Evidence map›Paper›PMID 22571741›Full record

ReviewRetrovirology2012

HLA-C and HIV-1: friends or foes?

Donato Zipeto, Alberto Beretta

Abstract readReview
In one paragraph

Review in Retrovirology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Natural Resistance to HIV Infection: Role of Immune Activation.Immunity, inflammation and disease · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. HLA-Cw1 and Psoriasis.American journal of clinical dermatology · 2021
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. HLA-C: An Accomplice in Rheumatic Diseases.ACR open rheumatology · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  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

2 authors.

Donato ZipetoDepartment of Life and Reproduction Sciences, Section of Biology and Genetics, University of Verona, Verona, Italy.
Alberto Beretta

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The major histocompatibility complex class I protein HLA-C plays a crucial role as a molecule capable of sending inhibitory signals to both natural killer (NK) cells and cytotoxic T lymphocytes (CTL) via binding to killer cell Ig-like receptors (KIR). Recently HLA-C has been recognized as a key molecule in the immune control of HIV-1. Expression of HLA-C is modulated by a microRNA binding site. HLA-C alleles that bear substitutions in the microRNA binding site are more expressed at the cell surface and associated with the control of HIV-1 viral load, suggesting a role of HLA-C in the presentation of antigenic peptides to CTLs. This review highlights the role of HLA-C in association with HIV-1 viral load, but also addresses the contradiction of the association between high cell surface expression of an inhibitory molecule and strong cell-mediated immunity. To explore additional mechanisms of control of HIV-1 replication by HLA-C, we address specific features of the molecule, like its tendency to be expressed as open conformer upon cell activation, which endows it with a unique capacity to associate with other cell surface molecules as well as with HIV-1 proteins.

Indexed as

Gene Expression RegulationHIV-1HIV InfectionsHLA-C AntigensHumansKiller Cells, NaturalRNA Processing, Post-TranscriptionalVirus ReplicationHLA-C Antigens

Identifiers

PMID22571741
PMCPMC3386009

What OpenQuestion holds

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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.