0000000000148217

AUTHOR

Mark W. Lingen

showing 4 related works from this author

Evidence for a multistep mechanism for cell-cell fusion by herpes simplex virus with mutations in the syn 3 locus using heparin derivatives during fu…

1994

Addition of heparin-Na+ as well as related substances of high and intermediate MW (Arteparon and polyanion SP54) 3 h after infection inhibit fusion from within (FFWI) induced by HSV strains with mutations in the syn 3 locus only. The concentration of heparin-Na+ required to inhibit FFWI is 10-fold higher (1 mg/ml) than that needed to inhibit adsorption. Instead of fusion, cell rounding is observed. The effect is readily reversible. A low MW heparin disaccharide is ineffective. Neomycin, at a concentration of 8 mM, inhibits FFWI induced by all HSV-1 but not HSV-2 strains, whereas adsorption is inhibited at 3 mM. We conclude from our observations that cell-cell fusion (FFWI) induced by syn 3 …

SyncytiumCell fusionHeparinCellMutantGeneral MedicineBiologyGiant CellsVirologyCell membranemedicine.anatomical_structureMutagenesisCell cultureCell surface receptorVirologyChlorocebus aethiopsmedicineVero cellAnimalsSimplexvirusVero CellsCells CulturedArchives of Virology
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Two mutations in gB-1 and gD-1 of herpes simplex virus type 1 are involved in the "fusion from without" phenotype in different cell types.

1996

Previous studies have shown that certain strains of herpes simplex viruses type 1 (HSV-1) are able to induce “fusion from without” (FFWO) which means no transcription or translation of the viral genome happens. The main determinants for FFWO in BHK cells are mutations in the C-terminal part of gB-1. But single mutations in this part of the genome are not sufficient to transfer the FFWO phenotype also to Vero cells. Here, we report that FFWO of HSV strains indeed need additional mutations in the N-terminal part of gD in order to produce the FFWO phenotype in BHK and Vero cells. By marker transfer we are able to show that loss of mutations in the N-terminal part of gD influences the ability t…

Cell typevirusesCellMolecular Sequence DataGenome ViralHerpesvirus 1 HumanBiologymedicine.disease_causeTransfectionGiant CellsVirusCell LineViral Envelope ProteinsTranscription (biology)VirologyCricetinaeChlorocebus aethiopsGeneticsmedicineBaby hamster kidney cellAnimalsHumansAmino Acid SequenceMolecular BiologyVero CellsBase SequenceGeneral MedicineVirologyPhenotypemedicine.anatomical_structureHerpes simplex virusPhenotypeDNA ViralMutationVero cellVirus genes
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Single amino acid substitutions in the glycoprotein B carboxy terminus influence the fusion from without property of herpes simplex virus type 1.

1995

Syncytial mutations of herpes simplex virus type 1 (HSV-1) strains ANG, ANG path, HFEM, tsB5 and HSZP cause extensive cell fusion and were mapped to the cytoplasmic domain of glycoprotein B (gB), within the syn 3 locus. These strains are so far the only ones which show the phenotype ‘fusion from without’ (FFWO): 60 min after infection with high m.o.i., cells in a tissue culture are fused without transcription and translation of the viral genome. In this report we detected, using the recombinants 27/III and K-7, that an amino acid exchange from Ala to Val at aa position 854 of gB is the main determinant for FFWO activity of strains ANG, ANG path and recombinant K-7. The transfer of this muta…

virusesMutantRestriction MappingEnzyme-Linked Immunosorbent AssayHerpesvirus 1 HumanBiologymedicine.disease_causeKidneylaw.inventionCell FusionCytopathogenic Effect ViralViral Envelope ProteinslawVirologyCyclosporin aCricetinaeChlorocebus aethiopsmedicineBaby hamster kidney cellAnimalsAmino Acid SequenceAmino AcidsPeptide sequenceVero CellsRecombination GeneticCell fusionAlanineValineVirologyHerpes simplex virusPhenotypeRecombinant DNAVero cellThe Journal of general virology
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Mixed vaginal infections of Balb/c mice with low virulent herpes simplex type 1 strains result in restoration of virulence properties: vaginitis/vulv…

1997

Vaginal infections of BALB/c Ann mice with herpes simplex virus type 1 (HSV-1) were studied. Mice were inoculated with virulent strains ANG path and 17 syn+ or low-virulent recombinant strains 27/III and 17-syn3 that differ from parental strains in their glycoprotein B (gB) gene sequences. When low-virulent strains were inoculated separately, no vaginitis/vulvitis was produced despite replication in the vagina. In contrast, after coinfection of mice with the two low-virulent strains, vaginitis/vulvitis was produced and virus could be recovered from the central nervous system (CNS). Two of the CNS isolates produced vaginitis/vulvitis, neuroinvasiveness and death of mice after vaginal infecti…

Microbiology (medical)Central Nervous SystemImmunologyMolecular Sequence DataVirulenceHerpesvirus 1 Humanmedicine.disease_causePolymerase Chain ReactionVirusBALB/cMicrobiologyMiceVaginal diseasemedicineImmunology and AllergyAnimalsAmino Acid SequenceEncephalomyelitisVaginitisRecombination GeneticMice Inbred BALB CbiologyGeneral MedicineSequence Analysis DNAmedicine.diseasebiology.organism_classificationVulvovaginitisVirologyHerpes simplex virusVulvitisCoinfectionFemalemedicine.symptomMedical microbiology and immunology
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