Conserved Herpesvirus Protein Kinases Target SAMHD1 to Facilitate Virus Replication.

Abstract:

:To ensure a successful infection, herpesviruses have developed elegant strategies to counterbalance the host anti-viral responses. Sterile alpha motif and HD domain 1 (SAMHD1) was recently identified as an intrinsic restriction factor for a variety of viruses. Aside from HIV-2 and the related simian immunodeficiency virus (SIV) Vpx proteins, the direct viral countermeasures against SAMHD1 restriction remain unknown. Using Epstein-Barr virus (EBV) as a primary model, we discover that SAMHD1-mediated anti-viral restriction is antagonized by EBV BGLF4, a member of the conserved viral protein kinases encoded by all herpesviruses. Mechanistically, we find that BGLF4 phosphorylates SAMHD1 and thereby inhibits its deoxynucleotide triphosphate triphosphohydrolase (dNTPase) activity. We further demonstrate that the targeting of SAMHD1 for phosphorylation is a common feature shared by beta- and gamma-herpesviruses. Together, our findings uncover an immune evasion mechanism whereby herpesviruses exploit the phosphorylation of SAMHD1 to thwart host defenses.

journal_name

Cell Rep

journal_title

Cell reports

authors

Zhang K,Lv DW,Li R

doi

10.1016/j.celrep.2019.04.020

subject

Has Abstract

pub_date

2019-07-09 00:00:00

pages

449-459.e5

issue

2

issn

2211-1247

pii

S2211-1247(19)30485-1

journal_volume

28

pub_type

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