Viral Genes Modify Herpes Simplex Virus Latency both in Mouse Footpad and Sensory Ganglia

Al-Saadi, S. A.; Clements, G. B.; Subak‐Sharpe, J. H.

doi:10.1099/0022-1317-64-5-1175

Cited by 31 publications

(11 citation statements)

References 25 publications

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“…In conjunction with evidence from the mouse model system, where HSV has been shown to be latent in the skin of the footpad (A1- Saadi et al, 1983), our work would support the hypothesis that HSV does not require cells of neurological origin in order to establish and maintain a latent infection.…”

Section: Discussionsupporting

confidence: 74%

Herpes Simplex Virus Type 1 Latency in Rabbit Corneal Cells in Vitro: Reactivation and Recombination Following Intratypic Superinfection of Long Term Cultures

1987

Journal of General Virology

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SUMMARYHerpes simplex virus type 1 (HSV-1) has been isolated from explanted human corneas after cultivation in vitro. To determine whether HSV-1 is persistent or latent in corneal cells, a system to study HSV-1 infection of rabbit corneal cells in vitro was developed. By elevation of the incubation temperature to 42 °C before and during HSV-1 infection it was shown that both keratocytes and epithelial cells support a nonproductive rather than a productive infection. On subsequent temperature reduction to 37 °C, infectious virus was released from both cell types. Addition of the viral inhibitor acycloguanosine during the last 5 days of a 14 day incubation at 42 °C did not reduce the frequency of viral shedding following transfer to 37 °C, indicating that corneal cells support a latent as opposed to persistent infection. Cultures which failed to shed virus spontaneously up to 29 days post-inoculation were superinfected at 37 °C, with an XbaI site deletion mutant of HSV-1. Restriction endonuclease analysis of progeny identified both the initial infecting virus and recombinants between the parental and superinfecting genomes.

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Section: Discussionsupporting

confidence: 74%

Herpes Simplex Virus Type 1 Latency in Rabbit Corneal Cells in Vitro: Reactivation and Recombination Following Intratypic Superinfection of Long Term Cultures

1987

Journal of General Virology

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“…HSV-1 has been isolated from the ear skin, which was the initial site of inoculation, in 8% of mice latently infected with the virus in the absence of detectable clinical lesions [11]. HSV-2 and HSV-1 have both been recovered independently from the FP as well as from the DRG of latently infected mice [1,32,33]. In the guinea pig both HSV-1 and HSV-2 have been isolated from the site of primary infection (the FP and vagina) long after inoculation [9,[25][26][27].…”

Section: Discussionmentioning

confidence: 99%

“…The interval between explantation and the first appearance of HSV antigens in cultured dissociated dorsal root ganglion cells of latently infected mice is 3-4 days and infectious virus is released from day 4 [15]. Ganglia tend to shed virus at earlier times than FP [1]. This could suggest that there exist differences in the mechanism of latency reactivation in the different tissues.…”

Section: Discussionmentioning

confidence: 99%

“…However, evidence is accumulating from a variety of experimental systems for there being peripheral latency in non-neuronal cells. HSV-1 and HSV-2 have been recovered from explanted and cultured rear footpads (FP) of mice three months or more after inoculation at that site [1,32,33]. At the time of explantation virus could not be detected--infectious virus has only been isolated from explanted tissue after several days in culture.…”

Section: Introductionmentioning

confidence: 99%

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Reactivation of latent Herpes simplex virus-1 (HSV) from mouse footpad cells demonstrated by in situ hybridization

Clements

Jamieson

1989

Archives of Virology

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HSV-1 specific RNA sequences became detectable by in situ hybridization 5-6 days after culture of footpads (FP) explanted from latently infected mice. HSV-specific RNA first appeared in basal cells of hair follicles and cells of the hair root sheath, in epithelial cells of sebaceous glands and in cells within the epidermis. When first detected graining was light and usually present over individual cells, subsequently graining became heavy and present over large groups of cells. HSV reactivation from latency could be demonstrated in individual cells and therefore identified those cells in which the virus has been latent. The heavy graining over clumps of cells characteristic of a lytic infection was seen at later times after explantation; we infer that the infection had spread progressively from the initial foci of reactivation from latency.

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“…Extraneural latency is controversial. There are reports compatible with latency in mouse footpad [Alsaadi et al, 1982;Alsaadi et al, 1987;Clements and Subak-Sharpe, 19881 and in ocular tissue of experimental animals and humans, including the retina [Openshaw, 19821 and the cornea [Shimeld et al, 1982;Tullo et al, 1985;Cook and Brown, 1986;Cook et al, 1987;Abghari and Stulting, 1988;O'Brien and Taylor, 1989;Claove et al, 1990;O'Brien et al, 19913. Latency in these studies was defined by the absence of infectious virus in cell-free tissue homogenates, with isolation of HSV from tissue explants (in vitro reactivation).…”

Section: Introductionmentioning

confidence: 95%

Herpes simplex Virus dna in normal corneas: Persistence without viral shedding from ganglia

Openshaw

McNeill

Lin

et al. 1995

Journal of Medical Virology

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Herpes simplex virus type 1 (HSV-1) DNA has been shown to persist in the cornea not only after inoculation of experimental animals but also in surgical samples from patients with herpes keratitis. The further observation of corneal HSV-1 DNA in subjects without known HSV eye disease prompted the present study of the presence and distribution of HSV-1 in eye bank corneas. Prior to DNA extraction, the corneas were trephined, separating the central and peripheral cornea. With polymerase chain reaction (PCR) for HSV-1 thymidine kinase (TK) and glycoprotein D (gD) gene sequences, we found HSV-1 in 10 of 24 eye bank corneas, from the 4 mm wide corneal rim in 8 eyes and from the 8 mm diameter central cornea in 2 eyes. In 9 subjects, both eyes were assayed, and HSV-1 was detected in 6 subjects. In only one subject was HSV-1 detected in both eyes and in only one subject was HSV-1 detected in the central and peripheral cornea of the same eye. The biological role of HSV-1 DNA corneal sequences is unknown. To investigate this, a rabbit animal model was established by transplantation of corneas containing viral DNA sequences in HSV-1 naive recipients. Followed for 5 months, there was no evidence of sheeding of HSV-1 in the tear film or seroconversion of the recipient rabbits. At the end of this time, HSV-1 DNA was detected in the corneal graft at a similar intensity to the PCR signal from the donor rims.(ABSTRACT TRUNCATED AT 250 WORDS)

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Viral Genes Modify Herpes Simplex Virus Latency both in Mouse Footpad and Sensory Ganglia

Cited by 31 publications

References 25 publications

Herpes Simplex Virus Type 1 Latency in Rabbit Corneal Cells in Vitro: Reactivation and Recombination Following Intratypic Superinfection of Long Term Cultures

Herpes Simplex Virus Type 1 Latency in Rabbit Corneal Cells in Vitro: Reactivation and Recombination Following Intratypic Superinfection of Long Term Cultures

Reactivation of latent Herpes simplex virus-1 (HSV) from mouse footpad cells demonstrated by in situ hybridization

Herpes simplex Virus dna in normal corneas: Persistence without viral shedding from ganglia

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