Search results for "Viral transformation"

showing 5 items of 5 documents

Inhibition of human T-cell leukemia virus type I replication in primary human T cells that express antisense RNA

1989

The human T-cell leukemia virus type I is associated with adult T-cell leukemia-lymphoma in humans, a disease which is induced by a malignant transformation of T lymphocytes. Retrovirus vectors carrying human T-cell leukemia virus type I-derived sequences in reversed transcriptional orientation were used to express antisense RNA transcripts in primary human leukocytes. Human T-cell leukemia virus type I replication and virus-mediated immortalization were inhibited in cells harboring antisense constructs. This study suggests that retrovirus-mediated antisense RNA inhibition can be used to protect primary human T-lymphocytes from human T-cell leukemia virus type I-mediated cell transformation.

DNA ReplicationT-LymphocytesvirusesGenetic VectorsImmunologyViral transformationVirus ReplicationMicrobiologyVirusCell LineRetrovirushemic and lymphatic diseasesVirologymedicineHumansRNA AntisenseHuman T-lymphotropic virus 1biologyRNAbiology.organism_classificationmedicine.diseaseVirologyMolecular biologyAntisense RNALeukemiaGene Expression RegulationViral replicationInsect ScienceHuman T-lymphotropic virus 1RNACell DivisionResearch ArticleJournal of Virology
researchProduct

Posttranslational N-glycosylation of the hepatitis B virus large envelope protein

2007

Abstract Background The addition of N-linked glycans to proteins is normally a cotranslational process that occurs during translocation of the nascent protein to the endoplasmic reticulum. Here, we report on an exception to this rule occurring on the hepatitis B virus (HBV) large L envelope protein that is a subject to co-plus posttranslational N-glycosylation. Results By using an improved detection system, we identified so far unrecognized, novel isoforms of L. Based on mutational analyses, the use of N-glycosylation inhibitors, and pulse-chase studies, we showed that these isoforms are due to posttranslational N-glycan addition to the asparagines 4 and 112 within the preS domain of L. Whi…

Gene Expression Regulation ViralHepatitis B virusGlycosylationGlycosylationViral transformationBiologymedicine.disease_causeHepatitis B virus PRE betaCell Linelcsh:Infectious and parasitic diseaseschemistry.chemical_compoundViral Envelope ProteinsN-linked glycosylationViral entryVirologymedicineHumansProtein Isoformslcsh:RC109-216Hepatitis B viruschemistry.chemical_classificationResearchEndoplasmic reticulumEpithelial CellsVirologyProtein Structure TertiaryCell biologycarbohydrates (lipids)Infectious DiseaseschemistryGlycoproteinProtein Processing Post-TranslationalVirology Journal
researchProduct

Molecular hybridization techniques in current diagnosis of chronic hepatitis B in childhood.

1992

Following the cloning and sequencing of the hepatitis B virus genome, molecular hybridization techniques have been established to detect hepatitis B virus (HBV) DNA in serum and liver tissue. Analyses can be performed by dot blot, Southern blot and in situ hybridization. HBV DNA is regarded to be the most sensitive marker of viral replication and infectivity which was previously related to the presence of hepatitis B e antigen in serum and hepatitis B core antigen in liver cells. In liver tissue different molecular patterns can be recognized as free viral DNA and integrated sequences. Furthermore, introduction of the polymerase chain reaction allows the detection of very small amounts of vi…

Hepatitis B virusHepatitis B virusHepatitis B virus DNA polymeraseNucleotide MappingNucleic Acid HybridizationViral transformationIn situ hybridizationBiologymedicine.disease_causeHepatitis BVirologyPolymerase Chain ReactionHepatitis B virus PRE betalaw.inventionViral replicationlawPediatrics Perinatology and Child HealthDNA ViralmedicineHumansChildPolymerase chain reactionSouthern blotHepatitis ChronicEuropean journal of pediatrics
researchProduct

The Major Virus-Producing Cell Type during Murine Cytomegalovirus Infection, the Hepatocyte, Is Not the Source of Virus Dissemination in the Host

2008

SummaryThe course of systemic viral infections is determined by the virus productivity of infected cell types and the efficiency of virus dissemination throughout the host. Here, we used a cell-type-specific virus labeling system to quantitatively track virus progeny during murine cytomegalovirus infection. We infected mice that expressed Cre recombinase selectively in vascular endothelial cells or hepatocytes with a murine cytomegalovirus for which Cre-mediated recombination would generate a fluorescently labeled virus. We showed that endothelial cells and hepatocytes produced virus after direct infection. However, in the liver, the main contributor to viral load in the mouse, most viruses…

MaleCancer ResearchCell typeMuromegalovirusMICROBIOvirusesGreen Fluorescent ProteinsCongenital cytomegalovirus infectionCre recombinaseViral transformationMice TransgenicBiologyVirus ReplicationMicrobiologyVirusMicrobiologyCell LineMiceImmunology and Microbiology(all)VirologymedicineAnimalsMolecular BiologyRecombination GeneticIntegrasesViral cultureEndothelial CellsHerpesviridae InfectionsFibroblastsmedicine.diseaseVirologyMice Inbred C57BLmedicine.anatomical_structureLiverHepatocyteHepatocytesParasitologyFemaleCELLBIOViral loadCell Host & Microbe
researchProduct

Replication of hepatitis C virus

2000

Viral pathogenesisHepatitis C virusVirus AssemblyViral transformationHepatitis CHepacivirusBiologymedicine.diseasemedicine.disease_causeTransfectionVirus ReplicationMicrobiologyVirologyPathogenesisViral ProteinsViral replicationReplication (statistics)medicineAnimalsRNA ViralOncovirusCells Cultured
researchProduct