarly journals PEGylation of a Vesicular Stomatitis Virus G Pseudotyped Lentivirus Vector Prevents Inactivation in Serum

2004 ◽  
Vol 78 (2) ◽  
pp. 912-921 ◽  
Author(s):  
Maria A. Croyle ◽  
Shellie M. Callahan ◽  
Alberto Auricchio ◽  
Gregg Schumer ◽  
Klause D. Linse ◽  
...  
Keyword(s):  
Ethylene Glycol ◽  
Vesicular Stomatitis Virus ◽  
Transduction Efficiency ◽  
Virus Particles ◽  
Pharmacokinetic Profiles ◽  
Vesicular Stomatitis ◽  
Poly Ethylene ◽  
Lentivirus Vectors

ABSTRACT One disadvantage of vesicular stomatitis virus G (VSV-G) pseudotyped lentivirus vectors for clinical application is inactivation of the vector by human serum complement. To prevent this, monomethoxypoly(ethylene) glycol was conjugated to a VSV-G-human immunodeficiency virus vector expressing Escherichia coli beta-galactosidase. The modification did not affect transduction efficiency in vitro and protected the vector from inactivation in complement-active human and mouse sera. Blood from mice dosed intravenously with either the unmodified or the PEGylated virus particles was assayed for active vector by a limiting-dilution assay to evaluate transduction efficiency and for p24, an indicator of the total number of virus particles present. PEGylation extended the circulation half-life of active vector by a factor of 5 and reduced the rate of vector inactivation in the serum by a factor of 1,000. Pharmacokinetic profiles for the total number of virus particles present in the circulation were unaffected by PEGylation. Modification of the vector with poly(ethylene) glycol significantly enhanced transduction efficiency in the bone marrow and in the spleen 14 days after systemic administration of the virus. These results, in concert with the pharmacokinetic profiles, indicate that PEGylation does protect the virus from inactivation in the serum and, as a result, improves the transduction efficiency of VSV-G pseudotyped lentivirus vectors in susceptible organs in vivo.

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