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The current mechanism proposed for protection of the virus by HIV-1 Vif is to induce APOBEC3G degradation through a ubiquitination-dependent proteasomal pathway. However, a new study published in <jats:italic>Retrovirology<\/jats:italic> by Strebel and colleagues suggests that Vif-induced APOBEC3G destruction may not be required for Vif's virus-protective effect. Strebel and co-workers show that Vif and APOBEC3G can stably co-exist, and yet viruses produced under such conditions are fully infectious. This new result highlights the notion that depletion of APOBEC3G is not the sole protective mechanism of Vif and that additional mechanisms exerted by this protein can be envisioned which counteract APOBEC3G and enhance HIV infectivity.<\/jats:p>","DOI":"10.1186\/1742-4690-1-28","type":"journal-article","created":{"date-parts":[[2004,9,23]],"date-time":"2004-09-23T06:23:34Z","timestamp":1095920614000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["HIV-1 Vif and APOBEC3G: Multiple roads to one goal"],"prefix":"10.1186","volume":"1","author":[{"given":"Joao","family":"Goncalves","sequence":"first","affiliation":[]},{"given":"Mariana","family":"Santa-Marta","sequence":"additional","affiliation":[]}],"member":"297","published-online":{"date-parts":[[2004,9,21]]},"reference":[{"key":"28_CR1","doi-asserted-by":"publisher","first-page":"27","DOI":"10.1186\/1742-4690-1-27","volume":"1","author":"S Kao","year":"2004","unstructured":"Kao S, Miyagi E, Khan MA, Takeuchi H, Opi S, Goila-Gaur R, Strebel K: Production of infectious human immunodeficiency virus type 1 does not require depletion of APOBEC3G from virus-producing cells. 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