Passive immunization in experimental Herpesvirus hominis infection of newborn mice

Luyet, F; Samra, D.; Soneji, A.; Marks, Melvin I.

doi:10.1128/iai.12.6.1258-1261.1975

Cited by 48 publications

(11 citation statements)

References 29 publications

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“…It is clear that virus-reactive antibodies can play an important role in immune protection (2, 6, 7, 10, 15, [18][19][20][22][23][24][25]. Kapoor et al.…”

Section: Discussionmentioning

confidence: 99%

Immunogenicity of herpes simplex virus glycoproteins gC and gB and their role in protective immunity

Glorioso¹,

Schröder²,

Kümel³

et al. 1984

J Virol

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The relative antigenicity of the individual herpes simplex virus type 1 (KOS) glycoproteins gC and gB was analyzed in BALB/c mice by using KOS mutants altered in their ability to present these antigens on cell surface membranes during infection. The mutants employed were as follows: syn LD70, a non-temperaturesensitive mutant defective in the synthesis of cell surface membrane gC; tsF13, a temperature-sensitive mutant defective in the processing of the precursor form of gB to the mature cell surface form at 39°C; and ts606, an immediate early temperature-sensitive mutant defective in the production of all early and late proteins including the glycoproteins. By comparing the relative susceptibility to immunolysis of mouse 3T3 cells infected at 39°C with wild-type virus, presenting the full complement of the glycoprotein antigens, gC, gB, and gD, with target cells infected with mutants presenting only subsets of these antigens, we determined that a major portion of cytolytic antibody contained in hyperimmune anti-herpes simplex virus type 1 (KOS) mouse antiserum was directed against glycoproteins gC and gB. The relative immunogenicity of wild-type and mutant virus-infected cells also was compared in BALB/c mice. Immunogen lacking the mature form of gB induced a cytolytic antibody titer comparable to that of the wild-type virus, whereas that lacking the mature form of gC showed a 70% reduction in titer. The absence of the mature cell surface forms of gB and gC in immunogen preparations resulted in a 4-to 15-fold reduction in virus neutralizing titer. Animals immunized with ts606-infected cells (39°C) induced relatively little virus-specific cytolytic and neutralizing antibody. Analysis of the glycoprotein specificities of these antisera by radioimmunoprecipitation showed that the antigens immunoprecipitated reflected the viral plasma membrane glycoprotein profiles of the immunogens. The absence of the mature forms of gC or gB in the immunizing preparation did not appreciably affect the immunoprecipitating antibody response to other antigens. Mice immunized with wildtype and mutant virus-infected cells were tested for their resistance to intracranial and intraperitoneal challenge with the highly virulent WAL strain of herpes simplex virus type 1. Despite the observed alterations in serum virus-specific antibody induced with the individual immunogens, all animals survived an intraperitoneal challenge of 10 50% lethal doses. However, differences in the survival of animals were obtained upon intracranial challenge. Protection could be induced most efficiently with wild-type virus, less well with the gC and gB mutants, and the least with the early mutant ts606. The level of protection did not strictly correlate with the relative titers of virus-neutralizing antibodies; however, in general, a reduction in titer was associated with increased susceptibility to virus challenge. These findings suggest that antibody with neutralizing activity in vitro may contribute to protection against neurological herpes simplex virus infec...

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“…It is clear that virus-reactive antibodies can play an important role in immune protection (2, 6, 7, 10, 15, [18][19][20][22][23][24][25]. Kapoor et al.…”

Section: Discussionmentioning

confidence: 99%

Immunogenicity of herpes simplex virus glycoproteins gC and gB and their role in protective immunity

Glorioso¹,

Schröder²,

Kümel³

et al. 1984

J Virol

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“…Subcutaneous infection of mice with herpes simplex virus (HSV) type 1 (HSV-1) or 2 (HSV-2) usually results in ascending neurological illness and death (3,9). Passive immunization with antiviral antibody has been shown to prevent this lethal outcome (1,4,10,12,13,(18)(19)(20), and the protective ability of the antibody depends upon the time of administration after infection and the presence of immunocompetent thymusderived lymphocytes. Effective protection was seen when antibody was given within 48 h of infection (12,20), and animals immunosuppressed by irradiation, cyclophosphamide, or antithymocyte serum were not protected (17,18,20).…”

mentioning

confidence: 99%

Protection against lethal challenge of BALB/c mice by passive transfer of monoclonal antibodies to five glycoproteins of herpes simplex virus type 2

Balachandran¹,

Bacchetti²,

Rawls³

1982

Infect Immun

196

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Monoclonal antibodies secreted by six hybridomas and recognizing antigenic sites on glycoproteins gC, gAB, gD, gE, and gF of herpes simplex virus type 2 were examined for their ability to protect BALB/c mice from lethal infection by the virus. Administration of monoclonal antibodies to individual glycoproteins intraperitoneally 3 h before footpad challenge with 10 times the 50% lethal dose of virus protected between 35 and 75% of the mice, except for one of two monoclonal antibodies recognizing antigens on gC. The antibodies did not neutralize virus in vitro and protected A/J mice deficient in the fifth component of complement as efficiently as complement-sufficient BALB/c mice. A good correlation was found between protection and titers of monoclonal antibodies assessed by antibody-dependent cell-mediated cytolysis. The results indicate that any of the glycoproteins can serve as antigens for a protective immune response. In addition, the data are compatible with protection being mediated by an antibodydependent cell-mediated cytolysis mechanism.

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“…Recently, it became evident that passive maternal antibodies influence the course of infections of newborns (42). The same finding was made in the mouse model (5,22). The degree of protection apparently depends on the amount of antibodies (4).…”

mentioning

confidence: 77%

Kinetics and genetics of herpes simplex virus-induced antibody formation in mice

Knoblich¹,

Görtz²,

Harle-Grupp³

et al. 1983

Infect Immun

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The kinetics of antibody synthesis was investigated after intraperitoneal, subcutaneous, and footpad infection of various strains of mice with herpes simplex virus. Immunoglobulin M antibodies appeared 5 days after and immunoglobulin G antibodies appeared 10 to 12 days after intraperitoneal infection with herpes simplex virus type 1. The major histocompatibility complex and the background genome of inbred mice were not found to have a systematical influence on antibody synthesis. Female mice, however, consistently produced more antibodies than did male if the infection was done intraperitoneally, but not if it was done subcutaneously or into footpads. Castration considerably increased the amount of antibodies produced by male mice. The difference in antibody formation between females and males could be abolished by injection of silica; moreover, antibody titers were enhanced by this treatment. This has also been found by immunization with a Formalin-inactivated herpes simplex virus vaccine. The effect of silica in enhancing antibody formation could be observed up to 12 days after infection. Infectious virus could be detected up to 2 days after infection, and herpes simplex virus type 1 antibody-stimulating antigens could be detected up to 4 days in ultrasonicates of macrophages. The assumption is made that androgen-sensitive cell populations, including macrophages and their soluble products, are involved in antibody-depressing mechanisms.

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Passive immunization in experimental Herpesvirus hominis infection of newborn mice

Cited by 48 publications

References 29 publications

Immunogenicity of herpes simplex virus glycoproteins gC and gB and their role in protective immunity

Immunogenicity of herpes simplex virus glycoproteins gC and gB and their role in protective immunity

Protection against lethal challenge of BALB/c mice by passive transfer of monoclonal antibodies to five glycoproteins of herpes simplex virus type 2

Kinetics and genetics of herpes simplex virus-induced antibody formation in mice

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