Kaposi's Sarcoma-Associated Herpesvirus Induction of AP-1 and Interleukin 6 during Primary Infection Mediated by Multiple Mitogen-Activated Protein Kinase Pathways

Xie, Jianping; Pan, Heng; Yoo, Seung‐Min; Gao, Shou‐Jiang

doi:10.1128/jvi.79.24.15027-15037.2005

Cited by 104 publications

(143 citation statements)

References 76 publications

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“…The requirement for IL-6 during KSHV infection is well documented [30][31][32][33][34][35][36][37][38], but the role of GADD45B may be more nuanced. While we demonstrated that it escapes host shutoff during lytic KSHV infection and appears important for viral reactivation in the iSLK.219 model, GADD45B expression is repressed by viral miRNAs during latency to avoid its cell cycle arrest and pro-apoptotic functions [73].…”

Section: Discussionmentioning

confidence: 99%

“…IL-6 expression is required for survival of B cells infected with KSHV, and the virus engages a number of strategies to drive production of this cytokine [30][31][32][33][34][35][36][37][38]. The IL-6 mRNA is directly refractory to SOX cleavage and thus remains robustly induced during host shutoff due to the presence of a specific 'SOX resistance element' (SRE) [26,29].…”

Section: Introductionmentioning

confidence: 99%

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Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases

Muller

Glaunsinger

2017

Preprint

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During lytic Kaposi's sarcoma-associated herpesvirus (KSHV) infection, the viral endonuclease SOX promotes widespread degradation of cytoplasmic messenger RNA (mRNA). However, select mRNAs, including the transcript encoding interleukin-6 (IL-6), escape SOX-induced cleavage. IL-6 escape is mediated through a 3' UTR RNA regulatory element that overrides the SOX targeting mechanism. Here, we reveal that this protective RNA element functions to broadly restrict cleavage by a range of homologous and non-homologous viral endonucleases. However, it does not impede cleavage by cellular endonucleases. The IL-6 protective sequence may be representative of a larger class of nuclease escape elements, as we identified a similar protective element in the GADD45B mRNA. The IL-6 and GADD45B-derived elements display similarities in their sequence, putative structure, and several associated RNA binding proteins. However, the overall composition of their ribonucleoprotein complexes appears distinct, leading to differences in the breadth of nucleases restricted. These findings highlight how RNA elements can selectively control transcript abundance in the background of widespread virus-induced mRNA degradation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases

Muller

Glaunsinger

2017

Preprint

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“…Disruption of EBV latency by BRLF1 is prevented by inhibitors of p38 or JNK (Adamson et al, 2000). Another human herpesvirus, Kaposi's sarcoma-associated herpesvirus (HHV-8), has been reported to activate the ERK, p38 and JNK MAP kinase pathways during primary infection (Naranatt et al, 2003;Xie et al, 2005), and the activation of these pathways is essential for HHV-8 infection (Pan et al, 2006). Inhibitors of all three MAP kinase pathways reduce HHV-8 infectivity by reducing lytic replication and, as a result, the yield of infectious virions (Pan et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Human herpesvirus 6B induces phosphorylation of p53 in its regulatory domain by a CK2- and p38-independent pathway

Øster

Bundgaard

Hupp

et al. 2008

Journal of General Virology

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Here, we demonstrate that human herpesvirus 6B (HHV-6B) infection upregulates the tumour suppressor p53 and induces phosphorylation of p53 at Ser392. Interestingly, phosphorylation at the equivalent site has previously been shown to correlate with p53 tumour suppression in murine models. Although the signalling pathways leading to Ser392 phosphorylation are poorly understood, they seem to include casein kinase 2 (CK2), double-stranded RNA-activated protein kinase (PKR), p38 or cyclin-dependent kinase 9 (Cdk9). By using column chromatography and in vitro kinase assays, CK2 and p38, but not PKR or Cdk9, eluted in column fractions that phosphorylated p53 at Ser392. However, treatment of cells with neither the CK2 and Cdk9 inhibitor 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole (DRB) nor p38 kinase inhibitors reduced HHV-6B-induced Ser392 phosphorylation significantly. Knockdown of the CK2β subunit or p38α by small interfering RNA had no effect on HHV-6B-induced phosphorylation of p53 at Ser392. Thus, HHV-6B induces p53 Ser392 phosphorylation by an atypical pathway independent of CK2 and p38 kinases, whereas mitogen-activated protein (MAP) kinase signalling pathways are involved in viral replication.

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“…These signaling events mediate several functions, such as activation of the cytoskeleton, endocytosis, gene expression, cell motility, attachment, the cell cycle, cell growth, apoptosis, and differentiation (10,11,19,32,48). During early times of infection, KSHV induces integrin-mediated FAK phosphorylation that is followed by the activation of a variety of focal adhesion-associated signal molecules, such as Src, PI-3K, Rho GTPases (RhoA, Rac, and Cdc42), and Diaphanous 2 (Dia2), as well as several downstream effector molecules, such as AKT, Ezrin, PKC-, MEK, ERK1/2, NF-B, and p38MAPK (4,18,30,35,37,39,41,42,47,49,(50)(51)(52)(53)(55)(56)(57) (Fig. 3).…”

Section: Kshv Induces Host Cell Preexisting Signal Molecules Early Dumentioning

confidence: 99%

Early Events in Kaposi's Sarcoma-Associated Herpesvirus Infection of Target Cells

Chandran

2010

J Virol

143

184

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Kaposi's sarcoma-associated herpesvirus (KSHV), the most recently identified member of the herpesvirus family, infects a variety of target cells in vitro and in vivo. This minireview surveys current information on the early events of KSHV infection, including virus-receptor interactions, involved envelope glycoproteins, mode of entry, intracellular trafficking, and initial viral and host gene expression programs. We describe data supporting the hypothesis that KSHV manipulates preexisting host cell signaling pathways to allow successful infection. The various signaling events triggered by infection, and their potential roles in the different stages of infection and disease pathogenesis, are summarized.

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Kaposi's Sarcoma-Associated Herpesvirus Induction of AP-1 and Interleukin 6 during Primary Infection Mediated by Multiple Mitogen-Activated Protein Kinase Pathways

Abstract: Kaposi's sarcoma is an angioproliferative disseminated tumor of endothelial cells linked to infection with

Cited by 104 publications

References 76 publications

Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases

Nuclease escape elements protect messenger RNA against cleavage by multiple viral endonucleases

Human herpesvirus 6B induces phosphorylation of p53 in its regulatory domain by a CK2- and p38-independent pathway

Early Events in Kaposi's Sarcoma-Associated Herpesvirus Infection of Target Cells

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