Evidence map›Paper›PMID 31848275›Full record

ArticlemBio2019

Tryptophan Metabolism Activates Aryl Hydrocarbon Receptor-Mediated Pathway To Promote HIV-1 Infection and Reactivation.

Yan-Heng Zhou, Li Sun, Jun Chen, Wei-Wei Sun, Li Ma, Yang Han, Xia Jin, Qing-Xia Zhao, Taisheng Li, Hongzhou Lu and 2 more

Open access · goldAbstract read
In one paragraph

Article in mBio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

34 citing papers in PubMed, 49 citations in OpenAlex.

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  11. Article
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  13. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
    Review
  14. Article
  15. Article
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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

12 authors at 4 institutions in 1 country.

Yan-Heng ZhouThe Joint Center for Infection and Immunity between Guangzhou Institute of Pediatrics, Guangzhou Women and Children`s Medical Center, Guangzhou, China, and Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China.
Li SunCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Jun ChenDepartment of Infections and Immunity, Shanghai Public Health Clinical Center, Shanghai, China.
Wei-Wei SunCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Li MaCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Yang HanDepartment of Infectious Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Xia JinCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
Qing-Xia ZhaoDepartment of Infection, Zhengzhou Sixth People's Hospital, Zhengzhou, China.
Taisheng LiDepartment of Infectious Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China.
Hongzhou LuDepartment of Infections and Immunity, Shanghai Public Health Clinical Center, Shanghai, China.
Xiu QiuThe Joint Center for Infection and Immunity between Guangzhou Institute of Pediatrics, Guangzhou Women and Children`s Medical Center, Guangzhou, China, and Institut Pasteur of Shanghai, Chinese Academy of Sciences (CAS), Shanghai, China qiu.xiu@bigcs.org jh_wang@sibs.ac.cn.
Jian-Hua WangCAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China qiu.xiu@bigcs.org jh_wang@sibs.ac.cn.
Institut Pasteur of Shanghai · CNPeking Union Medical College Hospital · CNShanghai Public Health Clinical Center · CNThe Sixth People's Hospital of Zhengzhou · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple cellular metabolic pathways are altered by HIV-1 infection, with an impact on immune activation, inflammation, and acquisition of non-AIDS comorbid diseases. The dysfunction of tryptophan (Trp) metabolism has been observed clinically in association with accelerated HIV-1 pathogenesis, but the underlying mechanism remains unknown. In this study, we demonstrated that the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, is activated by Trp metabolites to promote HIV-1 infection and reactivation. AHR directly binds to the HIV-1 5' long terminal repeat (5'-LTR) at the molecular level to activate viral transcription and infection, and AHR activation by Trp metabolites increases its nuclear translocation and association with the HIV 5'-LTR; moreover, the binding of AHR with HIV-1 Tat facilitates the recruitment of positive transcription factors to viral promoters. These findings not only elucidate a previously unappreciated mechanism through which cellular Trp metabolites affect HIV pathogenesis but also suggest that a downstream target AHR may be a potential target for modulating HIV-1 infection.

Indexed as

Host-Pathogen InteractionsSignal TransductionVirus ActivationAntiretroviral Therapy, Highly ActiveCD4 Lymphocyte CountGene Expression Regulation, ViralHIV-1HIV InfectionsHIV Long Terminal RepeatHumansModels, BiologicalReceptors, Aryl Hydrocarbontat Gene Products, Human Immunodeficiency VirusTranscriptional ActivationTryptophanViral LoadReceptors, Aryl Hydrocarbontat Gene Products, Human Immunodeficiency VirusTryptophanaryl hydrocarbon receptorHIV-1transcriptiontryptophan metabolite

Identifiers

PMID31848275
PMCPMC6918076
OpenAlexW2995180378

What OpenQuestion holds

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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.