Linked Life Data

21763505

Source:http://linkedlifedata.com/resource/pubmed/id/21763505

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-7-18
pubmed:abstractText
Human immunodeficiency virus type 1 (HIV-1) infection significantly increases the risk and development of Kaposi's sarcoma (KS) in individuals infected with KS-associated herpesvirus (KSHV). Previously, we reported that HIV-1 Tat protein induced KSHV replication by modulating the Janus kinase/signal transducers and activators of transcription signaling pathway. Here, we further investigated the possible signaling pathways involved in HIV-1-induced reactivation of KSHV. We showed that HIV-1 infection of primary effusion lymphoma cell lines triggered the reactivation of KSHV, as demonstrated by the expression of KSHV replication and transcription activator, the early viral lytic protein vIL-6 and ORF59 and the production of progeny virions. By utilizing microarray gene expression analyses, transfecting a series of dominant negative mutants, and adding pharmacologic inhibitors, we identified a group of diverse cellular signaling proteins and found that HIV-1 infection of BCBL-1 cells activated phosphatidylinositol 3-kinase/AKT (also called protein kinase B, PKB) pathway and inactivated phosphatase and tensin homolog deleted on chromosome ten and glycogen synthase kinase-3?, which partially modulated HIV-1-induced KSHV reactivation. Furthermore, activation of Ras/c-Raf/MAPK/ERK kinase1/2 pathway contributed to HIV-1-induced KSHV replication. Finally, we discovered that HIV-1 infection activated nuclear factor ?B signaling, which exhibits an inhibitory effect on KSHV reactivation in BCBL-1 cells. Collectively, our data demonstrated that HIV-1 infection stimulated these cell signaling pathways that, in turn, contributed to KSHV reactivation, which may be of therapeutic value in acquired immunodeficiency syndrome-related KS patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1089-8638
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
29
pubmed:volume
410
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1035-51
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:21763505-Animals, pubmed-meshheading:21763505-Cell Line, pubmed-meshheading:21763505-Enzyme Activation, pubmed-meshheading:21763505-Glycogen Synthase Kinase 3, pubmed-meshheading:21763505-HIV-1, pubmed-meshheading:21763505-Herpesvirus 8, Human, pubmed-meshheading:21763505-Humans, pubmed-meshheading:21763505-Mice, pubmed-meshheading:21763505-Mitogen-Activated Protein Kinase Kinases, pubmed-meshheading:21763505-NF-kappa B, pubmed-meshheading:21763505-PTEN Phosphohydrolase, pubmed-meshheading:21763505-Phosphatidylinositol 3-Kinases, pubmed-meshheading:21763505-Proto-Oncogene Proteins c-akt, pubmed-meshheading:21763505-Proto-Oncogene Proteins c-raf, pubmed-meshheading:21763505-Signal Transduction, pubmed-meshheading:21763505-Up-Regulation, pubmed-meshheading:21763505-Vesiculovirus, pubmed-meshheading:21763505-Virus Replication, pubmed-meshheading:21763505-ras Proteins
pubmed:year
2011
pubmed:articleTitle
Human immunodeficiency virus type 1 induces lytic cycle replication of Kaposi's-sarcoma-associated herpesvirus: role of Ras/c-Raf/MEK1/2, PI3K/AKT, and NF-?B signaling pathways.
pubmed:affiliation
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing 210029, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't