Role of Lyt‐1 Positive Immune T Cells in Recovery from Herpes Simplex Virus Infection in Mice

Nagafuchi, Seiho; Hayashida, Isao; Higa, Kazuo; Wada, Toshinori; Mori, Ryoichi

doi:10.1111/j.1348-0421.1982.tb00186.x

Cited by 29 publications

(17 citation statements)

References 16 publications

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“…In previous studies from this and other laboratories, it has been shown that Lyt 1 + T cells may play a central role in protection against HSV infeetion (17,19,22). Immune cells of this phenotype confer protective activity by elieitation of the delayed-type hypersensitivity reaction (17,19) or accelerated antibody production (22).…”

Section: Discussionmentioning

confidence: 93%

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

Yasumoto

Okabe

Mori

1986

Archives of Virology

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To investigate the role of epidermal Langerhans cells (LC) in resistance to herpes simplex virus (HSV) infection, nonadherent spleen cells taken from BALB/c mice immunized with HSV were cultured with syngeneic epidermal cells (EC) and ultraviolet light-inactivated HSV antigen. After five days of culture, T cell-dependent proliferative response was determined by 3H-thymidine incorporation. Treatment of EC with anti-Iad monoclonal antibody plus complement before cultivation prevented this proliferation, which suggested that LC induced stimulation of immune T cells. When these stimulated spleen cells were transferred to intracutaneously infected nude mice, the virus titer in the skin was reduced markedly and the formation of zosteriform skin lesions was completely inhibited. On the other hand, transfer of unstimulated cells, which were cultured with HSV antigen only or with HSV antigen and EC treated with anti-Iad monoclonal antibody plus complement, resulted in delayed viral clearance and development of the lesions. These results indicate that LC are of importance as accessory cells in the control of cutaneous HSV infection. Furthermore, Lyt 1+ T cells in the stimulated population were shown to have greater protective activity than Lyt 2+ T cells.

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Section: Discussionmentioning

confidence: 93%

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

Yasumoto

Okabe

Mori

1986

Archives of Virology

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“…Both protection against and recovery from HSV infections were shown to depend on the presence of I-regionrestricted helper T cells (32,33). The mechanisms underlying these results may involve the production of y-interferon (34) and the differentiation of HSV-specific cytotoxic T cells (35), both of which are mediated by T helper cells.…”

Section: Resultsmentioning

confidence: 99%

Human T-lymphocyte response in vitro to synthetic peptides of herpes simplex virus glycoprotein D.

DeFreitas¹,

Dietzschold²,

Koprowski³

1985

Proc. Natl. Acad. Sci. U.S.A.

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Immunization of mice with a synthetic peptide that corresponds to a murine antibody-defined immunodominant domain of herpes simplex virus (HSV) glycoprotein D (gD) induced neutralizing antibodies against HSV types 1 and 2 and protected animals against a lethal challenge with HSV type 2 (Dietzschold, B., Eisenberg, R., Ponce de Leon, M., Golub, E., Hudecz, F., Varicchio, A. & Cohen, G. (1984) J. Virol. 52,[431][432][433][434][435]. We report here that human peripheral blood T cells from HSV-seropositive and -seronegative adult donors are activated by this synthetic peptide in vitro. Interleukin-2-dependent T-cell lines established from these cultures respond specifically to peptides containing residues 1-23 of HSV gD and to a panel of overlapping peptides within this domain. The T-cell proliferative response was maximal when the majority of interleukin-2-propagated T cells were of the helper phenotype and the peptides were at least 16 amino acids long. Peptides of 8 or 12 amino acids from the carboxyl terminus were nonstimulatory. Peptide-activated T-cell lines from seronegative donors less than 11 years old could be established in vitro, but most cells were of the suppressor/cytotoxic phenotype and demonstrated no antigen-specificity when tested with the panel of synthetic peptides.The immune response to herpes simplex virus (HSV) has been shown to involve a variety of effector mechanisms which include production of virus-neutralizing antibody, cytotoxic T lymphocytes, natural killer (NK) cells, antibodydependent cellular cytotoxicity, and T-cell-derived lymphokines (43). The pivotal role of helper T-cells in the induction of these responses has been well documented (44,45).The nature of the HSV-specified antigens that act as immunostimulants has not been completely identified, but several lines of evidence implicate the major viral glycoproteins (1). One of these, glycoprotein D (gD), has been shown to induce type-common viral-neutralizing antibody (2, 3), and passive administration of monoclonal antibody (mAb) specific for gD protects mice from a lethal challenge with HSV (4). Moreover, gD appears to be recognized on HSV-infected cells by cytolytic effector cells (5).An antibody-defined immunodominant determinant of HSV type 1 (HSV-1) gD was localized and a peptide corresponding to residues 8-23 of the mature glycoprotein was synthesized. This peptide was recognized by an anti-gD mAb known to neutralize HSV-1 and -2 (6). Moreover, immunization of mice with this synthetic molecule induces viral-neutralizing antibodies and confers protection against a lethal challenge with HSV-2 (7). MATERIALS AND METHODSSynthesis of HSV gD Peptides. Peptides were manually synthesized as described (6) by using the Merrifield solidphase method (8). The completed peptides were simultaneously deprotected and cleaved from the resin with anhydrous HF containing thioanisole as an organic cation scavenger. The crude peptides were purified by gel filtration on Bio-Gel P-2 or P-4 (Bio-Rad) columns. Homogeneity of the peptides w...

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“…Adoptive transfer of T lymphocytes specific for HSV-1 antigens can confer protection from lethal HSV-1 infections in immunocompetent and immunosuppressed mice (26)(27)(28)(29)(30). In this report we have demonstrated further that the immune response to HSV-1 is also critical for control of viral spread in the brain.…”

Section: Discussionmentioning

confidence: 99%

Interference with major histocompatibility complex class II-restricted antigen presentation in the brain by herpes simplex virus type 1: a possible mechanism of evasion of the immune response.

Lewandowski

Bloom

1993

Proc. Natl. Acad. Sci. U.S.A.

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Host survival of herpes simplex virus type 1 (HSV-1) infection depends on the establishment of latent infections in both peripheral and central nervous systems. Strains of HSV-1 that are successful in escaping the immune response produce a lethal infection. We now report a possible mechanism of immune response evasion used by HSV-1. After intraocular inoculation of mice, HSV-1 strain F established a latent infection in the brain, whereas strain KOS did not. The immune response to HSV-1 infection (strains KOS and F) in the brain was characterized by induction of major histocompatibility complex class II expression and recruitment of CD4+ and CD8+ cells to highly restricted sites of intracerebral viral infection. Major histocompatibility complex class H antigen expression was primarily intracellular in strain KOS infection centers and at the cell surface in strain F infection centers. We propose that major histocompatibiity complex class IIrestricted viral-antigen presentation to T cells is interrupted during strain KOS infections, thereby allowing KOS infection to evade T-cell-mediated events that would normally protect the host from a lethal infection. Immunocompromised mice (athymic or irradiated mice) could not survive strain F infections; however, latent F infections were established in irradiated mice reconstituted with naive lymph node and spleen cells.These data suggest that class 11-restricted presentation of viral antigens is required for the control of HSV-1 infections in the nervous system. Protection of a host from lethal herpes simplex virus type 1 (HSV-1) infections requires a functional immune response. The T-cell-mediated immune response that controls viral spread by clearance of the virus from peripheral lesion sites (1, 2) has also been indicated as a necessary component in the establishment of latent HSV-1 infections (3-6). In most instances, after a primary HSV-1 infection a latent viral infection is established in the peripheral and central nervous systems (7-9). If a latent infection is not established, the uncontrolled HSV-1 infection can spread through the peripheral and central nervous system and cause the death of the host. Recently, some attention has been given to the roles of major histocompatibility complex (MHC) class I-restricted CD8+ and MHC class II-restricted CD4+ T lymphocytes. Although the literature presents mixed results, both CD8+ and CD4+ cells are probably required for complete recovery from HSV-1 infections. Activation of both CD8+ and CD4+ lymphocytes requires viral-antigen presentation in the appropriate MHC complex (10-13). We now report that HSV-1 may cause a lethal infection by escaping the surveillance of the immune system and that a possible evasion mechanism is through interference of MHC class II-restricted antigen presentation.t MATERIALS AND METHODSInoculation of Mice with HSV-1. Female BALB/cByJ mice of at least 8 weeks of age were anesthetized by inhalation of Metofane and inoculated in the right eye with 105 plaqueforming units (pfu) of either strai...

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Role of Lyt‐1 Positive Immune T Cells in Recovery from Herpes Simplex Virus Infection in Mice

Cited by 29 publications

References 16 publications

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

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

Human T-lymphocyte response in vitro to synthetic peptides of herpes simplex virus glycoprotein D.

Interference with major histocompatibility complex class II-restricted antigen presentation in the brain by herpes simplex virus type 1: a possible mechanism of evasion of the immune response.

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