Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Knockdown of KSHV viral interferon-regulatory factor 3 (vIRF-3) in primary effusion lymphoma (PEL) cells by RNA-Interference

ABSTRACT: KaposiM-bM-^@M-^Ys sarcoma-associated hepesvirus (KSHV) encodes four genes with homology to human interferon regulatory factors (IRFs). One of these IRFs, the viral interferon regulatory factor 3 (vIRF-3) is expressed in latently infected PEL cells and required for their continuous proliferation. Moreover, vIRF-3 is known to be involved in modulation of the type I interferon response. In order to identify cellular genes regulated by vIRF-3, cells from the PEL cell line BC-3 (KSHV positive) were transfected with either siRNAs targeted at vIRF-3 (si463 or si716s) or a negative control siRNA without homology to a known gene (siN, siNs). A total of 4 samples were analyzed. This includes two samples with silencing of vIRF-3 expression via RNA-interference (si463 or si716s) and two samples transfected with a negative-control siRNA (siN, siNs). Expression of vIRF-3 was reduced by approximately 75% as estimated by Western blot analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Frank Neipel 

PROVIDER: E-GEOD-26661 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Kaposi's sarcoma-associated herpesvirus viral interferon regulatory factor 3 inhibits gamma interferon and major histocompatibility complex class II expression.

Schmidt Katharina K   Wies Effi E   Neipel Frank F  

Journal of virology 20110223 9

Kaposi's sarcoma-associated herpesvirus (KSHV) carries four genes with homology to human interferon regulatory factors (IRFs). One of these IRFs, the viral interferon regulatory factor 3 (vIRF-3), is expressed in latently infected primary effusion lymphoma (PEL) cells and required for their continuous proliferation. Moreover, vIRF-3 is known to be involved in modulation of the type I interferon (IFN) response. We now show that vIRF-3 also interferes with the type II interferon system and antigen  ...[more]

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