Evidence map›Paper›PMID 24725927›Full record

ArticleVirology2014

HIV-1 mutates to evade IFITM1 restriction.

Shilei Ding, Qinghua Pan, Shan-Lu Liu, Chen Liang

Open access · greenAbstract read
In one paragraph

Article in Virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. HIV envelope tail truncation confers resistance to SERINC5 restriction.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Mutations in the HIV-1 envelope glycoprotein can broadly rescue blocks at multiple steps in the virus replication cycle.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  14. Review
  15. Review
  16. Review
  17. Antiviral Protection by IFITM3 In Vivo.Current clinical microbiology reports · 2018
    Article
  18. Article
  19. Review
  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

4 authors at 2 institutions in 2 countries.

Shilei DingLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada H3T 1E2; Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada H3A 2B4.
Qinghua PanLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada H3T 1E2.
Shan-Lu LiuDepartment of Molecular Microbiology & Immunology, School of Medicine, Bond Life Sciences Center, University of Missouri, Columbia, MO 65211-7310, USA. Electronic address: liushan@missouri.edu.
Chen LiangLady Davis Institute, Jewish General Hospital, Montreal, QC, Canada H3T 1E2; Department of Microbiology and Immunology, McGill University, Montreal, QC, Canada H3A 2B4; Department of Medicine, McGill University, Montreal, QC, Canada H3A 2B4. Electronic address: chen.liang@mcgill.ca.
Jewish General Hospital · CAUniversity of Missouri · US

Funding

IFITM-mediated Inhibition of HIV Infection and Viral CountermeasuresR01AI112381 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI LIU, SHAN-LU · 2014 to 2018
$1.7M
Novel Cellular Factors Restricting Viral Membrane FusionR21AI105584 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI LIU, SHAN-LU · 2013 to 2014
$421k
CIHR HVI-98828CIHR MOP-77649NIAID NIH HHS R01 AI112381NIAID NIH HHS R01AI112381NIAID NIH HHS R21 AI105584NIAID NIH HHS R21AI105584
6 · The paper itself

Abstract

Interferon-induced transmembrane (IFITM) proteins inhibit the infection of a wide range of viruses including human immunodeficiency virus type 1 (HIV-1). At present, little is known about how viruses overcome IFITM restriction. In this study, we have utilized HIV-1 as a model and selected IFITM1-resistant viruses after multiple passages of HIV-1 in IFITM1-expressing SupT1 cells. Sequencing the entire viral genome revealed several mutations in the vpu and envelope genes, among which mutations Vpu34 and EnvG367E together enable efficient HIV-1 replication in IFITM1-expressing cells. Vpu34 introduces a stop codon at amino acid position 35 of Vpu, whereas EnvG367E changes the G367 residue at the CD4-binding site of gp120. These two mutations do not appear to overcome the downregulation of viral p24 expression caused by IFITM1, but rather enhance HIV-1 replication by promoting cell-to-cell virus transmission. Altogether, our data demonstrate that HIV-1 can mutate to evade IFITM1 restriction by increasing cell-to-cell transmission.

Indexed as

Immune EvasionMutationAntigens, DifferentiationCell LineDNA Mutational Analysisenv Gene Products, Human Immunodeficiency VirusHIV-1Human Immunodeficiency Virus ProteinsHumansSequence Analysis, DNASerial PassageViral Regulatory and Accessory ProteinsViroporin ProteinsAntigens, Differentiationenv Gene Products, Human Immunodeficiency VirusHuman Immunodeficiency Virus Proteinsleu-13 antigenViral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1Cell-to-cell transmissionEscape mutationsHIV-1IFITM1

Identifiers

PMID24725927
PMCPMC4274668
OpenAlexW2014098988

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.