作者: R. Suspene , M.-M. Aynaud , S. Koch , D. Pasdeloup , M. Labetoulle
DOI: 10.1128/JVI.00290-11
关键词: Herpes simplex virus 、 Activation-induced (cytidine) deaminase 、 Biology 、 Virus 、 Genetics 、 Cytidine deaminase 、 Viral replication 、 Genome 、 Virology 、 Viral transformation 、 Retrovirus
摘要: ABSTRACT Human APOBEC3 cytidine deaminases target and edit single-stranded DNA, which can be of viral, mitochondrial, or nuclear origin. Retrovirus genomes, such as human immunodeficiency virus (HIV) genomes deficient in the vif gene hepatitis B genome, are particularly vulnerable. The some DNA viruses, papillomaviruses, edited vivo transfection experiments. Accordingly, herpesviruses should no exception. This is indeed case for herpes simplex 1 (HSV-1) tissue culture, where APOBEC3C (A3C) overexpression reduce titers particle/PFU ratio ∼10-fold. Nonetheless, A3A, A3G, AICDA what presumably a small fraction HSV an experimental setting without seriously impacting viral titer. Hyperediting was found recovered from 4/8 uncultured buccal lesions. phenomenon not restricted to HSV, since hyperedited Epstein-Barr (EBV) were readily 4/5 established cell lines, indicating that episomes vulnerable editing. These findings suggest widely expressed A3C deaminase function restriction factor herpesviruses. That induced by type I interferons begs question whether encode antagonists.