Host defenses in herpes simplex infections of the nervous system: effect of antibody on disease and viral spread

McKendall, Robert R.; Klassen, Toni; Baringer, J. Richard

doi:10.1128/iai.23.2.305-311.1979

Cited by 87 publications

(39 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding no doubt reflects the increased acute clinical illness observed in these animal groups. These results mirror previous studies that have shown that passively administered hyperimmune serum will reduce the number of latently infected ganglia but will not prevent the establishment of latency [McKendall et al, 1979;Openshaw et al, 1979;Price and Schmitz, 19791. It is noteworthy, however, that our findings are somewhat in opposition to results provided by Mc-Kendall [1977], which showed that prior immunization of mice by HSV-1 infection would significantly protect against both acute and latent HSV-2 infection.…”

Section: Discussionsupporting

confidence: 89%

Acute and latent herpes simplex virus neurological disease in mice immunized with purified virus‐specific glycoproteins gB or gD

Dix

Mills

1985

Journal of Medical Virology

View full text Add to dashboard Cite

Groups of 5-week-old BALB/c mice were immunized intraperitoneally with approximately 10 micrograms of purified alum-precipitated glycoprotein gB or gD of either herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2) origin. Control mice received injections of alum-precipitated 1% bovine serum albumin (BSA). Following a second immunization 4 weeks later, seroconversion was confirmed by demonstrating the presence of glycoprotein-specific antibody by immune precipitation. All animals were challenged with lethal doses of either HSV-1 or HSV-2 by footpad inoculation and assessed for acute virus-induced neurological disease and the development of ganglionic latency. Whereas 70% of control (BSA-immunized) HSV-1-infected animals developed ascending myelitis and died, 100% of mice immunized with either gB-1, gB-2, gD-1, or gD-2 antigens remained free of clinical illness and survived HSV-1 challenge. In contrast, gB-1-or gB-2-immunized mice were not protected against acute HSV-2-induced neurological disease and showed a mortality rate of 60-90% (equivalent to that seen in controls), although mean survival times were prolonged. However, significant protection against HSV-2 challenge was observed with gD-1 or gD-2 immunization. When sacral ganglia were removed from surviving mice 9-12 months after virus challenge, latent virus was detected in all gB- or gD-immunized animals, although the extent of latent infection was restricted. These results provide evidence that glycoprotein gD might be superior to glycoprotein gB as an immunogen for the control of acute HSV-1 and HSV-2 neurological disease in mice. However, neither glycoprotein prevents ganglionic latency, the source of virus for recurrent herpesvirus infections.

show abstract

Section: Discussionsupporting

confidence: 89%

Acute and latent herpes simplex virus neurological disease in mice immunized with purified virus‐specific glycoproteins gB or gD

Dix

Mills

1985

Journal of Medical Virology

View full text Add to dashboard Cite

show abstract

“…Neutralizing antibody can inactivate extracellular viruses but cannot reach the intracellular viruses (12). Thus, cell to cell spreading of HSV within tissues is hardly blocked by the antibody (15,26). This failure of humoral immunity is effectively supplemented by the cell-mediated effector system against HSV infection.…”

Section: Discussionmentioning

confidence: 99%

Preparation of Stable Target Cells for Anti‐Herpes Simplex Virus Cytotoxic T Lymphocytes

Sonoda

Hitsumoto

Utsumi

et al. 1981

Microbiology and Immunology

View full text Add to dashboard Cite

Using an avirulent strain of herpes simplex virus (HSV), SKa, and a methylcholanthrene induced sarcoma cell line, Meth A cells, we have developed a reliable target cell system for detection of cell-mediated cytotoxicity directed against HSV-infected cells. SKa-infection in Meth A produced no progeny virus but induced HSV-specific surface antigens as revealed by radioimmunoassay using 125I-labeled HSV antibody. Spontaneous release of 51Cr from the SKa-infected Meth A cells was no more than that from uninfected control cells but a strong spontaneous 51Cr release was produced in Meth A cells infected with KOS, a virulent strain which produced a progeny virus in Meth A and was lytic for the cells. When used as a target, SKa-infected Meth A cells could detect HSV-specific cytotoxicity by spleen and lymph node lymphocytes of mice immunized with SKa and KOS. This system also detected effector cytotoxic lymphocytes stimulated in vitro by mixed cultures of immune spleen cells and KOS-infected Meth A cells. Thus, the system should be valuable in studies of cell-mediated cytotoxicity directed against HSV-infected cells.

show abstract

“…The protective effect of passively transferred antiviral antibody against primary herpes simplex virus (HSV) infection has been investigated extensively in mouse models (1,6,15,17). Relatively little is known, however, of the mechanisms by which the antibody prevents the spread of infection in vivo.…”

mentioning

confidence: 99%

Mechanism of Antibody‐Mediated Protection against Herpes Simplex Virus Infection in Athymic Nude Mice: Requirement of Fc Portion of Antibody

Hayashida

Nagafughi

Hayashi

et al. 1982

Microbiology and Immunology

View full text Add to dashboard Cite

Experiments were performed to investigate the resistance of the host due to antibody-mediated mechanisms to herpes simplex virus (HSV) infection. Transfer of hyperimmune anti-HSV mouse serum inhibited the development of skin lesions and prolonged the survival of lethally HSV-infected nude mice. Relatively high concentrations of antibody were required to achieve this protection. Antisera prepared in heterologous animals were also effective, while administration of anti-cowpox virus serum or interferon provided no protection. This type of protection is therefore due to specific antibody and cannot be attributed to interferon. In order to delineate the requirement for antibody in antibody-mediated protection, human gamma globulin preparations were transferred to lethally HSV-infected nude mice. Transfer of intact human gamma globulin (GG) was effective in controlling infection. S-sulfonation of GG did not diminish the protective ability. However, purified F(ab')2 did not have any protective action even when it was administered frequently to maintain serum neutralizing antibody titer. GG was effective in C5-deficient mice lethally infected with HSV. These results indicate that in vivo antibody-mediated protection to HSV infection requires the Fe region of the intact IgG molecule and suggest that antibody-dependent cell-mediated cytotoxicity may be operative in vivo.The protective effect of passively transferred antiviral antibody against primary herpes simplex virus (HSV) infection has been investigated extensively in mouse models (1,6,15,17). Relatively little is known, however, of the mechanisms by which the antibody prevents the spread of infection in vivo. Since extracellular antibodies are thought to be incapable of neutralizing intracellular virus particles (20) and since HSV can spread directly to contiguous cells, some mechanism other

show abstract

Host defenses in herpes simplex infections of the nervous system: effect of antibody on disease and viral spread

Cited by 87 publications

References 25 publications

Acute and latent herpes simplex virus neurological disease in mice immunized with purified virus‐specific glycoproteins gB or gD

Acute and latent herpes simplex virus neurological disease in mice immunized with purified virus‐specific glycoproteins gB or gD

Preparation of Stable Target Cells for Anti‐Herpes Simplex Virus Cytotoxic T Lymphocytes

Mechanism of Antibody‐Mediated Protection against Herpes Simplex Virus Infection in Athymic Nude Mice: Requirement of Fc Portion of Antibody

Contact Info

Product

Resources

About