A requirement for NF-κB induction in the production of replication-competent HHV-8 virions

Sgarbanti, Marco; Arguello, Meztli; tenOever, Benjamin R.; Battistini, Angela; Lin, Rongtuan; Hiscott, John

doi:10.1038/sj.onc.1207707

Cited by 36 publications

(41 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…vFLIP activates the NF-B pathway (11,36), and this pathway has an inhibitory effect on KSHV reactivation (6). Nevertheless, the mechanism of NF-B pathway-mediated inhibition of KSHV reactivation remains unclear, and contradictory observations have been reported (50). Previous studies have shown that activation of the AP-1 pathway is essential for KSHV lytic replication during both de novo primary infection and reactivation, in part by regulating the expression of RTA (42,57,59).…”

Section: Resultsmentioning

confidence: 99%

“…vFLIP is known to activate NF-B (11,36). While inhibition of NF-B led to the reactivation and expression of KSHV lytic proteins (6), it was also shown that induction of NF-B was required for the production of KSHV virions in PEL cells following induction with 12-O-tetradecanoylphorbol-13-acetate (TPA) (50). In the present study, we investigated the role of vFLIP in KSHV latency by using a reverse genetics approach.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-κB-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency

Zhou

Xie

et al. 2008

J Virol

103

View full text Add to dashboard Cite

Kaposi's sarcoma-associated herpesvirus (KSHV) latency is central to the evasion of host immune surveillances and induction of KSHV-related malignancies. The mechanism of KSHV latency remains unclear. Here, we show that the KSHV latent gene vFLIP promotes viral latency by inhibiting viral lytic replication. vFLIP suppresses the AP-1 pathway, which is essential for KSHV lytic replication, by activating the NF-B pathway. Thus, by manipulating two convergent cellular pathways, vFLIP regulates both cell survival and KSHV lytic replication to promote viral latency. These results also indicate that the effect of the NF-B pathway on KSHV replication is determined by the status of the AP-1 pathway and hence provide a mechanistic explanation for the contradictory role of the NF-B pathway in KSHV replication. Since the NF-B pathway is commonly activated during infection of gammaherpesviruses, these findings might have general implications for the control of gammaherpesviral latency.

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-κB-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency

Zhou

Xie

et al. 2008

J Virol

103

View full text Add to dashboard Cite

show abstract

“…IKK-␤ subunit is one of the kinases involved in phosphorylation of p65 at serine 536 (34). The native IKK complex exhibits a molecular mass of ϳ700 to 900 kDa.…”

Section: Resultsmentioning

confidence: 99%

Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Narayanan

Kehn-Hall

Senina

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Rift Valley fever virus is a single-stranded RNA virus that causes disease in humans and livestock. Results: Rift Valley fever virus infection activates the host NFB signaling cascade. Conclusion: NFB inhibitors, particularly curcumin, down-regulate virus in both in vitro and in vivo models. Significance: Novel versions of host components resulting from an infection make them ideal therapeutic targets.

show abstract

“…Consistent with persistent activation of NF-kB being involved in HHV-8-associated disease, inhibition of NF-kB induces apoptosis in PEL cells (Keller et al, 2006), and as with EBV-infected cells, this appears to be due to downregulation of NF-kB-dependent survival genes such as IAP, cFLIP and IL-6 (Keller et al, 2006). Moreover, inhibition of NF-kB by expression of the IkBa superrepressor blocks the production of infectious HHV-8 virions (Sgarbanti et al, 2004), demonstrating the importance of NF-kB activation in both latent and lytic infection.…”

Section: Involvement Of the V-rel Protein In Avian Rev-t-induced Retrmentioning

confidence: 84%

Manipulation of the nuclear factor-κB pathway and the innate immune response by viruses

et al. 2006

View full text Add to dashboard Cite

A requirement for NF-κB induction in the production of replication-competent HHV-8 virions

Cited by 36 publications

References 67 publications

Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-κB-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency

Kaposi's Sarcoma-Associated Herpesvirus Latent Gene vFLIP Inhibits Viral Lytic Replication through NF-κB-Mediated Suppression of the AP-1 Pathway: a Novel Mechanism of Virus Control of Latency

Curcumin Inhibits Rift Valley Fever Virus Replication in Human Cells

Manipulation of the nuclear factor-κB pathway and the innate immune response by viruses

Contact Info

Product

Resources

About