Hepatitis C virus upregulates B-cell receptor signaling: a novel mechanism for HCV-associated B-cell lymphoproliferative disorders View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-06

AUTHORS

B Dai, A Y Chen, C P Corkum, R J Peroutka, A Landon, S Houng, P A Muniandy, Y Zhang, E Lehrmann, K Mazan-Mamczarz, J Steinhardt, M Shlyak, Q C Chen, K G Becker, F Livak, T I Michalak, R Talwani, R B Gartenhaus

ABSTRACT

B-cell receptor (BCR) signaling is essential for the development of B cells and has a critical role in B-cell neoplasia. Increasing evidence indicates an association between chronic hepatitis C virus (HCV) infection and B-cell lymphoma, however, the mechanisms by which HCV causes B-cell lymphoproliferative disorder are still unclear. Herein, we demonstrate the expression of HCV viral proteins in B cells of HCV-infected patients and show that HCV upregulates BCR signaling in human primary B cells. HCV nonstructural protein NS3/4A interacts with CHK2 and downregulates its activity, modulating HuR posttranscriptional regulation of a network of target mRNAs associated with B-cell lymphoproliferative disorders. Interestingly, the BCR signaling pathway was found to have the largest number of transcripts with increased association with HuR and was upregulated by NS3/4A. Our study reveals a previously unidentified role of NS3/4A in regulation of host BCR signaling during HCV infection, contributing to a better understanding of the molecular mechanisms underlying HCV-associated B-cell lymphoproliferative disorders. More... »

PAGES

2979

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2015.364

DOI

http://dx.doi.org/10.1038/onc.2015.364

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1019682751

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26434584


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