Evidence map›Paper›PMID 35468896›Full record

ArticleSignal transduction and targeted therapy2022

Modulation of innate immune response to viruses including SARS-CoV-2 by progesterone.

Shan Su, Duo Hua, Jin-Peng Li, Xia-Nan Zhang, Lei Bai, Li-Bo Cao, Yi Guo, Ming Zhang, Jia-Zhen Dong, Xiao-Wei Liang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Shan Su *Department of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Duo Hua *Department of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Jin-Peng Li *Department of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Xia-Nan ZhangState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430071, China.
Lei BaiState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430071, China.
Li-Bo CaoDepartment of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Yi GuoState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430071, China.
Ming ZhangDepartment of Thyroid and Breast Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Jia-Zhen DongState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430071, China.
Xiao-Wei LiangState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430071, China.
Ke LanDepartment of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.ORCID 0000-0002-0384-8598
Ming-Ming HuDepartment of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China. mmhu@whu.edu.cn.
Hong-Bing ShuDepartment of Infectious Diseases, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China. shuh@whu.edu.cn.ORCID 0000-0001-9102-3272
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whether and how innate antiviral response is regulated by humoral metabolism remains enigmatic. We show that viral infection induces progesterone via the hypothalamic-pituitary-adrenal axis in mice. Progesterone induces downstream antiviral genes and promotes innate antiviral response in cells and mice, whereas knockout of the progesterone receptor PGR has opposite effects. Mechanistically, stimulation of PGR by progesterone activates the tyrosine kinase SRC, which phosphorylates the transcriptional factor IRF3 at Y107, leading to its activation and induction of antiviral genes. SARS-CoV-2-infected patients have increased progesterone levels, and which are co-related with decreased severity of COVID-19. Our findings reveal how progesterone modulates host innate antiviral response, and point to progesterone as a potential immunomodulatory reagent for infectious and inflammatory diseases.

Indexed as

COVID-19SARS-CoV-2AnimalsAntiviral AgentsHumansHypothalamo-Hypophyseal SystemImmunity, InnateMicePituitary-Adrenal SystemProgesteroneAntiviral AgentsProgesterone

Identifiers

PMID35468896
PMCPMC9035769
OpenAlexW4224313694

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.