Role of epidermal Langerhans cells in resistance to herpes simplex virus infection

Yasumoto, Shinichiro; Okabe, Nobuhiko; Mori, Ryoichi

doi:10.1007/bf01317375

Cited by 38 publications

(29 citation statements)

References 25 publications

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“…The observations that nude mice develop more severe blepharitis than normal mice (2) and that depletion of both CD4 ϩ and CD8 ϩ T cells before challenge enhances development of periocular skin lesions (16) suggest that T cells are important in clearance of virus from periocular skin and in limiting disease. Such a role for T cells in clearance from dermal lesions has been reported (32)(33)(34)51). It follows then that mice in which a stronger or more competent immune response has been induced would be able to more effectively prevent development of blepharitis (41).…”

Section: ϫ 10mentioning

confidence: 93%

Disruption of Virion Host Shutoff Activity Improves the Immunogenicity and Protective Capacity of a Replication-Incompetent Herpes Simplex Virus Type 1 Vaccine Strain

Geiss

Smith

Leib

et al. 2000

J Virol

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The virion host shutoff (vhs) protein encoded by herpes simplex virus type 1 (HSV-1) destabilizes both viral and host mRNAs. An HSV-1 strain with a mutation in vhs is attenuated in virulence and induces immune responses in mice that are protective against corneal infection with virulent HSV-1, but it has the capacity to establish latency. Similarly, a replication-incompetent HSV-1 strain with a mutation in ICP8 elicits an immune response protective against corneal challenge, but it may be limited in viral antigen production. We hypothesized therefore that inactivation of vhs in an ICP8؊ virus would yield a replication-incompetent mutant with enhanced immunogenicity and protective capacity. ؊ mutant virus. The data indicate that inactivation of vhs in a replicationincompetent virus significantly enhances its protective efficacy while retaining its safety for potential human vaccination. Possible mechanisms of enhanced immunogenicity are discussed.Herpes simplex virus type 1 (HSV-1) is a common human pathogen, infecting approximately 80% of individuals by adulthood (49). The virus typically enters the body at epithelial and mucosal surfaces, where lytic infection of epithelial cells and fibroblasts leads to infection of sensory neurons innervating the mucosa and to the rapid establishment of latent infection in the neuronal cell bodies. In this latent reservoir, HSV infection is maintained for the life of the host. Either initial infection or reactivation can result in serious human disease, including rare but devastating encephalitis and keratitis, which is the second most common cause of nontraumatic corneal blindness (49). A vaccine to obviate or therapeutically alleviate these HSV-1-mediated diseases is a desirable goal.Development of an antiviral vaccine requires consideration of both safety and immunogenicity. An effective balance between these can be difficult to achieve, especially when faced with HSV that has a complex and persistent lifestyle. Immunization with live attenuated virus has the potential advantages of generating immune responses to a broad spectrum of viral proteins and induction of type 1 T-cell as well as humoral responses. In the development of prototypic live virus vaccines, several viral proteins that regulate host cell and viral synthetic processes have been manipulated to advantage. During infection, one of the earliest viral activities is that mediated by the virion host shutoff (vhs) protein, a product of the UL41 gene. This viral tegument component exerts its effects immediately upon entry into the cell, prior to viral gene expression (13,39). The vhs protein is associated with degradation of both cellular and viral mRNAs (24-26, 36, 39, 43) and endoribonucleolytic activity (9, 52), and the destabilization of viral messages mediated by vhs has been theorized to promote the switch from transcription of one kinetic class of viral genes to the next (43). We have previously shown that mice immunized with an HSV-1 strain that is deficient in vhs activity, UL41NHB, are significantly pro...

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Section: ϫ 10mentioning

confidence: 93%

Disruption of Virion Host Shutoff Activity Improves the Immunogenicity and Protective Capacity of a Replication-Incompetent Herpes Simplex Virus Type 1 Vaccine Strain

Geiss

Smith

Leib

et al. 2000

J Virol

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“…It has been shown that Langerhans cells are the major antigen presenting cells for HSV in human epidermis (Vestey et al, 1990) and murine epidermis (Yasumoto et al, 1986), and that the density of Langerhans cells at the site of intradermal inoculation affects the severity of the infection, fewer resulting in greater morbidity (Sprecher & Becker, 1986). UV irradiation is known to have several effects on Langerhans cells.…”

Section: Discussionmentioning

confidence: 99%

The effect of UV-B irradiation on secondary epidermal infection of mice with herpes simplex virus type 1

El‐Ghorr

Norval²

1996

Journal of General Virology

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Previous studies have indicated that suberythemal ultraviolet B (UV-B) irradiation of C3H mice before primary infection with herpes simplex virus (HSV) type 1 does not result in increased morbidity or mortality, but a suppressed delayed type hypersensitivity (DH) to the virus can be demonstrated. Any effect of UV radiation on pathogenesis during secondary epidermal HSV infection has not been previously examined. Mice were immunized by subcutaneous injection of inactivated HSV and, 5 days later, one group was UV-B-irradiated.The next day all mice were challenged epidermally with HSV. Most of the mice (92 %) in the irradiated group developed severe lesions, whilst 59% of the nonirradiated group had mild lesions and 30 % no lesions. Infectious virus was not isolated from the adrenal glands after challenge in either group. In addition, the DH to the virus was not affected by the UV exposure. The numbers oflymphocytes and dendritic cells in the lymph nodes draining the site of epidermal infection were increased in the UV group compared with the nonirradiated group. Following challenge, the percentage of CD4 + and CD8 + lymphocytes in lymph nodes was unaltered but the MHC class II expression on dendritic cells in these lymph nodes was reduced by UV exposure. The lymphoproliferative response in vitro of lymph node cells revealed a suppressed response to HSV and to the mitogen concanavalin A in the irradiated group. Thus, UV irradiation prior to epidermal secondary infection with HSV led to more severe infections due, perhaps, to a modulation in local antigen presentation.

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“…Recently, an important role for Langerhans cells in host defence against herpes virus infection has been dem onstrated [3][4][5]. Yasumotoet al [3] have discovered that nonadherent spleen cells from mice immunized with her pes simplex virus (HSV) produced no increase in thymi dine uptake when stimulated only by HSV antigen that was inactivated by ultraviolet light. However, addition of synergic epidermal cells to these spleen cells induced a remarkable increase in thymidine uptake.…”

Section: Commentsmentioning

confidence: 99%

Contact Dermatitis Sparing the Eruption of Herpes zoster and Its Periphery

Katayama

Karube²,

Ueki³

et al. 1990

Dermatology

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A 63-year-old male developed allergic contact dermatitis with antibiotic ointment applied to the skin eruptions of herpes zoster. From the result of patch test fradiomycin sulf ate contained in the ointment was identified as the contact sensitizing antigen. Strangely, this contact dermatitis was confined to the area surrounding the sores, sparing the lesions and their periphery. We postulated that a decrease in Langerhans cell activity in the herpes zoster lesions and their peripheral area was primarily responsible for this phenomenon, since an important role of Langerhans cells in host defence against herpes virus infection has recently been demonstrated.

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Role of epidermal Langerhans cells in resistance to herpes simplex virus infection

Cited by 38 publications

References 25 publications

Disruption of Virion Host Shutoff Activity Improves the Immunogenicity and Protective Capacity of a Replication-Incompetent Herpes Simplex Virus Type 1 Vaccine Strain

Disruption of Virion Host Shutoff Activity Improves the Immunogenicity and Protective Capacity of a Replication-Incompetent Herpes Simplex Virus Type 1 Vaccine Strain

The effect of UV-B irradiation on secondary epidermal infection of mice with herpes simplex virus type 1

Contact Dermatitis Sparing the Eruption of Herpes zoster and Its Periphery

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