Evidence map›Paper›PMID 35869417›Full record

ArticleJournal of medical virology2022

A soluble DR5-Fc chimeric protein attenuates inflammatory responses induced by coronavirus MHV-A59 and SARS-CoV-2.

Hong Peng, Birong Zheng, Sidi Yang, Jie Du, Liu Cao, Lihong Liu, Zengyi Ma, Junyu Wu, Chunmei Li, Hailong Zhang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of medical virology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Advances in the study of death receptor 5.Frontiers in pharmacology · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. 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 3 institutions in 1 country.

Hong PengDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.ORCID 0000-0003-0027-0855
Birong ZhengDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Sidi YangDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Jie DuDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Liu CaoDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Lihong LiuDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Zengyi MaDepartment of Neurosurgery, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Junyu WuDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Chunmei LiDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Hailong ZhangDepartment of Cell and Molecular Immunology, Joint National Laboratory for Antibody Drug Engineering, the First Affiliated Hospital, Henan University, Kaifeng, China.
Deyin GuoDepartment of Infection and Immunity, MOE Key Laboratory of Tropical Disease Control, School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.ORCID 0000-0002-8297-0814
Sun Yat-sen University · CNFirst Affiliated Hospital of Henan University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mortality in coronavirus disease 2019 (COVID-19) patients has been linked to the presence of a "cytokine storm" induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which involves elevated levels of circulating cytokines and immune-cell hyperactivation. Targeting cytokines during the management of COVID-19 patients has the potential to improve survival rates and reduce mortality. Although cytokine blockers and immune-host modulators are currently being tested in severely ill COVID-19 patients to cope with the overwhelming systemic inflammation, there is not too many successful cases, thus finding new cytokine blockers to attenuate the cytokine storm syndrome is meaningful. In this paper, we significantly attenuated the inflammatory responses induced by mouse hepatitis viruses A59 and SARS-CoV-2 through a soluble DR5-Fc (sDR5-Fc) chimeric protein that blocked the TNF-related apoptosis-inducing ligand-death receptor 5 (TRAIL-DR5) interaction. Our findings indicates that blocking the TRAIL-DR5 pathway through the sDR5-Fc chimeric protein is a promising strategy to treat COVID-19 severe patients requiring intensive care unit  admission or with chronic metabolic diseases.

Indexed as

COVID-19 Drug TreatmentSARS-CoV-2AnimalsCytokine Release SyndromeCytokinesMiceReceptors, TNF-Related Apoptosis-Inducing LigandRecombinant Fusion ProteinsCytokinesReceptors, TNF-Related Apoptosis-Inducing LigandRecombinant Fusion ProteinsMHV-A59proinflammatory cytokineSARS-CoV-2sDR5-Fc

Identifiers

PMID35869417
PMCPMC9349787
OpenAlexW4286669452

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.