HIV-1 Nef promotes infection by excluding SERINC5 from virion incorporation
- A. Rosa, A. Chande, M. Pizzato
- BiologyNature
- 30 September 2015
This work identifies 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.
Cyclophilin A retrotransposition into TRIM5 explains owl monkey resistance to HIV-1
- D. Sayah, Elena Sokolskaja, L. Berthoux, J. Luban
- BiologyNature
- 7 July 2004
It is shown that knockdown of owl monkey CypA by RNA interference (RNAi) correlates with suppression of anti-HIV-1 activity, and that TRIMCyp arose after the divergence of New and Old World primates, the first vertebrate example of a chimaeric gene generated by this mechanism of exon shuffling.
Specific incorporation of cyclophilin A into HIV-1 virions
- E. K. Franke, H. Yuan, J. Luban
- BiologyNature
- 24 November 1994
It is demonstrated that cyclophilin A is specifically incorporated into HIV-1 virions but not into virions of other primate immunodeficiency viruses.
The retinoblastoma protein and BRG1 form a complex and cooperate to induce cell cycle arrest
- J. Dunaief, B. Strober, S. Goff
- BiologyCell
- 7 October 1994
TRIM5 is an innate immune sensor for the retrovirus capsid lattice
- Thomas Pertel, S. Hausmann, J. Luban
- BiologyNature
- 7 March 2011
The retroviral restriction factor TRIM5 has two additional activities that are linked to restriction: it constitutively promotes innate immune signalling and it acts as a pattern recognition receptor specific for the retrovirus capsid lattice.
Cyclophilin A is required for an early step in the life cycle of human immunodeficiency virus type 1 before the initiation of reverse transcription
- D. Braaten, E. K. Franke, J. Luban
- Biology, MedicineJournal of Virology
- 1 June 1996
Results indicate that CyPA is required for an early step in the HIV-1 life cycle following receptor binding and membrane fusion but preceding reverse transcription, the first cellular protein other than the cell surface receptor shown to be required for a early event in the life cycle of a retrovirus.
HIV-1 Vpu Neutralizes the Antiviral Factor Tetherin/BST-2 by Binding It and Directing Its Beta-TrCP2-Dependent Degradation
- B. Mangeat, Gustavo Gers-Huber, Martin Lehmann, M. Zufferey, J. Luban, V. Piguet
- BiologyPLoS Pathogens
- 1 September 2009
It is shown that HIV-1 Vpu induces the depletion of tetherin from cells and interacts with tetherin to direct its β-TrCP2-dependent proteasomal degradation, thereby alleviating the blockade to the release of infectious virions.
TNPO3 protects HIV-1 replication from CPSF6-mediated capsid stabilization in the host cell cytoplasm
- A. De Iaco, F. Santoni, A. Vannier, M. Guipponi, S. Antonarakis, J. Luban
- BiologyRetrovirology
- 15 February 2013
TNPO3 promotes HIV-1 infectivity indirectly, by shifting the CA-binding protein CPSF6 to the nucleus, thus preventing the excessive HIV- 1 CA stability that would otherwise result from cytoplasmic accumulation of CPSF4 and targeting CPSF 6 by fusion to a heterologous nuclear localization signal rescued HIV-2 from the inhibitory effects of TNPO3 knockdown.
Basic Residues in Human Immunodeficiency Virus Type 1 Nucleocapsid Promote Virion Assembly via Interaction with RNA
- A. Cimarelli, S. Sandin, S. Höglund, J. Luban
- BiologyJournal of Virology
- 1 April 2000
An inverse relationship between the number of NC basic residues replaced with alanine and NC's nonspecific RNA-binding activity, Gag's ability to polymerize in vitro and in vivo, and Gag’s capacity to assemble virions is found.
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