Evidence map›Paper›PMID 21238946›Full record

ArticleCell host & microbe2011

Compensatory changes in the cytoplasmic tail of gp41 confer resistance to tetherin/BST-2 in a pathogenic nef-deleted SIV.

Ruth Serra-Moreno, Bin Jia, Matthew Breed, Xavier Alvarez, David T Evans

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Multi-functional BST2/tetherin against HIV-1, other viruses and LINE-1.Frontiers in cellular and infection microbiology · 2022
    Review
  7. Article
  8. Residues TRetrovirology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Ruth Serra-MorenoDepartment of Microbiology and Molecular Genetics, Harvard Medical School, New England Primate Research Center, Southborough, MA 01772-9102, USA.
Bin Jia
Matthew Breed
Xavier Alvarez
David T Evans
Harvard University · USTulane University · US

Funding

ZETA CHAIN OF T CELL RECEPTOR INTERACTS W/ NEF OF SIV &HIV2P51RR000168 · NCRR · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WESTMORELAND, SUSAN V. · 1985 to 2011
$139.3M
ZCM:A NOVEL BROAD-SPECTRUM MICROBICIDE FOR SEXUALLY TRANSMITTED INFECTIONSP51RR000164 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI VEAZEY, RONALD S. · 1985 to 2011
$100.1M
Pathology and Veterinary Service CoreP01AI071306 · NIAID · HARVARD MEDICAL SCHOOL · PI JOHNSON, R. PAUL · 2007 to 2011
$18.3M
KIR and MHC Class I Immunogenetics in SIV InfectionR01AI095098 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI EVANS, DAVID T · 2012 to 2016
$2.7M
MOUSE MODELS OF CANCER, BONE DISEASE, AND LACTATIONK26RR000168 · NCRR · OHIO STATE UNIVERSITY · PI ROSOL, THOMAS J · 2000 to 2004
$547k
Mechanisms of Lentiviral Resistance to TetherinR21AI087498 · NIAID · HARVARD MEDICAL SCHOOL · PI EVANS, DAVID T · 2010 to 2011
$475k
NCRR NIH HHS K26 RR000168NCRR NIH HHS P51 RR000164NCRR NIH HHS P51 RR000168NCRR NIH HHS RR000164NCRR NIH HHS RR000168NIAID NIH HHS AI071306NIAID NIH HHS AI087498NIAID NIH HHS P01 AI071306NIAID NIH HHS R21 AI087498
6 · The paper itself

Abstract

Tetherin (BST-2 or CD317) is an interferon-inducible transmembrane protein that inhibits virus release from infected cells. Whereas HIV-1 Vpu and HIV-2 Env counteract human tetherin, most SIVs use Nef to antagonize the tetherin proteins of their nonhuman primate hosts. Here, we show that compensatory changes in the cytoplasmic domain of SIV gp41, acquired by a nef-deleted virus that regained a pathogenic phenotype in infected rhesus macaques, restore resistance to tetherin. These changes facilitate virus release in the presence of rhesus tetherin, but not human tetherin, and enhance virus replication in interferon-treated primary lymphocytes. The substitutions in gp41 result in a selective physical association with rhesus tetherin, and the internalization and sequestration of rhesus tetherin by a mechanism that depends on a conserved endocytosis motif in gp41. These results are consistent with HIV-2 Env antagonism of human tetherin and suggest that the ability to oppose tetherin is important for lentiviral pathogenesis.

Indexed as

Mutation, MissenseAnimalsAntigens, CDCells, CulturedHost-Pathogen InteractionsLeukocytes, MononuclearMacaca mulattaMembrane GlycoproteinsMolecular Sequence DataMutant ProteinsRetroviridae ProteinsSequence Analysis, DNASimian Immunodeficiency VirusViral Regulatory and Accessory ProteinsAntigens, CDMembrane GlycoproteinsMutant ProteinsNEF protein, SIVRetroviridae ProteinsSIV envelope protein gp41Viral Regulatory and Accessory Proteins

Identifiers

PMID21238946
PMCPMC3023977
OpenAlexW2093060109

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.