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We now show that although both SERINC antagonists can in principle similarly enhance HIV-1 replication, glycoGag is unable to substitute for Nef in primary human cells and in a T cell line called MOLT-3. In MOLT-3 cells, Nef remained crucial for HIV-1 replication even in the absence of SERINC3 and SERINC5. The pronounced effect of Nef on HIV-1 spreading in MOLT-3 cells correlated with the ability of Nef to engage cellular endocytic machinery and to downregulate the HIV-1 receptor CD4 but nevertheless persisted in the absence of CD4 downregulation. Collectively, our results provide evidence for a potent novel restriction activity that affects even relatively SERINC-resistant HIV-1 isolates and is counteracted by Nef.<\/jats:p>","DOI":"10.1128\/mbio.01071-19","type":"journal-article","created":{"date-parts":[[2019,6,10]],"date-time":"2019-06-10T14:20:12Z","timestamp":1560176412000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Potent Enhancement of HIV-1 Replication by Nef in the Absence of SERINC3 and SERINC5"],"prefix":"10.1128","volume":"10","author":[{"given":"Yuanfei","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balaji","family":"Olety","sequence":"additional","affiliation":[{"name":"Department of Molecular, Cell and Cancer Biology, University 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