The Genome Sequence of Herpes Simplex Virus Type 2

Dolan, Aidan; Jamieson, Fiona E.; Cunningham, Charles; Barnett, Barbara C.; McGeoch, Duncan J.

doi:10.1128/jvi.72.3.2010-2021.1998

Cited by 326 publications

(134 citation statements)

References 84 publications

(87 reference statements)

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“…Herpes simplex virus (HSV) type 1 and type 2 are very closely related, showing a homology at the DNA level of 83% in protein coding regions and less in noncoding regions [6]. The genetic map of the two herpes simplex viruses is colinear [6], and the genomes are of approximately the same size, HSV-1 of 152 kbp [7] and HSV-2 of 155 kbp, and code for corresponding genes [6]. The minor sequence variations give different cleavage sites for restriction endonucleases, which has been used intensively as an important epidemiological tool [8][9][10].…”

Section: Herpes Simplex Virusmentioning

confidence: 99%

Macrophages and cytokines in the early defence against herpes simplex virus

Ellermann-Eriksen

2005

Virol J

113

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Herpes simplex virus (HSV) type 1 and 2 are old viruses, with a history of evolution shared with humans. Thus, it is generally well-adapted viruses, infecting many of us without doing much harm, and with the capacity to hide in our neurons for life. In rare situations, however, the primary infection becomes generalized or involves the brain.Normally, the primary HSV infection is asymptomatic, and a crucial element in the early restriction of virus replication and thus avoidance of symptoms from the infection is the concerted action of different arms of the innate immune response. An early and light struggle inhibiting some HSV replication will spare the host from the real war against huge amounts of virus later in infection. As far as such a war will jeopardize the life of the host, it will be in both interests, including the virus, to settle the conflict amicably. Some important weapons of the unspecific defence and the early strikes and beginning battle during the first days of a HSV infection are discussed in this review.Generally, macrophages are orchestrating a multitude of anti-herpetic actions during the first hours of the attack. In a first wave of responses, cytokines, primarily type I interferons (IFN) and tumour necrosis factor are produced and exert a direct antiviral effect and activate the macrophages themselves. In the next wave, interleukin (IL)-12 together with the above and other cytokines induce production of IFN-γ in mainly NK cells. Many positive feed-back mechanisms and synergistic interactions intensify these systems and give rise to heavy antiviral weapons such as reactive oxygen species and nitric oxide. This results in the generation of an alliance against the viral enemy.However, these heavy weapons have to be controlled to avoid too much harm to the host. By IL-4 and others, these reactions are hampered, but they are still allowed in foci of HSV replication, thus focusing the activity to only relevant sites. So, no hero does it alone. Rather, an alliance of cytokines, macrophages and other cells seems to play a central role. Implications of this for future treatment modalities are shortly considered.

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Section: Herpes Simplex Virusmentioning

confidence: 99%

Macrophages and cytokines in the early defence against herpes simplex virus

Ellermann-Eriksen

2005

Virol J

113

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“…HSV viruses are enveloped, double stranded, DNA viruses made up of 152 kbp (HSV-1) and 155 kbp (HSV-2) in length (Dolan et al, 1998). The HSV life cycle begins when viral glycoproteins bind host epithelial cellular receptors.…”

Section: Introductionmentioning

confidence: 99%

Antiviral activity of theaflavin digallate against herpes simplex virus type 1

Oliveira

Prince

et al. 2015

Antiviral Research

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Tea is the second most consumed drink in the world. The beneficial effects of tea have been mostly attributed to its catechin content. Black tea is derived from the leaves of Camellia sinensis plant, and it is rich in theaflavin polyphenols, in particular theaflavin (TF1), theaflavin-3-monogallate (TF2A), theaflavin-3'-monogallate (TF2B), and theaflavin-3,3'-digallate (TF3). Vero and A549 cells were used to evaluate the effect of purified individual black tea theaflavins as anti-herpes simplex virus 1 agents. With the rise of HSV resistant strains, there is a critical need to develop novel antiherpesviral treatments. Results of the cytotoxicity assay tested by MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxy-phenyl)-2-(4-sulfophenyl)-2H-tetrazolium] showed that TF1, TF2, and TF3 are not toxic to Vero and A549 cells at a concentration up to 75 μM. The antiviral activity of the individual theaflavins was tested by plaque reduction assay, MTS assay, flow cytometric analysis and confocal microscopy observations. The results showed that TF1, TF2, and TF3 exhibit potent, dose-dependent anti-HSV-1 effect, with TF3 being the most efficient in both Vero and A549 cells. A concentration of 50 μM TF3 and above was sufficient to inhibit >99% of the production of HSV-1 viral particles. The anti-HSV-1 effect of TF3 is due to a direct effect on the virions, and treating Vero or A549 cells with TF3 for 1h prior to infection, or treating the cells at different times post infection does not inhibit HSV-1 production. TF3 is stable at vaginal pH, indicating its potential to be a promising natural and affordable remedy against herpes simplex viral infections.

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“…Several HSV-1 genomic sequences have been determined (Macdonald et al, 2012a, b;McGeoch et al, 1988;McGeoch et al, 1986;Szpara et al, 2010), but the complete genome of only one strain of HSV-2 has been determined. The only available HSV-2 genomic sequence, that of the HG52 laboratory strain (Timbury, 1971), was determined a number of years ago (Dolan et al, 1998) and defined the genome size as 154,476 basepairs (bps). The HG52 DNA sequence was recently updated by Andrew Davison and provided in GenBank (JN561323.1), but the original sequence still serves as the reference genome for HSV-2.…”

Section: Introductionmentioning

confidence: 99%

Genomic sequences of a low passage herpes simplex virus 2 clinical isolate and its plaque-purified derivative strain

et al. 2014

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Herpes simplex virus 2 is an important human pathogen as the causative agent of genital herpes, neonatal herpes, and increased risk of HIV acquisition and transmission. Nevertheless, the only genomic sequence that has been completed is the attenuated HSV-2 HG52 laboratory strain. In this study we defined the genomic sequence of the HSV-2 SD90e low passage clinical isolate and a plaque-purified derivative, SD90-3P. We found minimal sequence differences between SD90e and SD90-3P. However, in comparisons with the HSV-2 HG52 reference genome sequence, the SD90e genome ORFs contained numerous point mutations, 13 insertions/delections (indels), and 9 short compensatory frameshifts. The indels were true sequence differences, but the compensatory frameshifts were likely sequence errors in the original HG52 sequence. Because HG52 virus is less virulent than other HSV-2 strains and may not be representative of wildtype HSV-2 strains, we propose that the HSV-2 SD90e genome serve as the new HSV-2 reference genome.

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The Genome Sequence of Herpes Simplex Virus Type 2

Cited by 326 publications

References 84 publications

Macrophages and cytokines in the early defence against herpes simplex virus

Macrophages and cytokines in the early defence against herpes simplex virus

Antiviral activity of theaflavin digallate against herpes simplex virus type 1

Genomic sequences of a low passage herpes simplex virus 2 clinical isolate and its plaque-purified derivative strain

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