Open AccessA Conserved Mechanism of APOBEC3 Relocalization by Herpesviral Ribonucleotide Reductase Large Subunits
Author(s) -
Adam Z. Cheng,
Sofia N. Moraes,
Claire Attarian,
Jaime Yockteng-Melgar,
Matthew C. Jarvis,
Matteo Biolatti,
Ganna Galitska,
Valentina Dell’Oste,
Lori Frappier,
Craig J. Bierle,
Stuart A. Rice,
Reuben S. Harris
Publication year - 2019
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.01539-19
Subject(s) - biology , ribonucleotide reductase , viral replication , lytic cycle , protein subunit , virus , dna replication , virology , ribonucleotide , viral protein , herpes simplex virus , microbiology and biotechnology , dna , genetics , gene , nucleotide
The APOBEC3 family of DNA cytosine deaminases constitutes a vital innate immune defense against a range of different viruses. A novel counterrestriction mechanism has recently been uncovered for the gammaherpesvirus EBV, in which a subunit of the viral protein known to produce DNA building blocks (ribonucleotide reductase) causes A3B to relocalize from the nucleus to the cytosol. Here, we extend these observations with A3B to include a closely related gammaherpesvirus, KSHV, and a more distantly related alphaherpesvirus, HSV-1. These different viral ribonucleotide reductases also caused relocalization of A3A, which is 92% identical to A3B. These studies are important because they suggest a conserved mechanism of APOBEC3 evasion by large double-stranded DNA herpesviruses. Strategies to block this host-pathogen interaction may be effective for treating infections caused by these herpesviruses.
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