Evidence map›Paper›PMID 41606386›Full record

ArticleCell death and differentiation2026

Parvovirus B19 targets hematopoietic stem cells to disrupt multilineage differentiation and drive pancytopenia.

Xu-Ying Pei, Zhuo-Jun Liu, Qiang Fu, Hsiang-Ying Lee, Qi Hu, Xiao-Su Zhao, Yan Wei, Fu-Ping You, Yu-Qian Sun, Lan-Ping Xu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Xu-Ying Pei *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Zhuo-Jun Liu *Peking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Qiang FuPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Hsiang-Ying LeePeking-Tsinghua Center for Life Sciences, Beijing, China.
Qi HuPeking-Tsinghua Center for Life Sciences, Beijing, China.
Xiao-Su ZhaoPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Yan WeiPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Fu-Ping YouInstitute of Systems Biomedicine, Department of Immunology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.ORCID 0000-0002-7444-729X
Yu-Qian SunPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Lan-Ping XuPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Yu WangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Xiao-Hui ZhangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China.
Xiang-Yu ZhaoPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China. zhao_xy@bjmu.edu.cn.ORCID 0000-0002-8139-1773
Xiao-Jun HuangPeking University People's Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing Key Laboratory of Cell and Gene Therapy for Hematologic Malignancies, Peking University, Beijing, China. huangxiaojun@bjmu.edu.cn.ORCID 0000-0002-2145-6643

Funding

Beijing Municipal Science and Technology Commission Z211100002921071National Natural Science Foundation of China (National Science Foundation of China) 82293630
6 · The paper itself

Abstract

Human parvovirus B19 (B19V) infection is a significant but underrecognized complication, commonly linked not only to aplastic anemia but also pancytopenia, especially in hematopoietic stem cell transplantation (HSCT) recipients. While B19V's tropism for erythroid progenitor cells (EPCs) is well-documented, its restriction to EPCs fails to fully explain the pathogenesis of pancytopenia. In this study, we used PrimeFlow RNA assay, and single-cell full-length transcriptome sequencing (scFAST-seq) to show that B19V could infect hematopoietic stem cells (HSCs) and initiate viral transcription, resulting in increased apoptosis, impaired self-renewal and multilineage differentiation of HSCs, which may contribute directly to pancytopenia. Further analysis revealed that B19V could activate the JAK2/STAT5 signaling pathway in HSCs to promote viral persistence. Pharmacological inhibition with baricitinib markedly reduced the viral load and partially restored hematopoietic differentiation capacity in vitro. Taken together, our findings reveal B19V as a previously unrecognized HSC-tropic virus that disrupts function of HSCs and may drive pancytopenia. Targeting the JAK2/STAT5 signaling by baricitinib shows promising therapeutic potential for reversing virus-induced bone marrow failure. This work not only deepens our understanding of viral tropism and pathogenesis in the hematopoietic niche, but also opens up new possibilities for treating bone marrow damage after transplantation and in other hematological diseases.

Indexed as

Cell DifferentiationHematopoietic Stem CellsPancytopeniaParvoviridae InfectionsParvovirus B19, HumanAnimalsApoptosisCell LineageHumansJanus Kinase 2MiceSignal TransductionSTAT5 Transcription FactorJanus Kinase 2STAT5 Transcription Factor

Identifiers

PMID41606386
PMCPMC13433991

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.