DOI: 10.1101/457937Oct 31, 2018Paper

Human APOBEC3G prevents emergence of infectious endogenous retrovirus in mice

BioRxiv : the Preprint Server for Biology
Rebecca TregerAkiko Iwasaki


Endogenous retroviruses (ERV) are found throughout vertebrate genomes and failure to silence their activation can have deleterious consequences on the host. Introduction of mutations that subsequently prevent transcription of ERV loci is therefore an indispensable cell-intrinsic defense mechanism that maintains the integrity of the host genome. Abundant in vitro and in silico evidence have revealed that APOBEC3 cytidine-deaminases, including human APOBEC3G (hA3G) can potently restrict retrotransposition; yet in vivo data demonstrating such activity is lacking, particularly since no replication competent human ERV has been identified. In mice deficient for Toll-like receptor 7 (TLR7), transcribed ERV loci can recombine and generate infectious ERV. In this study, we show that mice deficient in the only copy of Apobec3 in the genome did not have spontaneous reactivation of ERVs, nor elevated ERV reactivation when crossed to Tlr7-/- mice. In contrast, expression of a human APOBEC3G transgene abrogated emergence of infectious ERV in the Tlr7-/- background. No ERV RNA was detected in the plasma of hA3G+Apobec3-/-Tlr7-/- mice, and infectious ERV virions could not be amplified through co-culture with permissive cells. These data reveal...Continue Reading

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