Evidence map›Paper›PMID 32161622›Full record

ReviewCellular & molecular biology letters2020

Metabolic host response and therapeutic approaches to influenza infection.

Mohsen Keshavarz, Farid Solaymani-Mohammadi, Haideh Namdari, Yaser Arjeini, Mohammad Javad Mousavi, Farhad Rezaei

Open access · goldAbstract readReview
In one paragraph

Review in Cellular & molecular biology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.7field-weighted citation impact, top 1% 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

62 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Mohsen Keshavarz1The Persian Gulf Tropical Medicine Research Center, The Persian Gulf Biomedical Sciences Research Institute, Bushehr University of Medical Sciences, Bushehr, Iran.
Farid Solaymani-Mohammadi2Department of Biological Sciences, North Dakota State University, Fargo, North Dakota USA.
Haideh Namdari3Iranian Tissue Bank and Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Yaser Arjeini4Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Mohammad Javad Mousavi5Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Farhad Rezaei4Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Tehran University of Medical Sciences · IRBushehr University of Medical Sciences · IRNorth Dakota State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Based on available metabolomic studies, influenza infection affects a variety of cellular metabolic pathways to ensure an optimal environment for its replication and production of viral particles. Following infection, glucose uptake and aerobic glycolysis increase in infected cells continually, which results in higher glucose consumption. The pentose phosphate shunt, as another glucose-consuming pathway, is enhanced by influenza infection to help produce more nucleotides, especially ATP. Regarding lipid species, following infection, levels of triglycerides, phospholipids, and several lipid derivatives undergo perturbations, some of which are associated with inflammatory responses. Also, mitochondrial fatty acid β-oxidation decreases significantly simultaneously with an increase in biosynthesis of fatty acids and membrane lipids. Moreover, essential amino acids are demonstrated to decline in infected tissues due to the production of large amounts of viral and cellular proteins. Immune responses against influenza infection, on the other hand, could significantly affect metabolic pathways. Mainly, interferon (IFN) production following viral infection affects cell function via alteration in amino acid synthesis, membrane composition, and lipid metabolism. Understanding metabolic alterations required for influenza virus replication has revealed novel therapeutic methods based on targeted inhibition of these cellular metabolic pathways.

Indexed as

Energy MetabolismLipid MetabolismFatty Acid SynthasesGlucoseGlycolysisHost-Pathogen InteractionsHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInfluenza, HumanInterferonsMetabolic Networks and PathwaysNitric OxideFatty Acid SynthasesGlucoseIndoleamine-Pyrrole 2,3,-DioxygenaseInterferonsNitric OxideFatty acid synthesisGlycolysisIndoleamine-2,3-dioxygenaseInfluenzaMetabolism

Identifiers

PMID32161622
PMCPMC7059726
OpenAlexW3010645269

What OpenQuestion holds

Textmetadata
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.