ArticleThe Journal of infectious diseases2024
Viral Genomic Variation and the Severity of Genital Herpes Simplex Virus-2 Infection as Quantified by Shedding Rate: A Viral Genome-Wide Association Study.
Article in The Journal of infectious diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Article
- Nonlinear fractional stochastic delay modeling and computational analysis of herpes simplex virus type II dynamics.Scientific reports · 2026Article
- Progress and prospects for herpesvirus vaccination using gB antigens.Frontiers in immunology · 2026Review
- Article
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Authors and funding
9 authors.
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Abstract
backgroundThe clinical severity of genital herpes simplex virus-2 (HSV-2) infection varies widely among infected persons with some experiencing frequent genital lesions while others are asymptomatic. The viral genital shedding rate is closely associated with, and has been established as, a surrogate marker of clinical severity.
methodsTo assess the relationship between viral genetics and shedding, we assembled a set of 145 persons who had the severity of their genital herpes quantified through determination of their HSV genital shedding rate. An HSV-2 sample from each person was sequenced and biallelic variants among these genomes were identified.
resultsWe found no association between metrics of genome-wide variation in HSV-2 and shedding rate. A viral genome-wide association study identified the minor alleles of 3 individual unlinked variants as significantly associated with higher shedding rate (P < 8.4 × 10-5): C44973T (A512T), a nonsynonymous variant in UL22 (glycoprotein H); A74534G, a synonymous variant in UL36 (large tegument protein); and T119283C, an intergenic variant. We also found an association between the total number of minor alleles for the significant variants and shedding rate (P = 6.6 × 10-7).
conclusionsThese results add to a growing body of literature for HSV suggesting a connection between viral genetic variation and clinically important phenotypes of infection.
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