Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Iannello, Alexandre; Débbeche, Olfa; Arabi, Raoudha El; Samarani, Suzanne; Hamel, D.; Rozenberg, Flore; Heveker, Nikolaus; Ahmad, Ali

doi:10.1089/vim.2010.0083

Cited by 22 publications

(18 citation statements)

References 40 publications

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“…The authors also showed that FasL expression on monocytes acts as an immune evasion mechanism by causing the death of interacting human CD4+ and CD8+ T cells, and natural killer (NK) cells [18].…”

Section: Discussionmentioning

confidence: 99%

“…Iannello et al (2011) showed that HSV-1, whose genome is collinear with HSV-2, induced the de novo expression of FasL on the surface of human monocytes and macrophages, which caused death of monocytic cells growing in suspension, but not in monolayers (e.g., macrophages) [18]. The authors also showed that FasL expression on monocytes acts as an immune evasion mechanism by causing the death of interacting human CD4+ and CD8+ T cells, and natural killer (NK) cells [18].…”

Section: Discussionmentioning

confidence: 99%

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HSV-2 Regulates Monocyte Inflammatory Response via the Fas/FasL Pathway

et al. 2013

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Monocytic cells represent important cellular elements of the innate and adaptive immune responses in viral infections. We assessed the role of Fas/FasL in promoting monocyte apoptosis during HSV-2 infection by using an in vitro model based on the murine RAW 264.7 monocytic cell line and an in vivo murine model of HSV-2 infection applied to C57BL6, MRL-Faslpr/J (Fas−/−) and C3-Faslgld/J (FasL−/−) mice. HSV-2 infection of the monocytic cell line led to early induction of apoptosis, with no protective expression of anti-apoptotic Bcl-2. HSV-2 infected monocytes up-regulated Fas and FasL expression early during in vitro infection but were susceptible to Fas induced apoptosis. The vaginal monocytes in the HSV-2 murine model of infection up-regulated FasL expression and were susceptible to Fas induced apoptosis. HSV-2 infection of Fas and FasL- deficient mice led to decreased apoptosis of monocytes and impaired recruitment of NK, CD4+ and CD8+ T cells within the infection sites. The vaginal lavages of HSV-2 infected Fas and FasL- deficient showed decreased production of CXCL9, CXCL10 and TNF-α in comparison to HSV-2 infected wild-type mice strain. The decreased recruitment of immune competent cells was accompanied by delayed virus clearance from the infected tissue. Triggering of the Fas receptor on HSV-2 infected monocytes in vitro up-regulated the expression of CXCL9 chemokines and the cytokine TNF-α. Our study provides novel insights on the role of Fas/FasL pathway not only in apoptosis of monocytes but also in regulating local immune response by monocytes during HSV-2 infection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

HSV-2 Regulates Monocyte Inflammatory Response via the Fas/FasL Pathway

et al. 2013

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“…Finally, it culminates in latent infection, the majority in the trigeminal ganglion, nodose ganglion of the vagus, and dorsal root ganglia, as well as the superior cervical and vagal ganglions. Human monocytic cells are the vehicle of HSV-1 through bloodstream, in these cells virus-induced de novo expression of Fas or CD95 on the cell surfaces act as an immune evasion mechanism by causing the death of interacting human CD4+ T cells, CD8+ T cells, and natural killer cells (NKs) 13 . The glycophosphatidylinositol-linked host cells surface protein (cellular prion protein) expressed principally by neural tissue and the reduction of cellular toxicity by the inhibition of α gene expression influences the establishment of HSV-1 latency 14,15 .…”

Section: Infection Agentsmentioning

confidence: 99%

Infectious agents as potential triggers for autoimmunity in achalasia

Furuzawa‐Carballeda¹,

Coss‐Adame²,

Valdovinos³

et al. 2020

NGL

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“…For instance, infection of murine and human dendritic cells with HSV induces apoptosis, but after the virus has negatively modulated some of their properties ( [118][119][120] and below). Additionally, HSV has also been described to induce apoptosis in natural killer cell (NK cells) upon their interaction with infected macrophages that express Fas/FasL [121]. On the other hand, HSVs have been described to induce necroptosis in mouse fibroblasts through the direct interaction of viral ICP6 with host RIP3 (receptor-interacting kinase 3) [122].…”

Section: Hsv Modulation Of Cell Viabilitymentioning

confidence: 99%

“…More recent studies have revealed that HSV can also interfere with the expression of additional NK-activating ligands, such as ULBP1, ULBP2, and ULBP3 [171]. Importantly, HSVs can induce apoptosis in NK cells through Fas/FasL interaction between NK cells and HSV-infected macrophages, thus eliciting their deletion upon infection [121]. Although there is abundant evidence for negative modulation of NK cells by HSV, the contribution of these cells to HSV pathology remains somewhat controversial as both, negative and positive roles have been described for this cell population during HSV infection [172,173].…”

Section: Negative Modulation Of Nk and Nkt Functionmentioning

confidence: 99%

Immune Evasion by Herpes Simplex Viruses

Retamal-Díaz¹,

Tognarelli²,

Kalergis³

et al. 2016

Herpesviridae

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Infection with herpes simplex viruses type HSV-and type HSV-is extremely frequent in the human population, as well as recurrent reactivations due to lifelong infection. Infection and persistence of HSVs within healthy individuals likely results as a consequence of numerous molecular determinants evolved by these pathogens to escape both immediate and long-term host antiviral mechanisms. Indeed, HSVs harbor an arsenal of proteins that confer them stealth by negatively modulating immune function. Consequently, these viruses perpetuate within the host, altogether silently shedding onto other individuals. In this chapter, we discuss HSV determinants that interfere with cellular antiviral factors, as well as viral determinants that hamper innate and adaptive immune components intended to control such microbes. The identification of HSV evasion molecules that modulate the immune system, as well as the understanding of their mechanisms of action, should facilitate the design of novel prophylactic and therapeutic strategies to overcome infection and disease elicited by these viruses. This chapter is intended to provide an overview of the evasion mechanisms evolved by herpes simplex viruses to escape numerous host antiviral mediators.

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Herpes Simplex Virus Type 1-induced FasL Expression in Human Monocytic Cells and Its Implications for Cell Death, Viral Replication, and Immune Evasion

Cited by 22 publications

References 40 publications

HSV-2 Regulates Monocyte Inflammatory Response via the Fas/FasL Pathway

HSV-2 Regulates Monocyte Inflammatory Response via the Fas/FasL Pathway

Infectious agents as potential triggers for autoimmunity in achalasia

Immune Evasion by Herpes Simplex Viruses

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