Evidence map›Paper›PMID 40974064›Full record

ArticleThe Journal of infectious diseases2025

Mycobacterium tuberculosis PE_PGRS62 Protein Inhibits Type I Interferon Responses to Promote HIV-2 Replication by Directly Interacting With Interferon Regulatory Factor 3.

Chaohu Pan, Hui Xu, Min Huang, Junyan He, Siqi Li, Xiaoyu Tao, Tingzhi Cao, Guoliang Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of infectious diseases, 2025. 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

8 authors.

Chaohu PanNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Hui XuNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Min HuangNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Junyan HeNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Siqi LiNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Xiaoyu TaoNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Tingzhi CaoNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.
Guoliang ZhangNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, China.ORCID 0000-0002-3617-5449

Funding

China Postdoctoral Science Foundation 2022M711485Guangdong Basic and Applied Basic Research Foundation 2025A1515010641Guangdong Science Fund for Distinguished Young Scholars 0620220214National Key Research and Development 2020YFA0907201National Natural Science Foundation of China 82370012National Natural Science Foundation of China 82400010Sanming Project of Medicine in Shenzhen SZZYSM202311009Shenzhen High-Level Hospital Construction FundShenzhen Medical Research Fund B2402040Shenzhen Scientific and Technological Foundation JCYJ20230807153559003Shenzhen Scientific and Technological Foundation JCYJ20240813152610014Shenzhen Scientific and Technological Foundation KCXFZ20211020163545004Shenzhen Scientific and Technological Foundation RCJC20221008092726022
6 · The paper itself

Abstract

Coinfection with Mycobacterium tuberculosis (Mtb) and human immunodeficiency virus type 2 (HIV-2) increased the viral load of HIV-2. Type I interferons (IFNs) are essential for limiting HIV-2 progression. However, it is unclear whether and how Mtb affects HIV-2 coinfection by regulating type I IFNs. Here Mtb PE_PGRS62 protein was identified as an inhibitor of stimulator of interferon genes (STING)-mediated type I IFN expression. Ectopic expression of PE_PGRS62 impaired type I IFN expression stimulated by cytosolic DNA, while knockout of pe_pgrs62 potentiated Mtb-induced type I IFN expression. PE_PGRS62 interacts directly with IFN regulatory factor (IRF) 3 and inhibits the interaction of IRF3 with TANK-binding kinase 1 (TBK1) as well as the binding of IRF3 to the IFNβ promoter. Furthermore, reduced HIV viral load was observed in pe_pgrs62 knockout Mtb-infected macrophages compared with wild-type Mtb. These findings reveal an important mechanism by which Mtb infection promotes HIV-2 immune evasion.

Indexed as

Bacterial ProteinsHIV-2HIV InfectionsInterferon Regulatory Factor-3Interferon Type IMycobacterium tuberculosisVirus ReplicationCoinfectionHumansMacrophagesMembrane ProteinsProtein Serine-Threonine KinasesTuberculosisViral LoadBacterial ProteinsInterferon Regulatory Factor-3Interferon Type IIRF3 protein, humanMembrane ProteinsProtein Serine-Threonine KinasesTBK1 protein, humanHIV-2IRF3Mycobacterium tuberculosisPE_PGRS62type I IFN

Identifiers

PMID40974064
PMCPMC12718032

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Registered trials

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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.