ArticleNature medicine2008
Identification of calcium-modulating cyclophilin ligand as a human host restriction to HIV-1 release overcome by Vpu.
Article in Nature medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Restriction of Retroviral Replication by Tetherin/BST-2.Molecular biology international · 2012Article
- Background K(2P) channels KCNK3/9/15 limit the budding of cell membrane-derived vesicles.Cell biochemistry and biophysics · 2011Article
- Misdirection of membrane trafficking by HIV-1 Vpu and Nef: Keys to viral virulence and persistence.Cellular logistics · 2011Article
- Viral proteins function as ion channels.Biochimica et biophysica acta · 2011Review
- Molecular aspects of cyclophilins mediating therapeutic actions of their ligands.Cellular and molecular life sciences : CMLS · 2010Review
- Membrane potential depolarization as a triggering mechanism for Vpu-mediated HIV-1 release.Biophysical journal · 2010Article
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- Calcium-modulating cyclophilin ligand does not restrict retrovirus release.Nature medicine · 2010Article
- HIV-1 accessory protein Vpu internalizes cell-surface BST-2/tetherin through transmembrane interactions leading to lysosomes.The Journal of biological chemistry · 2009Article
- Effect of calcium-modulating cyclophilin ligand on human immunodeficiency virus type 1 particle release and cell surface expression of tetherin.Journal of virology · 2009Article
- Characterization of determinants important for hepatitis C virus p7 function in morphogenesis by using trans-complementation.Journal of virology · 2009Article
- Dynamics of HIV-1 assembly and release.PLoS pathogens · 2009Article
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- Partial inhibition of human immunodeficiency virus replication by type I interferons: impact of cell-to-cell viral transfer.Journal of virology · 2009Article
- Human cellular restriction factors that target HIV-1 replication.BMC medicine · 2009Review
- The formation of cysteine-linked dimers of BST-2/tetherin is important for inhibition of HIV-1 virus release but not for sensitivity to Vpu.Retrovirology · 2009Article
- Vpu directs the degradation of the human immunodeficiency virus restriction factor BST-2/Tetherin via a {beta}TrCP-dependent mechanism.Journal of virology · 2009Article
- The cell biology of HIV-1 virion genesis.Cell host & microbe · 2009Review
Corrections and comments
- Retraction · 2010-02-04Results Not Reproducible ·
- Commented on by
- Retracted
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The HIV-1 Vpu protein is required for efficient viral release from human cells. For HIV-2, the envelope (Env) protein replaces the role of Vpu. Both Vpu and HIV-2 Env enhance virus release by counteracting an innate host-cell block within human cells that is absent in African green monkey (AGM) cells. Here we identify calcium-modulating cyclophilin ligand (CAML) as a Vpu-interacting host factor that restricts HIV-1 release. Expression of human CAML (encoded by CAMLG) in AGM cells conferred a strong restriction of virus release that was reversed by Vpu and HIV-2 Env, suggesting that CAML is the mechanistic link between these two viral regulators. Depletion of CAML in human cells eliminated the need for Vpu in enhancing HIV-1 and murine leukemia virus release. These results point to CAML as a Vpu-sensitive host restriction factor that inhibits HIV release from human cells. The ability of CAML to inhibit virus release should illuminate new therapeutic strategies against HIV.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.