Evidence map›Paper›PMID 41974705›Full record

ArticleNature communications2026

Hydroxylation of the HIV-1 antisense protein promotes immune evasion of HIV-1 via modulation of TBK1.

Xinguang Lin, Wenrui Zhang, Manman Li, Chuanzhen Zhang, Jingna Xun, Wendong Han, Jun Chen, Yihua Zhang, Dapeng Yan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

9 authors.

Xinguang LinShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Wenrui ZhangShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Manman LiNingbo Research Institute, Fudan University, Ningbo, China.
Chuanzhen ZhangShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jingna XunShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Wendong HanBiosafety Level 3 Laboratory, Fudan University, Shanghai, China.
Jun ChenShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Yihua ZhangShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Dapeng YanShanghai Institute of Infectious Disease and Biosecurity, Department of Immunology, School of Basic Medical Sciences & Shanghai Public Health Clinical Center, Fudan University, Shanghai, China. dapengyan@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1977-8977

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32571090
6 · The paper itself

Abstract

HIV-1 evades host immunity via a number of virally encoded mediators. Here we show that the HIV-1 antisense protein (ASP) evades host immunity by interfering with the type I interferon (IFN-I) response. Mechanistically, host prolyl hydroxylase 3 (PHD3) hydroxylates ASP at Pro47, enabling the recruitment of the RING finger protein 114 (RNF114) to TANK-binding kinase 1 (TBK1). Subsequently, RNF114 mediates K6-linked ubiquitination of TBK1 at Lys236, suppressing TBK1 activation and the downstream IFN-I response. Conversely, mutation of ASP at Pro47 abolishes this inhibitory effect. In humanized mice, either ASP deletion or treatment with the RNF114 inhibitor EN219 or the PHD3 inhibitor Molidustat enhances antiviral immunity and reduces viral replication. Clinically, RNF114 and PHD3 transcript levels exhibit a positive correlation with viral load in treatment-naive patients. Here we show a distinct HIV-1 immune evasion mechanism involving proline hydroxylation and K6-linked ubiquitination, highlighting therapeutic potential.

Indexed as

HIV-1HIV InfectionsImmune EvasionProtein Serine-Threonine KinasesAnimalsHEK293 CellsHumansHydroxylationInterferon Type IMiceUbiquitinationUbiquitin-Protein LigasesVirus ReplicationInterferon Type IProtein Serine-Threonine KinasesTBK1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID41974705
PMCPMC13243506

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.