HIV-1 Nef promotes infection by excluding SERINC5 from virion incorporation

Annachiara Rosa, Ajit Chande, Serena Ziglio, Veronica De Sanctis, Roberto Bertorelli, Shih Lin Goh, Sean M. McCauley, Anetta Nowosielska, Stylianos E. Antonarakis, Jeremy Luban, Federico Andrea Santoni and Massimo Pizzato ()
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Annachiara Rosa: University of Trento, Centre for Integrative Biology
Ajit Chande: University of Trento, Centre for Integrative Biology
Serena Ziglio: University of Trento, Centre for Integrative Biology
Veronica De Sanctis: University of Trento, Laboratory of Biomolecular Sequence and Structure Analysis for Health, NGS facility
Roberto Bertorelli: University of Trento, Laboratory of Biomolecular Sequence and Structure Analysis for Health, NGS facility
Shih Lin Goh: University of Massachusetts Medical School, Program in Molecular Medicine
Sean M. McCauley: University of Massachusetts Medical School, Program in Molecular Medicine
Anetta Nowosielska: University of Massachusetts Medical School, Program in Molecular Medicine
Stylianos E. Antonarakis: University of Geneva
Jeremy Luban: University of Massachusetts Medical School, Program in Molecular Medicine
Federico Andrea Santoni: University of Geneva
Massimo Pizzato: University of Trento, Centre for Integrative Biology

Nature, 2015, vol. 526, issue 7572, 212-217

Abstract: Abstract HIV-1 Nef, a protein important for the development of AIDS, has well-characterized effects on host membrane trafficking and receptor downregulation. By an unidentified mechanism, Nef increases the intrinsic infectivity of HIV-1 virions in a host-cell-dependent manner. Here we identify the host transmembrane protein SERINC5, and to a lesser extent SERINC3, as a potent inhibitor of HIV-1 particle infectivity that is counteracted by Nef. SERINC5 localizes to the plasma membrane, where it is efficiently incorporated into budding HIV-1 virions and impairs subsequent virion penetration of susceptible target cells. Nef redirects SERINC5 to a Rab7-positive endosomal compartment and thereby excludes it from HIV-1 particles. The ability to counteract SERINC5 was conserved in Nef encoded by diverse primate immunodeficiency viruses, as well as in the structurally unrelated glycosylated Gag from murine leukaemia virus. These examples of functional conservation and convergent evolution emphasize the fundamental importance of SERINC5 as a potent anti-retroviral factor.

Date: 2015
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DOI: 10.1038/nature15399

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