Evidence map›Paper›PMID 28100616›Full record

ArticleJournal of virology2017

The V3 Loop of HIV-1 Env Determines Viral Susceptibility to IFITM3 Impairment of Viral Infectivity.

Yimeng Wang, Qinghua Pan, Shilei Ding, Zhen Wang, Jingyou Yu, Andrés Finzi, Shan-Lu Liu, Chen Liang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. HIV envelope tail truncation confers resistance to SERINC5 restriction.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Yimeng WangLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada.
Qinghua PanLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada.
Shilei DingCentre de Recherche du CHUM, Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Zhen WangLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada.
Jingyou YuCenter for Retrovirus Research, Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA.
Andrés FinziCentre de Recherche du CHUM, Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, Quebec, Canada.
Shan-Lu LiuCenter for Retrovirus Research, Department of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA.
Chen LiangLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada chen.liang@mcgill.ca.
Jewish General Hospital · CAThe Ohio State University · USCentre Hospitalier de l’Université de Montréal · CAMcGill University · CA

Funding

IFITM-mediated Inhibition of HIV Infection and Viral CountermeasuresR01AI112381 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI LIU, SHAN-LU · 2014 to 2018
$1.7M
NIAID NIH HHS R01 AI112381
6 · The paper itself

Abstract

Interferon-inducible transmembrane proteins (IFITMs) inhibit a broad spectrum of viruses, including HIV-1. IFITM proteins deter HIV-1 entry when expressed in target cells and also impair HIV-1 infectivity when expressed in virus producer cells. However, little is known about how viruses resist IFITM inhibition. In this study, we have investigated the susceptibilities of different primary isolates of HIV-1 to the inhibition of viral infectivity by IFITMs. Our results demonstrate that the infectivity of different HIV-1 primary isolates, including transmitted founder viruses, is diminished by IFITM3 to various levels, with strain AD8-1 exhibiting strong resistance. Further mutagenesis studies revealed that HIV-1 Env, and the V3 loop sequence in particular, determines the extent of inhibition of viral infectivity by IFITM3. IFITM3-sensitive Env proteins are also more susceptible to neutralization by soluble CD4 or the 17b antibody than are IFITM3-resistant Env proteins. Together, data from our study suggest that the propensity of HIV-1 Env to sample CD4-bound-like conformations modulates viral sensitivity to IFITM3 inhibition.

Indexed as

Amino Acid MotifsHEK293 CellsHIV-1HIV Envelope Protein gp120HIV InfectionsHumansImmune EvasionMembrane ProteinsRNA-Binding ProteinsViriongp120 protein, Human immunodeficiency virus 1HIV Envelope Protein gp120IFITM3 protein, humanMembrane ProteinsRNA-Binding Proteinsenvelope proteinhuman immunodeficiency virusIFITM

Identifiers

PMID28100616
PMCPMC5355610
OpenAlexW2572116825

What OpenQuestion holds

Textmetadata
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.