Evidence map›Paper›PMID 36467738›Full record

ReviewFrontiers in cellular and infection microbiology2022

HIV-1 replication and latency are balanced by mTOR-driven cell metabolism.

Jacqueline M Crater, Douglas F Nixon, Robert L Furler O'Brien

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Immuno-cell metabolic changes in HIV-1 infection.Infectious diseases & immunity · 2025
    Review
  13. Macropinosomes are a site of HIV-1 entry into primary CD4Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Salivary mycobiome alterations in HIV-infected MSM: dominance ofFrontiers in cellular and infection microbiology · 2025
    Article
  20. Editorial: The role of autophagy in cardiovascular disease.Frontiers in cell and developmental biology · 2025
    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 at 2 institutions in 1 country.

Jacqueline M CraterDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, NY, United States.
Douglas F NixonDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, NY, United States.
Robert L Furler O'BrienDivision of Infectious Diseases, Department of Medicine, Weill Cornell Medicine, New York, NY, United States.
Weill Cornell Medicine · USCornell University · US

Funding

REACH: Research Enterprise to Advance a Cure for HIVUM1AI164565 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Marina Caskey, R. Brad Jones · 2021 to 2026
$32.9M
BELIEVE: Bench to Bed Enhanced Lymphocyte Infusions to Engineer Viral EradicationUM1AI126617 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI JONES, R. BRAD, NIXON, DOUGLAS F · 2016 to 2020
$28.1M
Genetic Risk of HIV Acquisition: Mechanisms of ResilienceR21AI154956 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI NIXON, DOUGLAS F, POWELL, TIMOTHY · 2020 to 2021
$466k
NIAID NIH HHS R21 AI154956NIAID NIH HHS UM1 AI126617NIAID NIH HHS UM1 AI164565
6 · The paper itself

Abstract

Human Immunodeficiency virus type 1 (HIV-1) relies on host cell metabolism for all aspects of viral replication. Efficient HIV-1 entry, reverse transcription, and integration occurs in activated T cells because HIV-1 proteins co-opt host metabolic pathways to fuel the anabolic requirements of virion production. The HIV-1 viral life cycle is especially dependent on mTOR, which drives signaling and metabolic pathways required for viral entry, replication, and latency. As a central regulator of host cell metabolism, mTOR and its downstream effectors help to regulate the expression of enzymes within the glycolytic and pentose phosphate pathways along with other metabolic pathways regulating amino acid uptake, lipid metabolism, and autophagy. In HIV-1 pathogenesis, mTOR, in addition to HIF-1α and Myc signaling pathways, alter host cell metabolism to create an optimal environment for viral replication. Increased glycolysis and pentose phosphate pathway activity are required in the early stages of the viral life cycle, such as providing sufficient dNTPs for reverse transcription. In later stages, fatty acid synthesis is required for creating cholesterol and membrane lipids required for viral budding. Epigenetics of the provirus fueled by metabolism and mTOR signaling likewise controls active and latent infection. Acetyl-CoA and methyl group abundance, supplied by the TCA cycle and amino acid uptake respectively, may regulate latent infection and reactivation. Thus, understanding and exploring new connections between cellular metabolism and HIV-1 pathogenesis may yield new insights into the latent viral reservoirs and fuel novel treatments and cure strategies.

Indexed as

HIV-1Latent InfectionAmino AcidsHumansProto-Oncogene Proteins c-mycSignal TransductionTOR Serine-Threonine KinasesVirus ReplicationAmino AcidsMTOR protein, humanProto-Oncogene Proteins c-mycTOR Serine-Threonine KinasesCD4 + T cellglycolysisHIV-1immunometabolismmTOR

Identifiers

PMID36467738
PMCPMC9712982
OpenAlexW4309609834

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.