HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Liljeqvist, J. A. Articles by Norberg, P. Search for Related Content PubMed PubMed Citation Articles by Liljeqvist, J. A. Articles by Norberg, P. Agricola Articles by Liljeqvist, J. A. Articles by Norberg, P.

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

¹ Department of Clinical Virology, Göteborg University, Guldhedsgatan 10B, S-413 46 Göteborg, Sweden
² Department of Dermatovenereology, Göteborg University, Guldhedsgatan 10B, S-413 46 Göteborg, Sweden

Correspondence
Jan Åke Liljeqvist
jan-ake.liljeqvist{at}microbio.gu.se

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 1x10² to 2.8x10⁶ 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.

The GenBank/EMBL/DDBJ accession numbers for the sequences determined in this study are FJ455787 (JL, gI gene), FJ455788 (PT, gI gene), FJ455789 (FT, gI gene), FJ455790 (EL_040229, gI gene), FJ455791 (EL_040127, gI gene), FJ455792 (FT, gE gene) and FJ455793 (EL_040127, gE gene).