Evidence map›Paper›PMID 41031180›Full record

ReviewJournal of inflammation research2025

A Focus on the Mechanisms of Alteration in Host Lymphocyte Level Following Severe Fever with Thrombocytopenia Syndrome Virus (SFTSV) Infection.

Yundi Chen, Heather Miller, Kamel Benlagha, Maria G Byazrova, Alexander V Filatov, Ziyin Zhang, Lian Liu, Yan Ding, Lu Yang, Quan Gong and 1 more

Abstract readReview
In one paragraph

Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Multidimensional mechanisms of SFTSV-host interactions: viral protein functions, mFrontiers in cellular and infection microbiology · 2026
    Review
  5. Article
  6. 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.

Yundi ChenDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Heather MillerCytek Biosciences, R&D Clinical Reagents, Fremont, CA, USA.
Kamel BenlaghaInstitut de Recherche Saint-Louis, Université de Paris, Paris, France.ORCID 0000-0002-3251-9195
Maria G ByazrovaLaboratory of Immunochemistry, National Research Center Institute of Immunology, Federal Medical Biological Agency of Russia, Moscow, Russia.
Alexander V FilatovLaboratory of Immunochemistry, National Research Center Institute of Immunology, Federal Medical Biological Agency of Russia, Moscow, Russia.
Ziyin ZhangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Lian LiuDepartment of Immunology, School of Medicine, Yangtze University, Jingzhou, People's Republic of China.
Yan DingDepartment of Rheumatology and Immunology, Wuhan Children's Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Lu YangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.ORCID 0000-0003-0595-6311
Quan GongDepartment of Immunology, School of Medicine, Yangtze University, Jingzhou, People's Republic of China.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nowadays, severe fever with thrombocytopenia syndrome (SFTS), featuring clinical manifestation of fever with leukopenia, thrombocytopenia and multiple organ function impairment, has been paid more and more attention. It has become the pandemic for a few years and a quantity of people died of it. Severe fever with thrombocytopenia syndrome virus (SFTSV) infection may lead to the development of SFTS, which is characterized by decreased counts of lymphocyte subsets, especially T cells, B cells and natural killer cells, and disruptive release of cytokines, chemokines and growth factors. However, the deeper mechanism of this disease remains unidentified. To excavate the mechanisms of lymphopenia in SFTSV infection and to introduce the potential therapeutics, this paper focuses on lymphopenia as well as reviews the mechanisms and effects of lymphopenia caused by SFTSV infection, mainly through making analogies with other similar viruses to explain the details of programmed cell death. Other factors such as IL-6,IL-10, TNF-α and some vital immunocytes also play significant roles in eliciting lymphopenia. Eventually, the probable clinical implications have been discussed, mentioning that lymphopenia induced by multiple pathways in SFTSV infection may be associated with the severity of viral disease and opportunistic infection.

Indexed as

chemokinescytokinesimmune responseinfectionlymphopeniaSFTSV

Identifiers

PMID41031180
PMCPMC12477067

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.