Evidence map›Paper›PMID 18808677›Full record

ReviewRetrovirology2008

HIV-1 Nef: at the crossroads.

John L Foster, J Victor Garcia

Open access · goldAbstract readReview
In one paragraph

Review in Retrovirology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% 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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 209 citations in OpenAlex.

  1. HIV Genome-Wide Protein Associations: a Review of 30 Years of Research.Microbiology and molecular biology reviews : MMBR · 2016
    Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Navigating the Nexus: HIV and Breast Cancer-A Critical Review.International journal of molecular sciences · 2024
    Review
  11. Human transferrin receptor can mediate SARS-CoV-2 infection.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Cardiovascular Disease and Thrombosis in HIV Infection.Arteriosclerosis, thrombosis, and vascular biology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

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

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

2 authors at 1 institution in 1 country.

John L FosterDepartment of Internal Medicine, Division of Infectious Diseases, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. John.foster@utsouthwestern.edu
J Victor Garcia
The University of Texas Southwestern Medical Center · US

Funding

NEF FUNCTIONR01AI033331 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI GARCIA-MARTINEZ, J. VICTOR · 1994 to 2010
$4.4M
NIAID NIH HHS AI33331NIAID NIH HHS R01 AI033331
6 · The paper itself

Abstract

The development of anti-virals has blunted the AIDS epidemic in the Western world but globally the epidemic has not been curtailed. Standard vaccines have not worked, and attenuated vaccines are not being developed because of safety concerns. Interest in attenuated vaccines has centered on isolated cases of patients infected with HIV-1 containing a deleted nef gene. Nef is a multifunctional accessory protein that is necessary for full HIV-1 virulence. Unfortunately, some patients infected with the nef-deleted virus eventually lose their CD4+ T cells to levels indicating progression to AIDS. This renders the possibility of an attenuated HIV-1 based solely on a deleted nef remote. In this review we discuss the knowledge gained both from the study of these patients and from in vitro investigations of Nef function to assess the possibility of developing new anti-HIV-1 drugs based on Nef. Specifically, we consider CD4 downregulation, major histocompatibility complex I downregulation, Pak2 activation, and enhancement of virion infectivity. We also consider the recent proposal that simian immunodeficiency viruses are non-pathogenic in their hosts because they have Nefs that downregulate CD3, but HIV-1 is pathogenic because its Nef fails to downregulate CD3. The possibility of incorporating the CD3 downregulation function into HIV-1 Nef as a therapeutic option is also considered. Finally, we conclude that inhibiting the CD4 downregulation function is the most promising Nef-targeted approach for developing a new anti-viral as a contribution to combating AIDS.

Indexed as

Virulence FactorsAcquired Immunodeficiency SyndromeHIV-1Humansnef Gene Products, Human Immunodeficiency Virusnef Gene Products, Human Immunodeficiency Virusnef protein, Human immunodeficiency virus 1Virulence Factors

Identifiers

PMID18808677
PMCPMC2563024
OpenAlexW2073129612

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.