Evidence map›Paper›PMID 30918127›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Inhibition of the lncRNA SAF drives activation of apoptotic effector caspases in HIV-1-infected human macrophages.

Saikat Boliar, David W Gludish, Kondwani C Jambo, Raphael Kamng'ona, Leonard Mvaya, Henry C Mwandumba, David G Russell

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Ebola virus exploits host lncRNAbioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Non-coding RNA Networks in Infection.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Animal models for studies of HIV-1 brain reservoirs.Journal of leukocyte biology · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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

7 authors at 2 institutions in 3 countries.

Saikat BoliarMicrobiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.
David W GludishMicrobiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853.
Kondwani C JamboMalawi-Liverpool-Wellcome Trust Clinical Research Program, University of Malawi College of Medicine, Blantyre 3, Malawi.
Raphael Kamng'onaMalawi-Liverpool-Wellcome Trust Clinical Research Program, University of Malawi College of Medicine, Blantyre 3, Malawi.
Leonard MvayaMalawi-Liverpool-Wellcome Trust Clinical Research Program, University of Malawi College of Medicine, Blantyre 3, Malawi.
Henry C MwandumbaMalawi-Liverpool-Wellcome Trust Clinical Research Program, University of Malawi College of Medicine, Blantyre 3, Malawi.
David G RussellMicrobiology and Immunology, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853; dgr8@cornell.edu.ORCID 0000-0002-9748-750X
University of Liverpool · GBCornell University · US

Funding

How does HIV lead to increased susceptibility to tuberculosis?R01AI118582 · NIAID · CORNELL UNIVERSITY · PI RUSSELL, DAVID G · 2015 to 2019
$2.8M
Are HIV-1-Infected Alveolar Macrophages Productive Sites of Viral Persistence?R33AI136097 · NIAID · CORNELL UNIVERSITY · PI RUSSELL, DAVID G · 2020 to 2022
$1.2M
Are HIV-1-Infected Alveolar Macrophages Productive Sites of Viral Persistence?R21AI136097 · NIAID · CORNELL UNIVERSITY · PI RUSSELL, DAVID G · 2018 to 2019
$426k
Medical Research Council MR/P020526/1NIAID NIH HHS R01 AI118582NIAID NIH HHS R21 AI136097NIAID NIH HHS R33 AI136097Wellcome TrustWellcome Trust 088696/Z/09/ZWellcome Trust 105831/Z/14/Z
6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) impart significant regulatory functions in a diverse array of biological pathways and manipulation of these RNAs provides an important avenue to modulate such pathways, particularly in disease. Our knowledge about lncRNAs' role in determination of cellular fate during HIV-1 infection remains sparse. Here, we have identified the impact of the lncRNA SAF in regulating apoptotic effector caspases in macrophages, a long-lived cellular reservoir of HIV-1, that are largely immune to virus-induced cell death. Expression of SAF is significantly up-regulated in HIV-1-infected human monocyte-derived macrophages (MDM) compared with bystander and virus-nonexposed cells. A similar enhancement in SAF RNA expression is also detected in the HIV-1-infected airway macrophages obtained by bronchoalveolar lavage of HIV-1-infected individuals. Down-regulation of SAF with siRNA treatment increases caspase-3/7 activity levels in virus-infected MDMs. This induction of apoptotic caspases occurs exclusively in HIV-1-infected macrophages and not in bystander cells, leading to a significant reduction in HIV-1 replication and overall viral burden in the macrophage culture. This study identifies targeting of the lncRNA SAF as a potential means to specifically induce cell death in HIV-1-infected macrophages.

Indexed as

ApoptosisCaspase 3Caspase 7HIV-1HIV InfectionsHumansMacrophagesRNA, Long NoncodingVirus ReplicationCASP3 protein, humanCASP7 protein, humanCaspase 3Caspase 7long noncoding RNA Fas-AS1, humanRNA, Long NoncodingAIDSapoptosisHIVlncRNAmacrophage

Identifiers

PMID30918127
PMCPMC6462110
OpenAlexW2924199136

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.