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Adenovirus evasion of interferon-mediated innate immunity by direct antagonism of a cellular histone posttranslational modification.

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.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Fonseca GJ,Thillainadesan G,Yousef AF,Ablack JN,Mossman KL,Torchia J,Mymryk JS

doi

10.1016/j.chom.2012.05.005

subject

Has Abstract

pub_date

2012-06-14 00:00:00

pages

597-606

issue

6

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(12)00167-9

journal_volume

11

pub_type

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