In Vivo Protective Effect of Tumour Necrosis Factor   Against Experimental Infection with Herpes Simplex Virus Type 1

Rossol-Voth, R.; Rossol, S.; Schütt, K.-H.; Corridori, S; Cian, W. de; Falke, D.

doi:10.1099/0022-1317-72-1-143

Cited by 78 publications

(42 citation statements)

References 17 publications

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“…We have previously shown that B6 mice lacking either or both TNF receptors are as resistant to fatal HSE as are B6 control mice (43). However, a protective role for TNF is suggested by results showing that intraperitoneal administration of TNF can protect against fatal HSE (55). Hence, we compared HSV-1 infection in TNF Ϫ/Ϫ mice to that in C57BL/6 wild-type mice.…”

Section: Resultsmentioning

confidence: 99%

“…Local TNF has been reported to both exacerbate herpes stromal keratitis and mediate protection from corneal scarring in ocular mouse models (25,33). In a prior study, TNF pretreatment was shown to confer significant protection from lethal intraperitoneal HSV-1 challenge of resistant C57BL/6 mice by a mechanism independent of IFN production or natural killer cell activation (55). TNF and IFN-␥ have also been shown to be important for macrophage activation and control of HSV and murine cytomegalovirus replication, independent of T and B cells (29).…”

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confidence: 99%

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Tumor Necrosis Factor (TNF) Protects Resistant C57BL/6 Mice against Herpes Simplex Virus-Induced Encephalitis Independently of Signaling via TNF Receptor 1 or 2

Lundberg¹,

Welander²,

Edwards

et al. 2007

J Virol

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Tumor necrosis factor (TNF) is a multifunctional cytokine that has a role in induction and regulation of host innate and adaptive immune responses. The importance of TNF antiviral mechanisms is reflected by the diverse strategies adopted by different viruses, particularly members of the herpesvirus family, to block TNF responses. TNF binds and signals through two receptors, Tnfrsf1a (TNF receptor 1 [TNFR1], or p55) and Tnfrsf1b (TNFR2, or p75). We report here that herpes simplex virus 1 (HSV-1) infection of TNF ؊/؊ mice on the resistant C57BL/6 genetic background results in significantly increased susceptibility (P < 0.0001, log rank test) to fatal HSV encephalitis (HSE) and prolonged persistence of elevated levels of virus in neural tissues. In contrast, although virus titers in neural tissues of p55 ؊/؊ N13 mice were elevated to levels comparable to what was found for the TNF ؊/؊ mice, the p55 ؊/؊ N13 mice were as resistant as control C57BL/6 mice (P > 0.05). The incidence of fatal HSE was significantly increased by in vivo neutralization of TNF using soluble TNFR1 (sTNFR1) or depletion of macrophages in C57BL/6 mice (P ‫؍‬ 0.0038 and P ‫؍‬ 0.0071, respectively). Strikingly, in vivo neutralization of TNF in HSV-1-infected p55 ؊/؊ p75 ؊/؊ mice by use of three independent approaches (treatment with soluble p55 receptor, anti-TNF monoclonal antibody, or in vivo small interfering RNA against TNF) resulted in significantly increased mortality rates (P ‫؍‬ 0.005), comparable in magnitude to those for C57BL/6 mice treated with sTNFR1 (P ‫؍‬ 0.0018). Overall, these results indicate that while TNF is required for resistance to fatal HSE, both p55 and p75 receptors are dispensable. Precisely how TNF mediates protection against HSV-1 mortality in p55 ؊/؊ p75 ؊/؊ mice remains to be determined.Early innate and subsequent adaptive immune responses to viral and bacterial pathogens are critically dependent on the tumor necrosis factor (TNF) superfamily of cytokines. These TNF superfamily cytokines act as effectors of host defense and regulate peripheral lymphoid tissue organogenesis and differentiation of natural killer cells and lymphoid cells (42,46). TNF, a multifunctional cytokine produced primarily by activated macrophages (70), functions as a key regulator of leukocyte trafficking by affecting chemokine expression and stimulating antigen presentation, which it does by inducing dendritic cell maturation (26, 58). TNF exists in two forms, a precursor 26-kDa membrane-bound form (mTNF) and a 17-kDa soluble form (sTNF), both of which are bioactive (46, 71). TNF and the closely related ligand lymphotoxin-␣ (LT) bind as homotrimers to two receptors, TNF receptor 1 (TNFR1, or p55) and TNFR2 (p75), which are widely expressed on most cell types (71). Activation of p55 generally results in gene activation that leads to induction of inflammatory and cytotoxic responses, while activation of TNFR2 is associated with thymocyte proliferation and T-cell activation. In response to TNF binding, lipopolysaccharide (LPS) and several other s...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Tumor Necrosis Factor (TNF) Protects Resistant C57BL/6 Mice against Herpes Simplex Virus-Induced Encephalitis Independently of Signaling via TNF Receptor 1 or 2

Lundberg¹,

Welander²,

Edwards

et al. 2007

J Virol

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“…TNF-α may limit virus replication in neurons either by inducing apoptosis or in other ways. For example, in vivo, TNF-α decreases hepatitis B virus gene expression (Gilles et al, 1992), protects against infection with HSV-1 (Rossol-Voth et al, 1991) and in vitro (in combination with IFN-γ), it blocks an early step in HSV-1 gene expression (Feduchi et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Cytokine production in the nervous system of mice during acute and latent infection with herpes simplex virus type 1.

Shimeld

Whiteland

Williams

et al. 1997

Journal of General Virology

101

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“…Therefore, after infection with HSV-1, IFN-␣/␤, IL-12, and possibly direct cellcell contact (14) may not activate NK cells. The role of NK cells in acute infections with HSV-1 in mice is still controversial (1,3,5,15,19,38), and the role of NK cells in chronic infections should be evaluated separately (see below). Evaluation of NK cell function in vivo by eliminating cells with antibodies to NK1.1 or asialo-GM1 is difficult if not impossible to assess.…”

Section: Nk Cells or Mature T And B Cells Are Not Required To Resistmentioning

confidence: 99%

Interplay between Alpha/Beta and Gamma Interferons with B, T, and Natural Killer Cells in the Defense against Herpes Simplex Virus Type 1

Vollstedt

Arnold

Schwerdel

et al. 2004

J Virol

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The essential components of the immune system that control primary and chronic infection with herpes simplex virus type 1 (HSV-1) in mice were investigated. Infection within the first few days can be controlled by alpha/beta interferon (IFN-␣/␤) alone without significant contribution of B, T, or NK cells. IFN-␣/␤ and IFN-␥ cooperate in the elimination of virus in the absence of these lymphocytes. In contrast, B, T, or NK cells appear to be required to control persistent infection with HSV-1. These results suggest that distinct and essential immune elements are recruited in a time-dependent fashion to control acute and persistent HSV-1 infection.

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In Vivo Protective Effect of Tumour Necrosis Factor Against Experimental Infection with Herpes Simplex Virus Type 1

Cited by 78 publications

References 17 publications

Tumor Necrosis Factor (TNF) Protects Resistant C57BL/6 Mice against Herpes Simplex Virus-Induced Encephalitis Independently of Signaling via TNF Receptor 1 or 2

Tumor Necrosis Factor (TNF) Protects Resistant C57BL/6 Mice against Herpes Simplex Virus-Induced Encephalitis Independently of Signaling via TNF Receptor 1 or 2

Cytokine production in the nervous system of mice during acute and latent infection with herpes simplex virus type 1.

Interplay between Alpha/Beta and Gamma Interferons with B, T, and Natural Killer Cells in the Defense against Herpes Simplex Virus Type 1

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