Nature 435, 108–114 (2005)
The authors wish to retract this Letter because they have been unable to reproduce the experiments demonstrating APOBEC3G functions as a post-entry restriction factor in resting CD4 T cells. Two recent studies1,2 have also challenged this conclusion. However, the authors report that several findings described in this Letter are reproducible, including: (1) low-molecular-mass (LMM) forms of APOBEC3G predominate in resting CD4 T cells and monocytes; (2) LMM APOBEC3G is recruited in high-molecular-mass (HMM) APOBEC3G RNA–protein complexes after activation of T cells or differentiation of monocytes into macrophages; (3) HMM APOBEC3G does not exhibit enzymatic activity; (4) when HMM APOBEC3G is treated with RNase A, LMM APOBEC3G forms are generated and enzymatic activity is restored; and (5) Vif assembles with and polyubiquitylates APOBEC3G present in HMM complexes. Nevertheless, because a central finding of the paper cannot be replicated either internally or externally despite repeated attempts, the authors request that Nature retract the paper and regret any confusion that may have been created by the paper’s publication.
References
Kamata, M., Nagaoka, Y. & Chen, I. S. Y. Reassessing the role of APOBEC3G in human immunodeficiency virus type 1 infection of quiescent CD4+ T-cells. PLoS Pathogens 5, e1000342 (2009)
Santoni de Sio, F. R. & Trono, D. APOBEC3G-depleted resting CD4+ T cells remain refractory to HIV1 infection. PLoS ONE 4, e6571 (2009)
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The online version of the original article can be found at 10.1038/nature03493
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Chiu, YL., Soros, V., Kreisberg, J. et al. Retraction Note: Cellular APOBEC3G restricts HIV-1 infection in resting CD4+ T cells. Nature 466, 276 (2010). https://doi.org/10.1038/nature09254
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DOI: https://doi.org/10.1038/nature09254
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