Effect of Antithymocyte Serum on Herpesvirus Hominis (type 1) Infection in Adult Mice

Nahmias, André J.; Hirsch, M. S.; Kramer, Joel H.; Murphy, F. A.

doi:10.3181/00379727-132-34290

Cited by 58 publications

(21 citation statements)

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“…Furthermore, by using antisera, i.e. (heterologous and polyclonal) anti-thymocyte and anti-lymphocyte sera, an increase in susceptibility to HSV infection was found (Mort et al, 1965;Nahmias et al, 1969: Zisman et al, 1970. We have used here a monoclonal anti-theta antibody with an established high ability to deplete specifically the cells of the T cell lineage in vivo.…”

Section: Discussionmentioning

confidence: 99%

“…It is less clear whether T lymphocytes also contribute to antiviral defence in the non-immune host ('natural resistance'). There have been some reports that injection of anti-lymphocyte serum or of anti-thymocyte serum increased HSV-induced mortality upon primary virus infection (Hirsch & Murphy, 1968: Kirchner et al, 1978b: Mori et al, 1965: Nahmias et al, 1969: Zisman et al, 1970. However, it is now recognized that such antisera are not specific for T lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

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Injection of Anti-thy-1.2 Serum Breaks Genetic Resistance of Mice against Herpes Simplex Virus

Chmielarczyk¹,

Engler²,

Ernst³

et al. 1985

Journal of General Virology

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SUMMARYNude mice have been shown to be as resistant to intraperitoneal infection with herpes simplex virus type 1 (HSV) as their heterozygous littermates. Here we document that both activation of natural killer (NK) cells and interferon induction were normal in nu/nu mice after injection of HSV. Injection of silica caused increased mortality by HSV in C57BL/6 mice. Silica, in addition, led to a significant reduction of NK cell activity but had no effect on the interferon response. Treatment of C57BL/6 mice with anti-asialo GM1 (an antiserum with a predominant effect on NK cells) caused complete abolition of the NK cell response, but had no effect on interferon induction or virus-induced mortality. In further studies a monoclonal anti-thy-1.2 antibody was utilized which possessed high activity in rivo in depleting T cell responses in mice. Injection of anti-thy-1.2 decreased NK cell activation but was without effect on the interferon response. Unexpectedly, in view of the data in nu/nu mice, this antibody increased HSV-induced mortality in C57BL/6 mice. Similar data were obtained when anti-thy-l.2 was injected into nu/nu mice. Our results are compatible with the hypothesis that T cell precursors sensitive to anti-thy-1.2 present in homozygous nude mice play a role in resistance against HSV. Furthermore, the data in the euthymic mice may indicate a role of T cells in the primary resistance of mice against HSV.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Injection of Anti-thy-1.2 Serum Breaks Genetic Resistance of Mice against Herpes Simplex Virus

Chmielarczyk¹,

Engler²,

Ernst³

et al. 1985

Journal of General Virology

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“…In recent years it has been demonstrated that an immune response is critical in recovery from a number of experimental, primary viral infections (4)(5)(6)(7)(17)(18)(19)(20)(21). There are a number of possible mechanisms by which the immune response might contribute to recovery during a primary virus infection.…”

Section: Discussionmentioning

confidence: 99%

“…There are, however, at least two reports of instances in which transfer of antibody may have enhanced the recovery process (25,26). In addition, immunosuppression has generally not potentiated primary virus infection when the virus is introduced directly into the target organ (4,6,23,27). Exceptions to this general observation sometimes occur when experimental respiratory and intracranial viral infections are studied.…”

Section: Discussionmentioning

confidence: 99%

“…Neonatally thymectomized mice and anti-thymocyte serum (ATS)-treated mice have been shown to be more susceptible to certain virus infections, including herpes simplex, vaccinia, and reovirus (5)(6)(7)32). These two methods of immunosuppression have sometimes been regarded as specific methods of suppression of cellular immunity; this is clearly not a valid conclusion, because they have also been demonstrated to suppress antibody formation to a variety of antigens (33,34).…”

Section: Discussionmentioning

confidence: 99%

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Mechanism of Recovery From Systemic Vaccinia Virus Infection

Worthington

Rabson

Baron

1972

The Journal of Experimental Medicine

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Administration of Cytoxan in doses capable of inhibiting both humoral and cellular immunity markedly potentiated primary systemic vaccinia virus infection in mice. Immunosuppressed mice did not form neutralizing antibody to vaccinia virus and had a prolonged and more severe viremia than nonimmunosuppressed control mice. Passive transfer of physiologic amounts of neutralizing antibody late in the course of infection, at a time when nonimmunosuppressed mice had similar levels of serum antibody, largely reversed the effect of Cytoxan on vaccinia virus infection. Transfer of 100 million immune spleen cells was much less effective than antibody in reversing the effect of Cytoxan on vaccinia virus infection, and mice receiving these cells did make some antibody. Serum interferon levels were not affected by Cytoxan. The results suggest an essential role for humoral antibody, but not for cellular immunity, in recovery from primary vaccinia virus infection in the mouse.

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