ArticleJournal of clinical microbiology1999
Amplification of reiterated sequences of herpes simplex virus type 1 (HSV-1) genome to discriminate between clinical HSV-1 isolates.
Article in Journal of clinical microbiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Use of acyclovir for suppression of human immunodeficiency virus infection is not associated with genotypic evidence of herpes simplex virus type 2 resistance to acyclovir: analysis of specimens from three phase III trials.Journal of clinical microbiology · 2010Trial
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- Genomic analysis for virulence determinants in feline herpesvirus type-1 isolates.Virus genes · 2020Article
- Inferred father-to-son transmission of herpes simplex virus results in near-perfect preservation of viral genome identity and in vivo phenotypes.Scientific reports · 2017Article
- Worldwide circulation of HSV-2 × HSV-1 recombinant strains.Scientific reports · 2017Article
- Antiviral Activity of Favipiravir (T-705) against a Broad Range of Paramyxoviruses In Vitro and against Human Metapneumovirus in Hamsters.Antimicrobial agents and chemotherapy · 2016Article
- Article
- Molecular method development and establishment of a database for clinical and epidemiological herpes simplex virus 1 strain comparisons.Journal of clinical microbiology · 2014Article
- Evolution and diversity in human herpes simplex virus genomes.Journal of virology · 2014Article
- HIV-associated disruption of tight and adherens junctions of oral epithelial cells facilitates HSV-1 infection and spread.PloS one · 2014Article
- Rad51 and Rad52 are involved in homologous recombination of replicating herpes simplex virus DNA.PloS one · 2014Article
- Sequence variability in clinical and laboratory isolates of herpes simplex virus 1 reveals new mutations.Journal of virology · 2010Article
- Utilization of microsatellite polymorphism for differentiating herpes simplex virus type 1 strains.Journal of clinical microbiology · 2009Article
- Platinum(II) and palladium(II) complexes of pyridine-2-carbaldehyde thiosemicarbazone as alternative antiherpes simplex virus agents.Bioinorganic chemistry and applications · 2007Article
- Sequence-based methods for identifying epidemiologically linked herpes simplex virus type 2 strains.Journal of clinical microbiology · 2006Article
- Intratypic variability of a tandem repeat locus within the DNA polymerase gene of human herpes simplex virus type 2.Virus genes · 2004Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Herpes simplex virus type 1 (HSV-1)-related disease ranges from a localized, self-limiting illness to fatal disease in immunocompromised individuals. The corneal disease herpetic keratitis may develop after reactivation of a latent virus or reinfection with an exogenous herpesvirus. Molecular analysis of the virus involved may allow distinction between these two options. The HSV-1 genome contains several hypervariable regions that vary in numbers of reiterating regions (reiterations I to VIII [ReI to ReVIII]) between individual strains. Twenty-four HSV-1 clones, derived by subcloning of HSV-1 (strain F) twice in limiting dilutions, were tested in a PCR-based assay to analyze the stabilities of ReI, ReIII, ReIV, and ReVII. ReI and ReIII proved to vary in size upon subcloning, whereas ReIV and ReVII were stable. Subsequently, 37 unrelated isolates and 10 sequential isolates from five patients, all with HSV-1-induced keratitis, were genotyped for ReIV and ReVII. Of the 37 unrelated samples, 34 (92%) could be discriminated, while the genotypes of the viruses in sequential samples were identical for each individual. Conclusively, the data show that the approach presented allows the rapid and accurate discrimination of HSV-1 strains in studies that address the transmission and pathogenesis of HSV-1 infections.
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