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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pseudotypes of vesicular stomatitis virus were prepared with avian sarcoma viruses and avian leukemia viruses representing five different subgroups. These pseudotypes display a host range restricted to that of the avian tumor virus when assayed on avian cells and are neutralized by subgroup-specific antisera. The efficiency of penetration of mammalian cells was assayed by using these vesicular stomatitis virus pseudotypes. Pseudotypes of avian tumor viruses belonging to subgroup D and of B77 virus were able to plate on mammalian cells with a high efficiency, whereas pseudotypes of other strains were not. The efficiency of penetration of the vesicular stomatitis virus pseudotypes was 10-2-to 10-3-fold higher than the efficiency of transformation of the corresponding avian tumor virus strain assayed on mammalian cells, suggesting that there are postpenetration blocks to the expression of transformation in these cells.
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PMID:Virus envelope markers in mammalian tropism of avian RNA tumor viruses. 16 37

We investigated the capacity of lymphocytes and sera from chickens bearing tumors induced by avian sarcoma viruses (ASV) to interact with phenotypically mixed particles of vesicular stomatitis virus (VSV) and ASV. Immune chicken sera were able to specifically neutralize such VSV pseudotypes. This ability could be absorbed out, however, on purified preparations of avian retroviruses, suggesting that reactivity was primarily against avian retrovirus enveloped components. Supernatant fluids containing phenotypically mixed particles were unable to stimulate division of lymphocytes of tumor-bearing hosts, an ability possessed by culture fluids containing native ASV particles. Polyacrylamide gel analysis was unable to resolve any distinct pseudotype protein, which was not present in either of the parental virus types. Treatment with crude preparations of ultraviolet (UV)-irradiated VSV pseudotype material did not afford immunity against subsequent challenge with live ASV.
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PMID:Neutralization of pseudotypes of vesicular stomatitis virus by sera from avian retrovirus-infected hosts. 22 Jan 98

BHK-21/13 cells transformed with various chemical carcinogens and mutagens were tested for susceptibility to avian sarcoma virus infection. The chemically transformed BHK cells were highly tumorigenic. The treatment of these cells in vitro with avian sarcoma virus strain Schmidt-Ruppin D resulted in chemically transformed and viral infected cells with different rescuability of the integrated virus genome. The different rescuability is not due to the difference in virus penetration as was shown by vesicular stomatitis virus Schmidt-Ruppin virus pseudotype VSV(SR-D) technique. The sarcoma virus genome in the doubly transformed cells was not inducible by various virus inducers.
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PMID:Study of the avian sarcoma virus infection of chemically transformed cells. 23 51

The effect of glucosamine on phenotypic mixing between vesicular stomatitis virus (VSV) and avian sarcoma virus (ASV) was studied. Phenotypic mixing decreased with increase in glucosamine concentration, and, in the presence of 20 mM glucosamine, was no longer detectable. In the presence of 20 mM glucosamine, cells still produced 10(2)--10(3) focus forming units (FFU) of ASV and 10(6) plaque forming units (PFU) of VSV per milliliter. These results suggest that cells producing a relatively large amount of ASV (more than 10(3) FFU/ml) are essential for phenotypic mixing of VSV with ASV.
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PMID:Effect of glucosamine on phenotype mixing of vesicular stomatitis virus with avian sarcoma virus. 625 97

Among the protein kinases associated with vesicular stomatitis virus (VSV), one was identified by immunoprecipitation to be pp60src, the transformation-specific product coded for by avian sarcoma virus, or its endogenous cellular homolog. This activity phosphorylated only tyrosine. pp60src was enriched in the membranes, whereas the serine- and threonine-specific kinases were concentrated with viral cores. The content of pp60src in VSV can be manipulated by growing VSV in different host cells. Monolayer baby hamster kidney cells transformed by an avian sarcoma virus produced VSV progeny which contained 7-fold greater pp60src activity than progeny produced by control untransformed or revertant cells. In contrast, suspension cultures of baby hamster kidney cells which produced VSV with increased tyrosine-specific kinase activity did not affect the content of pp60src. When pp60src was specifically increased in cells, the endogenous phosphorylation of tyrosine residues in the VSV matrix M protein was also enhanced, to as much as 20-fold. The phosphorylation of serine or threonine in this protein or in the other VSV phosphoprotein NS was not affected. Cellular tyrosine-specific kinases other than pp60scr did not change the overall phosphorylation pattern of any VSV phosphoproteins. Experiments designed to test the effects of endogenous phosphorylation on the various functions of the M protein failed to detect any significant alterations.
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PMID:Host-dependent phosphorylation and kinase activity associated with vesicular stomatitis virus. 627 33

In order to identify cellular proteins required for early stages of retroviral replication, a high volume screening with mammalian somatic cells was performed. Ten pools of chemically mutagenized Chinese hamster ovary (CHO-K1) cells were challenged with a murine leukemia virus (MLV) vector pseudotyped with the vesicular stomatitis virus glycoprotein (VSV-G), and cells that failed to be transduced were enriched by cell sorting. Each pool yielded a clonally derived cell line with a 5-fold or greater resistance to virus infection, and five cell lines exhibited a >50-fold resistance. These five cell lines were efficiently infected by a human immunodeficiency virus vector pseudotyped with VSV-G. When engineered to express the TVA receptor for subgroup A avian sarcoma and leukosis virus (ASLV-A), the five cell lines were resistant to infection with a MLV vector pseudotyped with the ASLV-A envelope protein but were fully susceptible to infection with an ASLV-A vector. Thus, the defect in these cells resides after virus-cell membrane fusion and, unlike those in other mutant cell lines that have been described, is specific for the MLV core. To identify the specific stages of MLV infection that are impaired in the resistant cell lines, real-time quantitative PCR analyses were employed and two phenotypic groups were identified. Viral infection of three cell lines was restricted before reverse transcription; in the other two cell lines, it was blocked after reverse transcription, nuclear localization, and two-long terminal repeat circle formation but before integration. These data provide genetic evidence that at least two distinct intracellular gene products are required specifically for MLV infection. These cell lines are important tools for the biochemical and genetic analysis of early stages in retrovirus infection.
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PMID:Isolation of cell lines that show novel, murine leukemia virus-specific blocks to early steps of retroviral replication. 1618 99

The ability to introduce DNA elements into host cells and analyze the effects has revolutionized modern biology. Here we describe a protocol to generate Moloney murine leukemia virus (MMLV)-based, replication-incompetent pseudotyped retrovirus capable of infecting axolotls and incorporating genetic information into their genome. When pseudotyped with vesicular stomatitis virus (VSV)-G glycoprotein, the retroviruses can infect a broad range of proliferative axolotl cell types. However, if the retrovirus is pseudotyped with an avian sarcoma leukosis virus (ASLV)-A envelope protein, only axolotl cells experimentally manipulated to express the cognate tumor virus A (TVA) receptor can be targeted by infections. These strategies enable robust transgene expression over many cell divisions, cell lineage tracing, and cell subtype targeting for gene expression.
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PMID:Pseudotyped retroviruses for infecting axolotl. 2574 Apr 82