SENSITIVITY TO, AND PRODUCTION OF INTERFERON BY THREE VARIANTS OF MENGO VIRUS

1967 ◽  
Vol 13 (8) ◽  
pp. 931-937 ◽  
Author(s):  
James B. Campbell ◽  
John S. Colter
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Mouse Embryo ◽  
Defense Mechanism ◽  
Interferon Production ◽  
Mouse Embryo Fibroblasts ◽  
Primary Mouse ◽  
Vesicular Stomatitis ◽  
Mengo Virus ◽  
A Minor

The sensitivity to interferon, and interferon-producing capacities of three plaque variants of Mengo virus have been studied. It has been shown that the Mengo variants, which differ greatly in their pathogenicity for mice, induce the production of very little interferon in L cells or primary mouse embryo fibroblasts, and that all are about half as sensitive to inhibition by interferon as is vesicular stomatitis virus. Serum and brain interferon titers closely parallel serum and brain virus titers following the intraperitoneal injection of mice with 106 plaque-forming units (PFU) of each variant, but there is little difference in the amounts of interferon produced in lethal and in non-lethal infections. It is concluded that interferon production in vivo is unlikely to be more than a minor defense mechanism against infection with Mengo virus.

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 In vivo biodistribution of a highly attenuated recombinant vesicular stomatitis virus expressing HIV-1 Gag following intramuscular, intranasal, or intravenous inoculation

Vaccine ◽  
2009 ◽  
Vol 27 (22) ◽  
pp. 2930-2939 ◽  
Author(s):  
J. Erik Johnson ◽  
John W. Coleman ◽  
Narender K. Kalyan ◽  
Priscilla Calderon ◽  
Kevin J. Wright ◽  
...  
Keyword(s):  
Vesicular Stomatitis Virus ◽  
In Vivo Biodistribution ◽  
Vesicular Stomatitis ◽  
Intravenous Inoculation ◽  
Hiv 1

A minor β-structured conformation is the active state of a fusion peptide of vesicular stomatitis virus glycoprotein

2008 ◽  
Vol 14 (4) ◽  
pp. 429-435 ◽  
Author(s):  
Carolina G. Sarzedas ◽  
Carla S. Lima ◽  
Maria A. Juliano ◽  
Luiz Juliano ◽  
Ana Paula Valente ◽  
...  
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Fusion Peptide ◽  
Active State ◽  
Vesicular Stomatitis Virus Glycoprotein ◽  
Virus Glycoprotein ◽  
Vesicular Stomatitis ◽  
A Minor

scholarly journals Continuous replication of Friend virus complex (spleen focus-forming virus-lymphatic leukemia-inducing virus) in mouse embryo fibroblasts. Retention of leukemogenicity and loss of immunosuppressive properties.

1975 ◽  
Vol 142 (4) ◽  
pp. 936-948 ◽  
Author(s):  
R J Eckner
Keyword(s):  
Mouse Embryo ◽  
Helper Virus ◽  
Productive Infection ◽  
Friend Virus ◽  
Focus Formation ◽  
Lymphatic Leukemia ◽  
Mouse Embryo Fibroblasts ◽  
Embryo Fibroblasts

Exposure of NIH Swiss mouse embryo fibroblasts (MEF) to infectious Friend virus (FV) complex [containing defective spleen focus-forming virus (SFFV) and endogenous NB-tropic leukemia-inducing helper virus (LLV-F)] resulted in the productive infection of these cells by both SFFV and LLV-F. Stocks of SFFV derived after extensive growth in this Swiss MEF cell culture system are fully leukemogenic in adult mice for the induction of erythroleukemia and spleen foci. In addition, in vitro-derived LLV-F, when isolated free of SFFV, is fully leukemogenic for the induction of lymphatic leukemia when inoculated into susceptible newborn BALB/c mice. The host range of in vitro-derived FV complex (i.e., FV-TC) for focus formation in vivo is NB-tropic. Unlike in vivo-derived FV complex, FV-TC does not suppress the responsiveness of murine thymocytes to concanavalin A (Con A) in vitro. Rather, FV-TC acts as a mitogen to nonspecifically stimulate the proliferation of BALB/c thymocytes. The mitogenicity of in vitro-derived FV complex is directly associated with the presence of type-C virus particles, is a heat-labile and UV-sensitive property of the virus, and may be primarily due to LLV since equivalent amounts of LLV with or without SFFV present are equally mitogenic. One in vivo passage of FV-TC resulted in the total loss of this mitogenic property with the reappearance of full immunosuppressive properties. This result demonstrates a clear association between in vivo growth of FV and its ability to suppress mouse thymocytes, and suggests that FV complex (SFFV-LLV) is not inherently immunosuppressive for these cells. While the mechanism of this interconversion between immunostimulatory and fully suppressive virus is unknown, both virus markers appear to be dependent upon the presence of infectious FV.

scholarly journals Transfer of carbohydrates on to nascent glycoprotein of vesicular stomatitis virus

1979 ◽  
Vol 181 (2) ◽  
pp. 295-300 ◽  
Author(s):  
J Kruppa
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Viral Envelope ◽  
Pulse Labelling ◽  
Viral Envelope Protein ◽  
Viral Glycoprotein ◽  
Membrane Bound ◽  
Vesicular Stomatitis

I studied the glycosylation in vivo of a viral envelope protein, the glycoprotein of vesicular stomatitis virus (VSV), by pulse labelling of virus-infected HeLa cells with 3H-labelled monosaccharides (mannose, glucosamine). Radioactivity was incorporated into the fraction of membrane-bound polyribosomes, although metabolic conversion of [3H]-mannose into amino acids was negligible. Dissociation of bound polyribosomes revealed that the radioactively co-purified with the peptidyl-tRNA. The nascent peptides were released by alkaline hydrolysis, immunoprecipitated and analysed by polyacrylamide-gel electrophoresis. It is apparent from the size distribution of the [3H]mannose-labelled nascent chains that attachment of carbohydrate starts when approximately half of the amino acid sequence of the viral glycoprotein has been synthesized.

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 Vesicular Stomatitis Virus Genomic RNA Persists In Vivo in the Absence of Viral Replication

2009 ◽  
Vol 84 (7) ◽  
pp. 3280-3286 ◽  
Author(s):  
Ian D. Simon ◽  
Nico van Rooijen ◽  
John K. Rose
Keyword(s):  
Lymph Node ◽  
Lymph Nodes ◽  
Viral Replication ◽  
Vesicular Stomatitis Virus ◽  
Genomic Rna ◽  
Intramuscular Inoculation ◽  
Vesicular Stomatitis ◽  
High Level

ABSTRACT Our previous studies using intranasal inoculation of mice with vesicular stomatitis virus (VSV) vaccine vectors showed persistence of vector genomic RNA (gRNA) for at least 60 days in lymph nodes in the absence of detectable infectious virus. Here we show high-level concentration of virus and gRNA in lymph nodes after intramuscular inoculation of mice with attenuated or single-cycle VSV vectors as well as long-term persistence of gRNA in the lymph nodes. To determine if the persistence of gRNA was due to ongoing viral replication, we developed a tagged-primer approach that was critical for detection of VSV mRNA specifically. Our results show that VSV gRNA persists long-term in the lymph nodes while VSV mRNA is present only transiently. Because VSV transcription is required for replication, our results indicate that persistence of gRNA does not result from continuing viral replication. We also performed macrophage depletion studies that are consistent with initial trapping of VSV gRNA largely in lymph node macrophages and subsequent persistence elsewhere in the lymph node.

scholarly journals Differential Expression of Interferon (IFN) Regulatory Factors and IFN-Stimulated Genes at Early Times after West Nile Virus Infection of Mouse Embryo Fibroblasts

2007 ◽  
Vol 81 (21) ◽  
pp. 12005-12018 ◽  
Author(s):  
Svetlana V. Scherbik ◽  
Bronislava M. Stockman ◽  
Margo A. Brinton
Keyword(s):  
West Nile Virus ◽  
Mouse Embryo ◽  
Stress Responses ◽  
Host Response ◽  
West Nile Virus Infection ◽  
West Nile ◽  
Protein Levels ◽  
Mouse Embryo Fibroblasts ◽  
Primary Mouse ◽  
Embryo Fibroblasts

ABSTRACT Although lineage I West Nile virus (WNV) strain Eg101 induced beta interferon (IFN-β) production as early as 12 h after infection in primary mouse embryo fibroblasts and did not inhibit the JAK-STAT signaling pathway, it was still able to replicate efficiently. To gain insights about possible viral countermeasures used by this virus to suppress the host response, the cell transcriptional profile and the kinetics of IFN regulatory factor (IRF) expression and activation were examined at early times after infection. By 12 h after WNV infection, the majority of the up-regulated genes were ones involved in IFN pathways. However, comparison of IFN-stimulated gene (ISG) expression levels in mock-infected, IFN-treated, and virus-infected cells indicated that WNV infection suppressed the up-regulation of a subset of ISGs, including genes involved in transcriptional regulation, apoptosis, and stress responses, prior to 24 h after infection. Analysis of mRNA and protein levels for representative genes indicated that suppression was at the transcriptional and posttranscriptional levels. Translocation of IRF-3 to the nucleus was observed beginning at 8 h, IRF-7 expression was detected by 12 h, but IRF-1 expression was not detected until 24 h after infection. Virus-induced gene suppression was sufficient to overcome the effect of exogenous IFN pretreatment for 1 h but not for 4 h prior to infection. These data indicate that WNV can selectively counteract the host response at early times after infection by previously unreported mechanisms.

Decay of vesicular stomatitis virus mRNAs in Vivo

Virology ◽  
1979 ◽  
Vol 94 (2) ◽  
pp. 484-487 ◽  
Author(s):  
Diane Pennica ◽  
Kevin R. Lyncht ◽  
Paul S. Cohen ◽  
Herbert L. Ennis
Keyword(s):  
Vesicular Stomatitis Virus ◽  
Vesicular Stomatitis ◽  
Virus Mrnas
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