bioRxiv preprint doi: https://doi.org/10.1101/293001; this version posted April 3, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Primate immunodeficiency virus Vpx and Vpr counteract transcriptional repression of proviruses by the HUSH complex Leonid Yurkovetskiy1, Mehmet Hakan Guney1, Kyusik Kim1, Shih Lin Goh1, Sean McCauley1, Ann Dauphin1, William Diehl1, and Jeremy LuBan1,2* 1Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA 2Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA *Correspondence:
[email protected] (J.L.) bioRxiv preprint doi: https://doi.org/10.1101/293001; this version posted April 3, 2018. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 Drugs that inhibit HIV-1 replication and prevent progression to AIDS do not 2 eliminate HIV-1 proviruses from the chromosomes of long-lived CD4+ memory T 3 cells. To escape eradication by these antiviral drugs, or by the host immune 4 system, HIV-1 exploits poorly defined host factors that silence provirus 5 transcription. These same factors, though, must be overcome by all retroviruses, 6 including HIV-1 and other primate immunodeficiency viruses, in order to activate 7 provirus transcription and produce new virus.