Host Gene Induction and Transcriptional Reprogramming in Kaposi’s Sarcoma-Associated Herpesvirus (KSHV/HHV-8)-Infected Endothelial, Fibroblast, and B Cells

Naranatt, Pramod P.; Krishnan, Harinivas H.; Svojanovsky, Stan R.; Bloomer, Clark; Mathur, Sachin; Chandran, Bala

doi:10.1158/0008-5472.can-03-2767

Cited by 145 publications

(208 citation statements)

References 42 publications

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“…We observed significant induction of RDC1 gene expression in K13-ER TAM HUVEC cells following 48 h treatment with 4-OHT, whereas no induction was observed in control vector-expressing cells (Figure 3b). Similar to RDC1, the expression of CXCL3/GRO3 and cyclooxygenase-2 (COX-2), two genes previously known to be upregulated in HHV8-infected endothelial cells (Naranatt et al, 2004), was highly upregulated following induction of K13 activity (Figure 3b). We also observed a modest increase in the expression of dual-specificity phosphatase 5 (DUSP5) (Figure 3b), another gene which is moderately upregulated following HHV8 infection (Naranatt et al, 2004).…”

Section: K13 Induces Spindle Cell Transformation Of Endothelial Cellsmentioning

confidence: 83%

“…Similar to RDC1, the expression of CXCL3/GRO3 and cyclooxygenase-2 (COX-2), two genes previously known to be upregulated in HHV8-infected endothelial cells (Naranatt et al, 2004), was highly upregulated following induction of K13 activity (Figure 3b). We also observed a modest increase in the expression of dual-specificity phosphatase 5 (DUSP5) (Figure 3b), another gene which is moderately upregulated following HHV8 infection (Naranatt et al, 2004). Taken together, the above results demonstrate that K13-induced spindle cell transformation of HUVEC cells is accompanied by an increase in the expression of several genes, which have been previously linked to spindle cell transformation by HHV8.…”

Section: K13 Induces Spindle Cell Transformation Of Endothelial Cellsmentioning

confidence: 83%

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Induction of spindle cell morphology in human vascular endothelial cells by human herpesvirus 8-encoded viral FLICE inhibitory protein K13

et al. 2006

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Section: K13 Induces Spindle Cell Transformation Of Endothelial Cellsmentioning

confidence: 83%

Section: K13 Induces Spindle Cell Transformation Of Endothelial Cellsmentioning

confidence: 83%

Induction of spindle cell morphology in human vascular endothelial cells by human herpesvirus 8-encoded viral FLICE inhibitory protein K13

et al. 2006

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“…Although no formal demonstration of recognition of KSHV intermediate dsRNA structures by MDA-5 or TLR-3 have been documented, this virus is likely no exception considering that infection by this virus is associated with the synthesis and release of IFN-b [26,27]. During latency, v-FLIP is known to activate NF-jB, essential for the survival of the infected cells [3].…”

Section: Discussionmentioning

confidence: 99%

Synergistic activation of interferon‐β gene transcription by the viral FLICE inhibitory protein of Kaposi's sarcoma‐associated herpesvirus and type I IFN activators

2007

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Expression of Kaposi's sarcoma-associated herpesvirus v-FLIP leads to the spindle-shape morphology of endothelial cells and is essential for the survival of primary effusion lymphoma cells. Activation of the NF-jB transcription factor by v-FLIP is responsible for these effects. Considering that the interferon-b (ifn-b) gene is regulated partly through NF-jB, we sought to determine whether v-FLIP would activate the expression of the ifn-b gene. Our results indicate that when v-FLIP is expressed by itself it has no effect on ifn-b gene activation but when it is combined with known IFN-b inducers, a synergistic activation of the ifn-b gene occurs. This effect is strictly dependent on NF-jB and is mediated through the positive regulatory domain II of the IFN-b promoter. Furthermore, we report that protection from Fas-induced cell-death by v-FLIP is observed whether or not the type I IFN signaling pathway is activated. Our work therefore contributes to increase our knowledge on v-FLIP, highlighting the complex immunomodulatory properties of this anti-apoptotic viral protein.

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“…Exposure to patientderived exosomes increased cell migration and IL-6 production in recipient endothelial cells [125]. Additionally, like EBV, KSHV reprogrammed the cell profile of infected B cells [126]. Infection promoted a switch to glycolytic metabolism, and glycolysis by-products like pyruvate kinase and lactate dehydrogenase were packaged into exosomes [7,127].…”

Section: Epstein-barr Virusmentioning

confidence: 99%

Exosomes in Viral Disease

2016

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Viruses have evolved many mechanisms by which to evade and subvert the immune system to ensure survival and persistence. However, for each method undertaken by the immune system for pathogen removal, there is a counteracting mechanism utilized by pathogens. The new and emerging role of microvesicles in immune intercellular communication and function is no different. Viruses across many different families have evolved to insert viral components in exosomes, a subtype of microvesicle, with many varying downstream effects. When assessed cumulatively, viral antigens in exosomes increase persistence through cloaking viral genomes, decoying the immune system, and even by increasing viral infection in uninfected cells. Exosomes therefore represent a source of viral antigen that can be used as a biomarker for disease and targeted for therapy in the control and eradication of these disorders. With the rise in the persistence of new and reemerging viruses like Ebola and Zika, exploring the role of exosomes become more important than ever.

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Host Gene Induction and Transcriptional Reprogramming in Kaposi’s Sarcoma-Associated Herpesvirus (KSHV/HHV-8)-Infected Endothelial, Fibroblast, and B Cells

Cited by 145 publications

References 42 publications

Induction of spindle cell morphology in human vascular endothelial cells by human herpesvirus 8-encoded viral FLICE inhibitory protein K13

Induction of spindle cell morphology in human vascular endothelial cells by human herpesvirus 8-encoded viral FLICE inhibitory protein K13

Synergistic activation of interferon‐β gene transcription by the viral FLICE inhibitory protein of Kaposi's sarcoma‐associated herpesvirus and type I IFN activators

Exosomes in Viral Disease

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