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Adenovirus Evasion of Interferon-Mediated Innate Immunity by Direct Antagonism of a Cellular Histone Posttranslational Modification

Adenovirus Evasion of Interferon-Mediated Innate Immunity by Direct Antagonism of a Cellular Histone Posttranslational Modification

G J Fonseca, G Thillainadesan, A F Yousef, J N Ablack, K L Mossman, J Torchia, J S Mymryk

Cell Host Microbe. 2012 Jun 14;11(6):597-606.

PMID: 22704620

Abstract:

Overcoming the cellular type I interferon (IFN) host defense response is critical for a virus to ensure successful infection. Investigating the effects of human adenovirus (HAdV) infection on global cellular histone posttranslational modification (hPTM), we discovered that virus infection-induced activation of IFN signaling triggers a global increase in the monoubiquitination of histone 2B (H2B) at lysine 120, which is a mark for transcriptionally active chromatin. This hPTM, catalyzed by the hBre1/RNF20 complex, is necessary for activation of the cellular IFN-stimulated gene (ISG) expression program in response to viruses. To establish effective infection, the HAdV E1A protein binds to and dissociates the hBre1 complex to block IFN-induced H2B monoubiquitination and associated ISG expression. Together, these data uncover a key role for H2B monoubiquitination in the type I IFN response and a viral mechanism of antagonizing this hPTM to evade the IFN response.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42415052	RNF20 active human			Price

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