Evidence map›Paper›PMID 35534727›Full record

ArticleNature metabolism2022

A glucose-like metabolite deficient in diabetes inhibits cellular entry of SARS-CoV-2.

Liangqin Tong, Xiaoping Xiao, Min Li, Shisong Fang, Enhao Ma, Xi Yu, Yibin Zhu, Chunli Wu, Deyu Tian, Fan Yang and 21 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Interactions of SARS-CoV-2 with Human Target Cells-A Metabolic View.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. SARS-CoV-2 infection and its effects on the endocrine system.Best practice & research. Clinical endocrinology & metabolism · 2023
    Review
  13. Article
  14. Review
  15. Characteristics of animal models for COVID-19.Animal models and experimental medicine · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. In vivo (Athens, Greece)
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

31 authors at 12 institutions in 2 countries.

Liangqin Tong *Tsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.ORCID http://orcid.org/0000-0002-2717-919X
Xiaoping Xiao *Tsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Min Li *State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China.
Shisong Fang *Institute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Enhao MaTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Xi YuTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Yibin ZhuTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Chunli WuInstitute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Deyu TianCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Fan YangInstitute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Jing SunState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jing QuInstitute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
Nianzhen ZhengDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Shumin LiaoShenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Wanbo TaiInstitute of Infectious Diseases, Shenzhen Bay Laboratory, Shenzhen, China.
Shengyong FengTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Liming ZhangTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Yuhan LiTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Lin WangTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China.
Xuelian HanState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China.
Shihui SunState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China.
Long YangSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Hui ZhongBeijing Institute of Biotechnology, Academy of Military Medical Sciences, Beijing, China.ORCID http://orcid.org/0000-0003-2128-9686
Jincun ZhaoState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Wenjun LiuCAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology, Chinese Academy of Sciences, Beijing, China.
Xiaohui LiuSchool of Life Science, Tsinghua University, Beijing, China.
Penghua WangDepartment of Immunology, School of Medicine, the University of Connecticut Health Center, Farmington, CT, USA.ORCID http://orcid.org/0000-0002-7332-1871
Liang LiDepartment of Pharmacology, School of Medicine, Southern University of Science and Technology, Shenzhen, China. lil@sustech.edu.cn.ORCID http://orcid.org/0000-0003-1001-7837
Guangyu ZhaoState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Academy of Military Medical Sciences, Beijing, China. guangyu0525@163.com.ORCID http://orcid.org/0000-0002-0925-5216
Renli ZhangInstitute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, China. renlizhangszcdc@aliyun.com.ORCID http://orcid.org/0000-0001-5037-1035
Gong ChengTsinghua-Peking Joint Center for Life Sciences, School of Medicine, Tsinghua University, Beijing, China. gongcheng@mail.tsinghua.edu.cn.ORCID http://orcid.org/0000-0001-7447-5488
Center for Life Sciences · CNAcademy of Military Medical Sciences · CNShenzhen Center for Disease Control and Prevention · CNShenzhen Bay Laboratory · CNChinese Academy of Sciences · CNFirst Affiliated Hospital of Guangzhou Medical University · CNSouthern University of Science and Technology · CNKing Center · USShenzhen Institutes of Advanced Technology · CNTianjin University of Traditional Chinese Medicine · CNTsinghua University · CNUConn Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The severity and mortality of COVID-19 are associated with pre-existing medical comorbidities such as diabetes mellitus. However, the underlying causes for increased susceptibility to viral infection in patients with diabetes is not fully understood. Here we identify several small-molecule metabolites from human blood with effective antiviral activity against SARS-CoV-2, one of which, 1,5-anhydro-D-glucitol (1,5-AG), is associated with diabetes mellitus. The serum 1,5-AG level is significantly lower in patients with diabetes. In vitro, the level of SARS-CoV-2 replication is higher in the presence of serum from patients with diabetes than from healthy individuals and this is counteracted by supplementation of 1,5-AG to the serum from patients. Diabetic (db/db) mice undergo SARS-CoV-2 infection accompanied by much higher viral loads and more severe respiratory tissue damage when compared to wild-type mice. Sustained supplementation of 1,5-AG in diabetic mice reduces SARS-CoV-2 loads and disease severity to similar levels in nondiabetic mice. Mechanistically, 1,5-AG directly binds the S2 subunit of the SARS-CoV-2 spike protein, thereby interrupting spike-mediated virus-host membrane fusion. Our results reveal a mechanism that contributes to COVID-19 pathogenesis in the diabetic population and suggest that 1,5-AG supplementation may be beneficial to diabetic patients against severe COVID-19.

Indexed as

COVID-19Diabetes Mellitus, ExperimentalAnimalsGlucoseHumansMiceSARS-CoV-2Spike Glycoprotein, CoronavirusGlucoseSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2

Identifiers

PMID35534727
OpenAlexW4229451772

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.