Latent Multiple Infections by Herpes Simplex Virus type 1.

Terasaki, Shinichiro

doi:10.2739/kurumemedj.43.127

Cited by 6 publications

(4 citation statements)

References 14 publications

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“…An earlier study using RFLP analyses showed that 9/13 asymptomatically HSV-1-infected subjects with malignant tumours in the throat region shed multiple HSV-1 strains in saliva on different occasions, whilst 23 strains collected from 10 subjects with primary or clinical reactivations were all identical (Terasaki, 1996). Another interesting finding in the present study is that two of the three strains from the truly asymptomatic individuals (EL and FT) represented HSV-1 recombinants.…”

Section: Discussionsupporting

confidence: 64%

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

Liljeqvist

Norberg

2009

Journal of General Virology

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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 1¾10 2 to 2.8¾10 6 copies of virus DNA (ml saliva). 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. INTRODUCTIONHerpes simplex virus type 1 (HSV-1) is a DNA virus belonging to the family Herpesviridae encompassing more than 100 herpesviruses. The clinical spectrum of HSV-1 infection includes rare, severe manifestations such as encephalitis and disseminated neonatal infection, oral and genital clinical lesions, and asymptomatic shedding. Recrudescent disease has been estimated to occur in 32 % of blood donors resident in England (Cowan et al., 1996), and in Sweden, a recent study demonstrated that 26 % of HSV-1-infected individuals presented oral lesions (Lowhagen et al., 2002). Thus, a minority of HSV-1-infected subjects have clinical lesions. It is well-known that HSV-1-infected individuals shed virus in saliva during episodes of herpes labialis as well as during asymptomatic phases, and that asymptomatic oral shedding of HSV-1 is essential for transmission (Scott et al., 1997). The molecular basis for asymptomatic shedding is not well understood, i.e. the difference between subclinical reactivation with asymptomatic shedding and reactivation leading to clinical lesions.Although most HSV-1-infected individuals have an asymptomatic infection, recent phylogenetic analyses of HSV-1 based on DNA sequencing have been exclusively from HSV-1 isolates derived from clinical lesions. These analyses identified three evolutionary clades (A-C) with a genetic distance between t...

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Section: Discussionsupporting

confidence: 64%

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

Liljeqvist

Norberg

2009

Journal of General Virology

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“…Several reports identified that recombinant viruses are shed asymptomatically in some infected individuals, suggesting coinfection with more than one virus (101,179). However, it has not been demonstrated that individual neurons are coinfected with genetically distinct genomes.…”

Section: Herpes Simplex Virusmentioning

confidence: 99%

Targeted DNA Mutagenesis for the Cure of Chronic Viral Infections

Schiffer

Aubert

Weber

et al. 2012

J Virol

104

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Human immunodeficiency virus type 1 (HIV-1), hepatitis B virus (HBV), and herpes simplex virus (HSV) have been incurable to date because effective antiviral therapies target only replicating viruses and do not eradicate latently integrated or nonreplicating episomal viral genomes. Endonucleases that can target and cleave critical regions within latent viral genomes are currently in development. These enzymes are being engineered with high specificity such that off-target binding of cellular DNA will be absent or minimal. Imprecise nonhomologous-end-joining (NHEJ) DNA repair following repeated cleavage at the same critical site may permanently disrupt translation of essential viral proteins. We discuss the benefits and drawbacks of three types of DNA cleavage enzymes (zinc finger endonucleases, transcription activator-like [TAL] effector nucleases [TALENs], and homing endonucleases [also called meganucleases]), the development of delivery vectors for these enzymes, and potential obstacles for successful treatment of chronic viral infections. We then review issues regarding persistence of HIV-1, HBV, and HSV that are relevant to eradication with genome-altering approaches.

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“…In a previous study, strains isolated from oral lesions exhibited a low genetic variability while the subclinical isolates derived from immunosuppressed patients diverged substantially (29). Although sequence information regarding the gG-1 gene in clinical isolates is currently lacking, data on the genetic variability of other HSV glycoproteins are accumulating.…”

Section: Discussionmentioning

confidence: 99%

Variability of the Glycoprotein G Gene in Clinical Isolates of Herpes Simplex Virus Type 1

Rekabdar¹,

Liljeqvist²,

Bergström³

1999

Clin Diagn Lab Immunol

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Glycoprotein G (gG) of herpes simplex virus type 1 (HSV-1) has been used as a prototype antigen for HSV-1 type-specific serodiagnosis, but data on the sequence variability of the gene coding for this protein in wild-type strains are lacking. In this study, direct DNA sequencing of the gG-1 genes from PCR products was performed with clinical HSV-1 isolates from 11 subjects as well as with strains Syn 17+, F, and KOS 321. The reference strains Syn 17+ and F showed a high degree of conservation, while KOS 321 carried 13 missense mutations and, in addition, 12 silent mutations. Three clinical isolates showed mutations leading to amino acid alterations: one had a mutation of K122 to N, which is a gG-1–to–gG-2 alteration; another contained all mutations which were observed in KOS 321 except two silent mutations; and the third isolate carried five missense mutations. Two clinical isolates as well as strain KOS 321 showed a mutation (F111→V) within the epitope of a gG-1-reactive monoclonal antibody (MAb). When all viruses were tested for reactivity with the anti-gG-1 MAb, the three strains with the F111→V mutation were found to be unreactive. Furthermore, gG-1 antibodies purified from sera from the two patients carrying strains mutated in this epitope were less reactive when they were tested by an HSV-1-infected-cell assay. Therefore, our finding that the sequence variability of the gG-1 gene also affects B-cell epitope regions of this protein in clinical isolates may have consequences for the use of this protein as a type-specific antigen for serodiagnosis.

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Latent Multiple Infections by Herpes Simplex Virus type 1.

Cited by 6 publications

References 14 publications

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

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

Targeted DNA Mutagenesis for the Cure of Chronic Viral Infections

Variability of the Glycoprotein G Gene in Clinical Isolates of Herpes Simplex Virus Type 1

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