Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

Ennaciri, Jamila; Menezes, José; Proulx, François; Toledano, Baruch

doi:10.1203/01.pdr.0000191816.57544.b4

Cited by 16 publications

(13 citation statements)

References 35 publications

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“…The infection resulted in enhanced apoptosis of various cell types in the eye and brain of the infected mice (31). A relatively recent study has shown that HSV-1 induces expression of FasL on neonatal, but not on adult, neutrophils (32). The study demonstrated hastened death of the virusinfected neonatal neutrophils that could be inhibited with antagonistic anti-Fas or anti-FasL antibodies.…”

Section: Hsv-1 Infection Induces Apoptosis In Human Monocytic Cellsmentioning

confidence: 92%

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

et al. 2011

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Herpes simplex virus type 1 (HSV-1) is a ubiquitously occurring pathogen that infects humans early in childhood. The virus persists as a latent infection in dorsal root ganglia, especially of the trigeminal nerve, and frequently becomes reactivated in humans under conditions of stress. Monocytic cells constitute an important component of the innate and adaptive immune responses. We show here for the first time that HSV-1 stimulates human FasL promoter and induces de novo expression of FasL on the surface of human monocytic cells, including monocytes and macrophages. This virus-induced FasL expression causes death of monocytic cells growing in suspension, but not in monolayers (e.g., macrophages). The addition of a broad-spectrum caspase inhibitor, as well as anti-FasL antibodies, reduced cell death but increased viral replication in the virus-infected cell cultures. We also show here for the first time that the virus-induced de novo expression of FasL on the cell surface acts as an immune evasion mechanism by causing the death of interacting human CD4+ T cells, CD8+ T cells, and natural killer (NK) cells. Our study provides novel insights on FasL expression and cell death in HSV-infected human monocytic cells and their impact on interacting immune cells.

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Section: Hsv-1 Infection Induces Apoptosis In Human Monocytic Cellsmentioning

confidence: 92%

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

et al. 2011

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“…Briefly, HeLa cells were seeded into 96-well plates until they reached 70% confluence. A series of diluted supernatants were inoculated into HeLa cells at 37°C and 5% CO 2 for 72 h. Viral titer was measured by cytopathic effect using the Reed-Muench method [21]. …”

Section: Methodsmentioning

confidence: 99%

Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Dai

Zhang

et al. 2017

Med Sci Monit

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BackgroundAt present, the treatment of coxsackievirus-induced myocarditis remains difficult. Berberine (BBR), an isoquinoline alkaloid isolated from traditional medicine herbs, exhibits significant anti-viral efficacy against various viruses. However, the underlying mechanism by which BBR controls CVB3 infection has not yet been reported. The purpose of this study was to investigate the anti-viral efficacy of BBR against CVB3 infection and its mechanism.Material/MethodsIn our experiments, the protein levels of VP1 and MAPKs signal pathway were measured by Western blot. The mRNA level of VP1 was measured by RT-PCR. The virus titers were determined by TCID50 assay.ResultsWe found that BBR treatment significantly decreased CVB3 replication in HeLa cells. In addition, the BBR treatment reduced the phosphorylation levels of JNK and p38 MAPK upon CVB3 infection in both HeLa cells and primary rat myocardial cells.ConclusionsTaken together, these results suggest that BBR inhibits CVB3 replication through the suppression of JNK and p38 MAPK activation, shedding new light on the investigation of therapeutic strategies against CVB3-induced viral myocarditis.

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“…For example, in vitro studies of neutrophil apoptosis induced by herpes simplex virus (HSV)-131 and influenza virus-A (IVA)32 showed that the majority of apoptotic cells were not infected; in IM, only a small minority of blood neutrophils contain Epstein–Barr virus (EBV),33 though in vitro, a substantial proportion of neutrophils can bind EBV in spite of their lack of the EBV receptor, CD21 34. Virus-induced neutrophil apoptosis is attributed to upregulation of Fas and Fas-L on the few cells that are infected, with release of soluble Fas-L to then diffuse and bind to Fas-receptor on uninfected cells to initiate apoptosis 35.…”

Section: Discussionmentioning

confidence: 99%

“…It is also possible that the susceptibility of neutrophils in vitro to the destructive effect of tumour necrosis factor (TNF)-α35 renders them vulnerable in vivo as well to TNF-α released from apoptotic lymphocytes whose death accompanies neutrophil death in viral infection. Neonatal, in contrast to adult neutrophils, may be especially susceptible to viral destruction, at least by HSV-131 which correlates with the marked leucocyte death in neonatal herpes simplex viraemia (figure 1). 20…”

Section: Discussionmentioning

confidence: 99%

Virus-associated apoptosis of blood neutrophils as a risk factor for invasive meningococcal disease

et al. 2013

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AimsTo quantify a range of haematological indicators of viral infection (leucocyte apoptosis, cytopenia of normal lymphocytes, reactive lymphocyte increase, neutropenia) in patients with recent onset invasive meningococcal disease (IMD), with a view to test the association of viral infection with IMD and identify possible haematological risk factors for its development.Subjects and methods88 patients with recent onset IMD, classified on clinical severity as fatal (n=14), septic shock survived (n=26) and no shock (n=48), and 50 healthy controls were studied. Blood film microscopy and leucocyte counts were used to quantify the virus-associated indicators. Cocci-containing neutrophils were also quantified.ResultsAll viral parameters were significantly more frequent or higher in patients than controls, with leucocyte apoptosis found only in the patients. A significant gradient in accord with clinical severity was found for neutrophil and lymphocyte apoptosis, neutropenia and cocci-containing neutrophils. Crucially, apoptotic neutrophils did not contain cocci, and cocci-containing neutrophils were not apoptotic.ConclusionsThe correlation between magnitude of neutrophil apoptosis and severity of IMD suggests a cause–effect relationship. We propose that neutrophil apoptosis is more likely a facilitator rather than an effect of IMD for these reasons: (1) apoptotic neutrophils did not contain cocci and cocci-containing neutrophils were not apoptotic, (2) leucocyte apoptosis is a recognised viral effect and (3) Neisseria meningitidis is incapable of producing a Panton–Valentine type leucocidin. The lymphocyte apoptosis which accompanies neutrophil death may contribute to risk by impairing the generation of microbicidal antibody. Leucocyte apoptosis is a morphological expression of viral immunosuppression and, we suggest, is a likely contributor to a range of viral effects.

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Induction of Apoptosis by Herpes Simplex Virus-1 in Neonatal, But Not Adult, Neutrophils

Cited by 16 publications

References 35 publications

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

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

Berberine Restricts Coxsackievirus B Type 3 Replication via Inhibition of c-Jun N-Terminal Kinase (JNK) and p38 MAPK Activation In Vitro

Virus-associated apoptosis of blood neutrophils as a risk factor for invasive meningococcal disease

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