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Asymptomatically shed recombinant herpes simplex virus type 1 strains detected in saliva

Artikel i vetenskaplig tidskrift
Författare Jan-Åke Liljeqvist
Petra Tunbäck
Peter Norberg
Publicerad i Journal of General Virology
Volym 90
Nummer/häfte Pt 3
Sidor 559-66
ISSN 0022-1317
Publiceringsår 2009
Publicerad vid Institutionen för biomedicin, avdelningen för infektionssjukdomar
Institutionen för kliniska vetenskaper
Sidor 559-66
Språk en
Länkar dx.doi.org/10.1099/vir.0.007070-0
Ämnesord Adolescent, Adult, Child, DNA, Viral/analysis/genetics, Female, *Herpes Simplex/physiopathology/virology, Herpesvirus 1, Human/*classification/genetics/*isolation &, purification/pathogenicity, Humans, Male, Phylogeny, *Recombination, Genetic, Saliva/*virology, Sequence Analysis, DNA, *Virus Shedding
Ämneskategorier Dermatologi och venereologi

Sammanfattning

Herpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen infecting most individuals worldwide. The majority of HSV-1-infected individuals have no clinical symptoms but shed HSV-1 asymptomatically in saliva. Recent phylogenetic analyses of HSV-1 have defined three genetic clades (A-C) and recombinants thereof. These data have all been based on clinical HSV-1 isolates and do not cover genetic variation of asymptomatically shed HSV-1. The primary goal of this study was to investigate such variation. A total of 648 consecutive saliva samples from five HSV-1-infected volunteers was collected. Asymptomatic shedding was detected on 7.6 % of the days from four subjects. The HSV-1 genome loads were quantified with real-time PCR and varied from 1x10(2) to 2.8x10(6) copies of virus DNA (ml saliva)(-1). Phylogenetic network analyses and bootscanning were performed on asymptomatically shed HSV-1. The analyses were based on DNA sequencing of the glycoprotein I gene, and also of the glycoprotein E gene for putative recombinants. For two individuals with clinical HSV-1 infection, the same HSV-1 strain was shed asymptomatically as induced clinical lesions, and sequence analyses revealed that these strains clustered distinctly to clades A and B, respectively. For one of the subjects with no clinical HSV-1 infection, a recombinant strain was identified. The other truly asymptomatic individual shed evolutionarily distinct HSV-1 strains on two occasions. The first strain was classified as a recombinant and the other strain clustered in clade A. High replication rates of different strains in the same person may facilitate the creation of recombinant clinical HSV-1 strains.

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