Passive immunization protects the mouse eye from damage after herpes simplex virus infection by limiting spread of virus in the nervous system

Shimeld, C.; Hill, Terry; Blyth, W. A.; Easty, D L

doi:10.1099/0022-1317-71-3-681

Cited by 55 publications

(43 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…with virus in passively immunized mice (Shimeld et al, 1990b). This suggests long term persistence of immune cells in the cornea following recovery from the primary infection; a phenomenon also reported in the latently infected ganglion .…”

Section: Discussionmentioning

confidence: 82%

“…TG1, which contains the neurons which supply the cornea, yielded the highest incidence of virus. Isolation from TG2 was not surprising since this part of the ganglion also harbours latently infected neurons (Shimeld et al, 1990b). Reactivation in this part was to be expected since the lower eyelid, in addition to the cornea, was irradiated with UV and the eyelid is within the area innervated by TG2.…”

Section: Discussionmentioning

confidence: 99%

“…Twenty-four hours before inoculation with virus, animals were inoculated intraperitoneally (i.p.) with 0.5 ml of rabbit serum containing antibodies to HSV-1 (Shimeld et al, 1990b). The serum was diluted with PBS to give a dose of 8000 ED~o.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Immune cell infiltration in corneas of mice with recurrent herpes simplex virus disease

Shimeld¹,

Whiteland²,

Nicholls³

et al. 1996

Journal of General Virology

Self Cite

View full text Add to dashboard Cite

Reactivation of latent herpes simplex virus type 1 (HSV-1) infection was induced by UV irradiation of the corneas of latently infected mice. On days 1--4 after stimulation, infectious virus was sought in nervous and ocular tissue. On days 4, 7 and 10, eyes with either recurrent epithelial or stromal disease and appropriate controls were stained to identify immune cells and HSV-1 antigens. The maximum incidence of infectious virus was on day 2 when 5/10 ophthalmic parts of the trigeminal ganglion yielded HSV. Thus in this mouse model, as in humans, reactivation of virus in the trigeminal ganglion is the likely source of virus producing recurrent disease and shedding in the tear film. On day 4, when virus antigens were still present, granulocytes were the predominant infiltrating cell in corneas with either type of disease. Small numbers ofT cells, dendritic cells and cells expressing MHC class II were also present. In stromal disease, the granulocyte infiltrate persisted and T cells remained sparse. In contrast, in epithelial disease, granulocyte numbers rapidly declined and both CD4 + and CD8 + T cells (present at a ratio of 1:1) increased significantly. The secondary immune response to virus antigen is more rapid and vigorous than that during primary corneal infection. Granulocytes may play a role in the initial clearance of virus, however, the other types of cells present early on provide the potential for a local secondary immune response. The high proportion of CD8 ÷ cells in epithelial disease compared with stromal disease suggests that they may be acting as suppressors.

show abstract

Section: Discussionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Immune cell infiltration in corneas of mice with recurrent herpes simplex virus disease

Shimeld¹,

Whiteland²,

Nicholls³

et al. 1996

Journal of General Virology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The recurrent model which was described above was first published by Shimeld, et al [1][2][3] . They tested and our laboratory has been using a modified version of this model to publish many manuscripts over the years [4][5][6][7][8][9][10][11][12][13][14][15] .…”

Section: Representative Resultsmentioning

confidence: 99%

Recurrent Herpetic Stromal Keratitis in Mice, a Model for Studying Human HSK

Morris

Stuart

Rogge

et al. 2012

JoVE

View full text Add to dashboard Cite

Herpetic eye disease, termed herpetic stromal keratitis (HSK), is a potentially blinding infection of the cornea that results in over 300,000 clinical visits each year for treatment. Between 1 and 2 percent of those patients with clinical disease will experience loss of vision of the infected cornea. The vast majority of these cases are the result of reactivation of a latent infection by herpes simplex type I virus and not due to acute disease. Interestingly, the acute infection is the model most often used to study this disease. However, it was felt that a recurrent model of HSK would be more reflective of what occurs during clinical disease. The recurrent animal models for HSK have employed both rabbits and mice. The advantage of rabbits is that they experience reactivation from latency absent any known stimulus. That said, it is difficult to explore the role that many immunological factors play in recurrent HSK because the rabbit model does not have the immunological and genetic resources that the mouse has. We chose to use the mouse model for recurrent HSK because it has the advantage of there being many resources available and also we know when reactivation will occur because reactivation is induced by exposure to UV-B light. Thus far, this model has allowed those laboratories using it to define several immunological factors that are important to this disease. It has also allowed us to test both therapeutic and vaccine efficacy. Video LinkThe video component of this article can be found at

show abstract

“…Indeed, it is known that antibodies can preserve corneal clarity during primary ocular infection with HSV, and passively transferred anti-HSV antibody can inhibit spread of virus within the nervous system. (19,21,29,37). Thus, ⌬41⌬29-stimulated anti-HSV antibodies are likely an important factor in reducing disease manifestations such as opacity, encephalitis, and death after primary infection in prophylactically vaccinated mice as well as recipients of immune serum (Tables 1 and 2, Fig.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Immunization with a Virion Host Shutoff-Defective, Replication-Incompetent Herpes Simplex Virus Type 1 Strain Limits Recurrent Herpetic Ocular Infection

Keadle

Morrison

Morris

et al. 2002

J Virol

View full text Add to dashboard Cite

Immunization of mice with herpes simplex virus type 1 (HSV-1) mutant viruses containing deletions in the gene for virion host shutoff (vhs) protein diminishes primary and recurrent corneal infection with wild-type HSV-1. vhs mutant viruses are severely attenuated in vivo but establish latent infections in sensory neurons. A safer HSV-1 mutant vaccine strain, ⌬41⌬29, has combined vhs and replication (ICP8 ؊ ) deficits and protects BALB/c mice against primary corneal infection equivalent to a vhs ؊ strain (BGS41). Here, we tested the hypothesis that ⌬41⌬29 can protect as well as BGS41 in a therapeutic setting. Because immune response induction varies with the mouse and virus strains studied, we first determined the effect of prophylactic ⌬41⌬29 vaccination on primary ocular infection of NIH inbred mice with HSV-1 McKrae, a model system used to evaluate therapeutic vaccines. In a dose-dependent fashion, prophylactic ⌬41⌬29 vaccination decreased postchallenge tear film virus titers and ocular disease incidence and severity while eliciting high levels of HSV-specific antibodies. Adoptive transfer studies demonstrated a dominant role for immune serum and a lesser role for immune cells in mediating prophylactic protection. Therapeutically, vaccination with ⌬41⌬29 effectively reduced the incidence of UV-B-induced recurrent virus shedding in latently infected mice. Therapeutic ⌬41⌬29 and BGS41 vaccination decreased corneal opacity and delayed-type hypersensitivity responses while elevating antibody titers, compared to controls. These data indicate that replication is not a prerequisite for generation of therapeutic immunity by live HSV mutant virus vaccines and raise the possibility that genetically tailored replication-defective viruses may make effective and safe therapeutic vaccines.

show abstract

Passive immunization protects the mouse eye from damage after herpes simplex virus infection by limiting spread of virus in the nervous system

Cited by 55 publications

References 18 publications

Immune cell infiltration in corneas of mice with recurrent herpes simplex virus disease

Immune cell infiltration in corneas of mice with recurrent herpes simplex virus disease

Recurrent Herpetic Stromal Keratitis in Mice, a Model for Studying Human HSK

Therapeutic Immunization with a Virion Host Shutoff-Defective, Replication-Incompetent Herpes Simplex Virus Type 1 Strain Limits Recurrent Herpetic Ocular Infection

Contact Info

Product

Resources

About