Effects of Monoclonal Antibodies Directed against Herpes Simplex Virus-specific Glycoproteins on the Generation of Virus-specific and H-2-restricted Cytotoxic T-Lymphocytes

Sethi, K. K.

doi:10.1099/0022-1317-64-9-2033

Cited by 14 publications

(3 citation statements)

References 19 publications

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“…However, this mechanism is very unlikely since we could not detect the antibody in the genital secretions. Furthermore, generation of virusspecific cytotoxic T lymphocytes by the administered antibody as postulated by Sethi (1983) is also excluded since the MAb 2c is effective immediately after its intraperitoneal administration and also in CDS+-depleted mice.…”

Section: Discussionmentioning

confidence: 99%

Anti-glycoprotein B monoclonal antibody protects T cell-depleted mice against herpes simplex virus infection by inhibition of virus replication at the inoculated mucous membranes

Eis‐Hübinger

Schmidt

Schneweis

1993

Journal of General Virology

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A monoclonal antibody (MAb 2c) specific for glycoprotein B of herpes simplex virus (HSV) mediated clearance of the virus from the infected mucous membranes. Young adult C57BL/6J mice were inoculated intravaginally with HSV type 1 and injected intraperitoneally either 24 and 72 h or 65 and 265 h post-inoculation with a polyclonal immune serum or the MAb 2c, both adjusted to the same neutralizing capacity. Immunization with the polyclonal immune serum did not alter the duration of virus shedding from the genital mucous membranes although a lethal outcome of infection was clearly prevented. Immunization with the MAb, however, resulted in a rapid clearance of the virus from the genital tract thus completely inhibiting genital inflammation and lethality. The same effects were achieved in mice depleted in vivo of CD4 ÷ T cells although peripheral virus replication continued longer in these mice. In mice depleted of both CD4 + and CD8 + T cells the polyclonal immune serum was no longer able to protect against lethality, and virus replication in the mucous membranes persisted until the mice died. In contrast, after treatment with the MAb peripheral infection was quickly eliminated and all mice survived. These findings indicate that clearance of the virus from the primary site of replication can be mediated by humoral immunity. The relevance of this observation for vaccination against HSV is discussed.

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Section: Discussionmentioning

confidence: 99%

Anti-glycoprotein B monoclonal antibody protects T cell-depleted mice against herpes simplex virus infection by inhibition of virus replication at the inoculated mucous membranes

Eis‐Hübinger

Schmidt

Schneweis

1993

Journal of General Virology

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“…It is possible that although DTH is enhanced, it plays no important role in pre venting stromal disease. Other as yet un identified cells and/or factors induced by antibody treatment may effectively contain the infection while minimizing corneal in flammation [21,22], Additional experiments characterizing the early immune response will be needed in order to decipher how anti body treatment prevents blinding corneal opacity.…”

Section: Discussionmentioning

confidence: 99%

Effective Antibody Therapy in Herpes Simplex Virus Ocular Infection

Lausch

Staats²,

Metcalf³

et al. 1990

Intervirology

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The immunotherapeutic potential of a monoclonal antibody specific for glycoprotein D of herpes simplex virus was evaluated in a murine ocular infection model. Passive transfer of antibody at microgram concentrations was able to promote resolution of corneal opacity and hasten healing of blepharitis. Antibody treatment did not prevent development of either a cellular or humoral antiviral immune response. In fact, kinetic studies revealed that the early delayed-type hypersensitivity response was significantly more vigorous in the treated group than in the controls. Potential explanations as to how a single microgram inoculation of antibody could exert a therapeutic effect are discussed.

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“…It is also unlikely that antibody-dependent cell-mediated cytotoxic ity is responsible for protection against stromal keratitis, since destruction of the cor neal cells would increase the severity of the keratitis, not protect against it [34], Addi tional experiments are clearly needed to de termine the effect of these antibodies on the rate of virus elimination from the eyes and the effect of passive immunization on cellmediated immunity. Sethi [35] has suggested that monoclonal antibodies against the ma jor HSV glycoproteins generate virus-speci fic cytotoxic T cells which are partly respon sible for the protective effects of the antibod ies. Further studies will clarify this point and precisely define the protective mechanism.…”

Section: Discussionmentioning

confidence: 99%

Protection against Herpetic Ocular Disease by Immunotherapy with Monoclonal Antibodies to Herpes simplex Virus Glycoproteins

Metcalf

Chatterjee

Koga³

et al. 1988

Intervirology

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In this paper we describe the ability of monoclonal antibodies to prevent herpetic stromal or interstitial keratitis following corneal infection in an outbred mouse model. Monoclonal antibodies recognizing antigenic determinants on glycoproteins B, C, D, and E of herpes simplex virus type 1 were injected intraperitoneally into CF-1 outbred mice 24 or 48 h following inoculation of the cornea with the RE strain of herpes simplex virus type 1. Passive, postexposure immunization with monoclonal antibodies had little effect on the severity of the initial corneal infection or the frequency of latent viral infections in the trigeminal ganglia, except for virus-neutralizing antibodies specific for glycoproteins B and D. A significant correlation was found between the severity of epithelial keratitis and the frequency of latent ganglionic infections. However, immunization with monoclonal antibodies protected the mice against encephalitis and prevented the development of necrotizing stromal keratitis that leads to permanent corneal scarring and blindness. This form of herpetic ocular disease does not respond to antiviral chemotherapy. Since nonneutralizing monoclonal antibodies were just as effective in prevention of encephalitis and stromal keratitis as ones that neutralized the virus in vitro, and antibodies were not administered until 24 or 48 h after corneal inoculation, we suggest that inactivation of infectious virus is not the only protective mechanism in this model.

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Effects of Monoclonal Antibodies Directed against Herpes Simplex Virus-specific Glycoproteins on the Generation of Virus-specific and H-2-restricted Cytotoxic T-Lymphocytes

Cited by 14 publications

References 19 publications

Anti-glycoprotein B monoclonal antibody protects T cell-depleted mice against herpes simplex virus infection by inhibition of virus replication at the inoculated mucous membranes

Anti-glycoprotein B monoclonal antibody protects T cell-depleted mice against herpes simplex virus infection by inhibition of virus replication at the inoculated mucous membranes

Effective Antibody Therapy in Herpes Simplex Virus Ocular Infection

Protection against Herpetic Ocular Disease by Immunotherapy with Monoclonal Antibodies to Herpes simplex Virus Glycoproteins

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