Crimean Congo hemorrhagic fever virus infects human monocyte-derived dendritic cells

Connolly‐Andersen, Anne‐Marie; Douagi, Iyadh; Kraus, Annette; Mirazimi, Alì

doi:10.1016/j.virol.2009.06.010

Cited by 66 publications

(74 citation statements)

References 175 publications

(270 reference statements)

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“…Time line studies for transcript analysis for ICAM1, VCAM1, E-selectin, CCHFV NP, and GAPDH (glyceraldehyde-3-phosphate dehydrogenase) levels were performed by using manually designed primers for ICAM1, CCHFV NP, and GAPDH (11), and VCAM1 (PPH00623E), E-selectin (PPH00683E), and GAPDH (PPH00150E) were relatively quantified by the use of RT 2 quantitative PCR (qPCR) primer assays (SABiosciences Qiagen, MD). Analysis of VE-cadherin levels was performed using an RT 2 Profiler PCR array Human Endothelial Cell Biology kit ((PAHS-015C) SABiosciences Qiagen, MD).…”

Section: Methodsmentioning

confidence: 99%

“…Western blotting (WB) was performed as previously described (11). Briefly, lysis buffer was added to infected cells at designated time points, and polypeptides were separated on an SDS-PAGE gel.…”

Section: Methodsmentioning

confidence: 99%

“…The generation of moDCs was performed as previously described (11). Peripheral blood mononuclear cells (PBMCs) were enriched for monocytes by plastic adherence, followed by culturing with RPMI 1640 containing 200 ng/ml granulocyte-macrophage colony-stimulating factor (GM-CSF) (Peprotech), 75 ng/ml IL-4 (RnD Systems, United Kingdom), and 10% FCS, 2 mM L-glutamine, 100 U/ml penicillin, 100 M streptomycin, and 2% HEPES (Invitrogen Life Technologies).…”

Section: Downloaded Frommentioning

confidence: 99%

“…The involvement of the endothelium for CCHF and other VHFs has classically been explained by one of two theories: virus infection activates endothelial cells (i) directly or (ii) indirectly via infected leukocytes releasing soluble mediators with concomitant activation of the endothelium (20,34). Previously, studies have focused on the indirect role of the endothelium, since CCHFV infects dendritic cells and macrophages (11,30) and soluble mediators from CCHFV-infected dendritic cells activated ECs (30). Further support for an indirect effect of ECs for other VHFs comes from the identification of tumor necrosis factor alpha (TNF-␣) as a key mediator of endothelial cell activation (1,8,17).…”

mentioning

confidence: 99%

“…These cytokines were also released from CCHFV-infected dendritic cells (DCs) and macrophages (11,30). To our knowledge, no studies have been performed focusing on the ability of CCHFV to induce release of proinflammatory cytokines from ECs.…”

mentioning

confidence: 99%

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Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Connolly‐Andersen

Moll

Andersson

et al. 2011

J Virol

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Crimean-Congo hemorrhagic fever virus (CCHFV) causes viral hemorrhagic fever with high case-fatality rates and is geographically widely distributed. Due to the requirement for a biosafety level 4 (BSL-4) laboratory and the lack of an animal model, knowledge of the viral pathogenesis is limited. Crimean-Congo hemorrhagic fever (CCHF) is characterized by hemorrhage and vascular permeability, indicating the involvement of endothelial cells (ECs). The interplay between ECs and CCHFV is therefore important for understanding the pathogenesis of CCHF. In a previous study, we found that CCHFV-infected monocyte-derived dendritic cells (moDCs) activated ECs; however, the direct effect of CCHFV on ECs was not investigated. Here, we report that ECs are activated upon infection, as demonstrated by upregulation of mRNA levels for E-selectin, vascular cell adhesion molecule 1 (VCAM1), and intercellular adhesion molecule 1 (ICAM1). Protein levels and cell surface expression of ICAM1 responded in a dose-dependent manner to increasing CCHFV titers with concomitant increase in leukocyte adhesion. Furthermore, we examined vascular endothelial (VE) cadherin in CCHFVinfected ECs by different approaches. Infected ECs released higher levels of interleukin 6 (IL-6) and IL-8; however, stimulation of resting ECs with supernatants derived from infected ECs did not result in increased ICAM1 expression. Interestingly, the moDC-mediated activation of ECs was abrogated by addition of neutralizing tumor necrosis factor alpha (TNF-␣) antibody to moDC supernatants, thereby identifying this soluble mediator as the key cytokine causing EC activation. We conclude that CCHFV can exert both direct and indirect effects on ECs.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Downloaded Frommentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Connolly‐Andersen

Moll

Andersson

et al. 2011

J Virol

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Pathogenesis of Emerging and Novel Bunyaviruses in Humans

Jin

2015

Human Emerging and Re‐emerging Infections

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Relationship betweenIFNA1,IFNA5,IFNA10, andIFNA17gene polymorphisms and Crimean‐Congo hemorrhagic fever prognosis in a Turkish population range

Elaldı

Yilmaz

Bağcı

et al. 2016

Journal of Medical Virology

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Crimean-Congo hemorrhagic fever (CCHF) is a fatal emerging acute viral infection. Not much is known regarding the pathogenic mechanisms and the reasons behind severe or mild disease courses in CCHF. IFN-alpha (IFNA) is one of the essential cytokines in the immune system. Existence of single nucleotide gene polymorphisms (SNPs) in cytokines can cause susceptibility or resistance to viral agents and different clinical courses. Hence, the relationship between SNPs in genes encoding cytokines (IFNA1 -1823G/A (rs1332190), IFNA5 -2529T/A (rs758236), IFNA10 Cys20stop (rs10119910), and IFNA17 Ile184Arg (rs9298814) SNPs and disease susceptibility were investigated. The associations between SNPs and CCHF prognosis were also studied. Total 150 patients with CCHF and 170 healthy individuals were enrolled. Genotyping was performed by PCR-RFLP methods. The frequency of IFNA1 -1823 (rs1332190) GG genotype was significantly higher in control subjects than CCHF patients (20% vs. 8%; P = 0.01). For IFNA17 Ile184Arg (rs9298814) polymorphism, CCHF patients having TG genotype had a higher frequency than the control subjects (38% vs. 32.4%; P = 0.039). The distribution of TT + TG genotype frequencies was also significantly higher in CCHF group than the controls (97.3% vs. 91.8%; P = 0.049). Genotype and allele frequencies for IFNA subtypes between fatal and survivors were the same (P > 0.05). Genotype and allele frequencies between severe and mild/moderate CCHF patients were also the same (P > 0.05). The results show that IFNA1 rs1332190 and IFNA17 rs9298814 SNPs may play an important role in CCHF susceptibility. Determining the existence of other connections for IFNA SNPs and CCHF severity and fatality requires further investigations.

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Crimean Congo hemorrhagic fever virus infects human monocyte-derived dendritic cells

Cited by 66 publications

References 175 publications

Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Crimean-Congo Hemorrhagic Fever Virus Activates Endothelial Cells

Pathogenesis of Emerging and Novel Bunyaviruses in Humans

Relationship betweenIFNA1,IFNA5,IFNA10, andIFNA17gene polymorphisms and Crimean‐Congo hemorrhagic fever prognosis in a Turkish population range

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