Evidence map›Paper›PMID 32516328›Full record

ArticlePLoS pathogens2020

Human herpesvirus 6A promotes glycolysis in infected T cells by activation of mTOR signaling.

Zhisheng Wu, Junli Jia, Xianyi Xu, Mengyuan Xu, Guangyong Peng, Jingjing Ma, Xuefeng Jiang, Jialin Yao, Kun Yao, Lingyun Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Review
  5. Review
  6. Article
  7. Article
  8. Glucose-independent human cytomegalovirus replication is supported by metabolites that feed upper glycolytic branches.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  9. Article
  10. Pathogens and global health · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Evasion of the Host Immune Response by Betaherpesviruses.International journal of molecular sciences · 2021
    Review
  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

11 authors at 2 institutions in 2 countries.

Zhisheng WuDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.ORCID 0000-0002-1633-1360
Junli JiaDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Xianyi XuDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Mengyuan XuDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Guangyong PengDivision of Infectious Diseases, Allergy & Immunology and Department of Internal Medicine, Saint Louis University School of Medicine, Saint Louis, Missouri, United States of America.
Jingjing MaDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Xuefeng JiangDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Jialin YaoDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Kun YaoDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.
Lingyun LiDepartment of Medical Genetics, Nanjing Medical University, Nanjing, P. R. China.
Huamin TangDepartment of Immunology, Nanjing Medical University, Nanjing, P. R. China.ORCID 0000-0002-5724-3973
Nanjing Medical University · CNSaint Louis University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human herpesvirus 6 (HHV-6) is an important immunosuppressive and immunomodulatory virus worldwide. However, whether and how HHV-6 infection influences the metabolic machinery of the host cell to provide the energy and biosynthetic resources for virus propagation remains unknown. In this study, we identified that HHV-6A infection promotes glucose metabolism in infected T cells, resulting in elevated glycolytic activity with an increase of glucose uptake, glucose consumption and lactate secretion. Furthermore, we explored the mechanisms involved in HHV-6A-mediated glycolytic activation in the infected T cells. We found increased expressions of the key glucose transporters and glycolytic enzymes in HHV-6A-infected T cells. In addition, HHV-6A infection dramatically activated AKT-mTORC1 signaling in the infected T cells and pharmacological inhibition of mTORC1 blocked HHV-6A-mediated glycolytic activation. We also found that direct inhibition of glycolysis by 2-Deoxy-D-glucose (2-DG) or inhibition of mTORC1 activity in HHV-6A-infected T cells effectively reduced HHV-6 DNA replication, protein synthesis and virion production. These results not only reveal the mechanism of how HHV-6 infection affects host cell metabolism, but also suggest that targeting the metabolic pathway could be a new avenue for HHV-6 therapy.

Indexed as

GlycolysisSignal TransductionCell LineDeoxyglucoseDNA ReplicationDNA, ViralGlucoseHerpesvirus 6, HumanHumansLactic AcidMechanistic Target of Rapamycin Complex 1Proto-Oncogene Proteins c-aktRoseolovirus InfectionsT-LymphocytesTOR Serine-Threonine KinasesViral ProteinsDeoxyglucoseDNA, ViralGlucoseLactic AcidMechanistic Target of Rapamycin Complex 1MTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesViral Proteins

Identifiers

PMID32516328
PMCPMC7282626
OpenAlexW3033377892

What OpenQuestion holds

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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.