Evidence map›Paper›PMID 35764966›Full record

ReviewRetrovirology2022

Defective HIV-1 genomes and their potential impact on HIV pathogenesis.

Jeffrey Kuniholm, Carolyn Coote, Andrew J Henderson

Abstract readReview
In one paragraph

Review in Retrovirology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
–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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Comprehensive Transcriptome Annotation of Thousands of HIV-1 Genomes.bioRxiv : the preprint server for biology · 2025
    Article
  13. Observational
  14. Article
  15. Review
  16. Review
  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

3 authors.

Jeffrey KuniholmDepartment of Microbiology, Section of Infectious Diseases, Boston University School of Medicine, Boston, MA, 02116, USA.
Carolyn CooteDepartment of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, MA, 02116, USA.
Andrew J HendersonDepartment of Microbiology, Section of Infectious Diseases, Boston University School of Medicine, Boston, MA, 02116, USA. hender@bu.edu.

Funding

Translational ScienceP30AI042853 · NIAID · MIRIAM HOSPITAL · PI CURT G BECKWITH, DEBBIE M. CHENG · 1998 to 2026
$51.7M
RESEARCH TRAINING IN IMMUNOLOGYT32AI007309 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GUMMULURU, SURYARAM · 1988 to 2024
$7.4M
Single nuclei transcriptomics of Alzheimer's brain diseaseR61DA047032 · NIDA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI CHENG, CHRISTINE, HENDERSON, ANDREW J · 2018 to 2020
$3.5M
Signals that establish and maintain HIV latencyR01AI138960 · NIAID · BOSTON MEDICAL CENTER · PI HENDERSON, ANDREW J · 2018 to 2022
$2.2M
Effect of opioid use disorder on HIV latent reservoirs and immune dysfunction assessed by single-cell transcriptomicsR33DA047032 · NIDA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI CHENG, CHRISTINE, HENDERSON, ANDREW J · 2021 to 2022
$1.8M
NIAID NIH HHS P30 AI042853NIAID NIH HHS R01 AI138960NIAID NIH HHS T32 AI007309NIDA NIH HHS R33 DA047032NIDA NIH HHS R61 DA047032
6 · The paper itself

Abstract

Defective HIV-1 proviruses represent a population of viral genomes that are selected for by immune pressures, and clonally expanded to dominate the persistent HIV-1 proviral genome landscape. There are examples of RNA and protein expression from these compromised genomes which are generated by a variety of mechanisms. Despite the evidence that these proviruses are transcribed and translated, their role in HIV pathogenesis has not been fully explored. The potential for these genomes to participate in immune stimulation is particularly relevant considering the accumulation of cells harboring these defective proviruses over the course of antiretroviral therapy in people living with HIV. The expression of defective proviruses in different cells and tissues could drive innate sensing mechanisms and inflammation. They may also alter antiviral T cell responses and myeloid cell functions that directly contribute to HIV-1 associated chronic comorbidities. Understanding the impact of these defective proviruses needs to be considered as we advance cure strategies that focus on targeting the diverse population of HIV-1 proviral genomes.

Indexed as

HIV-1HIV InfectionsGenome, ViralHumansProvirusesDefective provirusesHIV latencyPersistent reservoirTranscription

Identifiers

PMID35764966
PMCPMC9238239

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.