Tumor suppressor cylindromatosis (CYLD) controls HIV transcription in an NF-κB-dependent manner.

ABSTRACT:

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Characterizing the cellular factors that play a role in the HIV replication cycle is fundamental to fully understanding mechanisms of viral replication and pathogenesis. Whole-genome small interfering RNA (siRNA) screens have identified positive and negative regulators of HIV replication, providing starting points for investigating new cellular factors. We report here that silencing of the deubiquitinase cylindromatosis protein (CYLD), increases HIV infection by enhancing HIV long terminal repeat (LTR)-driven transcription via the NF-κB pathway. CYLD is highly expressed in CD4(+) T lymphocytes, monocyte-derived macrophages, and dendritic cells. We found that CYLD silencing increases HIV replication in T cell lines. We confirmed the positive role of CYLD silencing in HIV

SUBMITTER: Manganaro L 

PROVIDER: S-EPMC4054419 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature