Evidence map›Paper›PMID 35632668›Full record

ReviewViruses2022

Multimodal Functionalities of HIV-1 Integrase.

Alan N Engelman, Mamuka Kvaratskhelia

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. The miRNomics of antiretroviral therapy-induced obesity.Functional & integrative genomics · 2025
    Review
  13. HIV-1 Integrase Inhibition Activity by Spiroketals Derived fromPharmaceuticals (Basel, Switzerland) · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Viruses · 2022
    Article
  19. Article
  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

2 authors at 2 institutions in 1 country.

Alan N EngelmanDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.ORCID 0000-0002-9709-2591
Mamuka KvaratskheliaDivision of Infectious Diseases, Anschutz Medical Campus, University of Colorado School of Medicine, Aurora, CO 80045, USA.
Harvard University · USUniversity of Colorado Anschutz Medical Campus · US

Funding

X-ray Crystallographic Fragment Screening CoreU54AI150472 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI OLSON, ARTHUR J. · 2019 to 2021
$15.7M
Integrase Structural VirologyR01AI070042 · NIAID · DANA-FARBER CANCER INST · PI ENGELMAN, ALAN N. · 2006 to 2020
$7.2M
Multimeric HIV-1 Integrase InhibitorsR01AI143649 · NIAID · UNIVERSITY OF COLORADO DENVER · PI KVARATSKHELIA, MAMUKA · 2019 to 2023
$2.5M
NIAID NIH HHS R01 AI070042NIAID NIH HHS R01 AI143649NIAID NIH HHS U54 AI150472NIAID NIH HHS U54AI150472; R01AI070042; R01AI143649
6 · The paper itself

Abstract

Integrase is the retroviral protein responsible for integrating reverse transcripts into cellular genomes. Co-packaged with viral RNA and reverse transcriptase into capsid-encased viral cores, human immunodeficiency virus 1 (HIV-1) integrase has long been implicated in reverse transcription and virion maturation. However, the underlying mechanisms of integrase in these non-catalytic-related viral replication steps have remained elusive. Recent results have shown that integrase binds genomic RNA in virions, and that mutational or pharmacological disruption of integrase-RNA binding yields eccentric virion particles with ribonucleoprotein complexes situated outside of the capsid shell. Such viruses are defective for reverse transcription due to preferential loss of integrase and viral RNA from infected target cells. Parallel research has revealed defective integrase-RNA binding and eccentric particle formation as common features of class II integrase mutant viruses, a phenotypic grouping of viruses that display defects at steps beyond integration. In light of these new findings, we propose three new subclasses of class II mutant viruses (a, b, and c), all of which are defective for integrase-RNA binding and particle morphogenesis, but differ based on distinct underlying mechanisms exhibited by the associated integrase mutant proteins. We also assess how these findings inform the role of integrase in HIV-1 particle maturation.

Indexed as

HIV-1HIV IntegraseHIV Integrase InhibitorsHumansRNA, ViralHIV IntegraseHIV Integrase Inhibitorsp31 integrase protein, Human immunodeficiency virus 1RNA, Viralaberrant integrase multimerizationallosteric integrase inhibitorHIVintegraseintegrase-RNA bindingvirus maturationvirus morphogenesis

Identifiers

PMID35632668
PMCPMC9144474
OpenAlexW4225140243

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.