Evidence map›Paper›PMID 42748357›Full record

ArticleEmerging microbes & infections2026

Differential pathogenesis and antiviral treatment outcomes of MPXV clade Ib and clade IIb in a BALB/c mouse model.

Yong Feng, Chenguang Shen, Penghui Jia, Bo Peng, Wei Yang, Shiman Chen, Yun Peng, Xiaowen Liang, Shengjie Zhang, Fangfang Chang and 6 more

Abstract read
In one paragraph

Article in Emerging microbes & infections, 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

16 authors.

Yong FengShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Chenguang ShenPublic Health, Southern Medical University, BSL-3 Laboratory (Guangdong), Guangdong Provincial Key Laboratory of Tropical Disease Research, Guangzhou, People's Republic of China.
Penghui JiaInstitute of Microbiology, Center for Disease Control and Prevention of Guangdong Province, Guangzhou, People's Republic of China.
Bo PengShenzhen Guangming District Center for Disease Control and Prevention, Shenzhen, People's Republic of China.
Wei YangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Shiman ChenShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Yun PengShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Xiaowen LiangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Shengjie ZhangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Fangfang ChangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Yuanlong LinShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Mingxia ZhangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Yingxia LiuShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Baisheng LiPublic Health, Southern Medical University, BSL-3 Laboratory (Guangdong), Guangdong Provincial Key Laboratory of Tropical Disease Research, Guangzhou, People's Republic of China.
Fuxiang WangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.
Yang YangShenzhen Key Laboratory of Pathogen and Immunity, Shenzhen Third People's Hospital, Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global emergence of monkeypox virus (MPXV) clade IIb since 2022, together with the recent spread of clade Ib, underscores the continuing public health threat posed by MPXV. Clinical and epidemiological observations suggest that clade Ib infection may differ from clade IIb infection, but the biological basis of these differences remains insufficiently defined. In this study, we established an intranasal BALB/c mouse model of MPXV clade Ib infection and compared its pathogenicity with that of clade IIb. Clade Ib caused lethal disease at an inoculation dose approximately ten-fold lower than that required for clade IIb. Compared with clade IIb, clade Ib infection showed faster disease progression, higher pulmonary viral burden at later stages of infection, and more severe lung pathology. Single-cell transcriptome and cytokine response analyses further uncovered clade-specific differences in pulmonary immune cell landscapes, the distribution of MPXV-positive cells, and the expression patterns of key inflammatory mediators at specific time points. Antiviral evaluation showed that tecovirimat and cidofovir were active against both clades, although a higher dose of cidofovir was required to achieve protection in the clade Ib infection model. Together, these findings establish a susceptible BALB/c mouse model for MPXV clade Ib and provide experimental evidence for clade-dependent differences in MPXV pathogenicity and antiviral treatment outcomes.

Indexed as

Antiviral AgentsMonkeypox virusMpox, MonkeypoxAnimalsCytokinesDisease Models, AnimalFemaleLungMiceMice, Inbred BALB CTreatment OutcomeViral LoadAntiviral AgentsCytokinesantiviral efficacyBALB/c mouse modelClade IbMPXVpathogenesis

Identifiers

PMID42748357
PMCPMC13587567

What Socratic 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 Socratic graph.