Evidence map›Paper›PMID 40373067›Full record

ArticlePLoS pathogens2025

PINLYP-mediated phospholipid metabolism reprogramming contributes to chronic herpesvirus infection.

Zhangmengxue Lei, Wendi Wei, Mingyu Wang, Yun Xu, Lei Bai, Ying Gao, Congwei Jiang, Fangxia Li, Na Tian, Linlin Kuang and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

15 authors.

Zhangmengxue LeiUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Wendi WeiUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Mingyu WangUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Yun XuUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Lei BaiState Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, China.
Ying GaoUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Congwei JiangUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Fangxia LiUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Na TianUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Linlin KuangUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Ruiliang ZhuUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Gang PangUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Ke LanState Key Laboratory of Virology, Modern Virology Research Center, College of Life Sciences, Wuhan University, Wuhan, China.
Suihan FengUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.
Xiaozhen LiangUniversity of Chinese Academy of Sciences, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-2460-0532

Funding

National Key Research and Development Program of ChinaNatural Science Foundation of ChinaShanghai Municipal Science and Technology Major Project
6 · The paper itself

Abstract

Many viruses alter the phospholipid metabolism to benefit their own life cycles. It is unclear whether the host or the virus is driving phospholipid metabolism reprogramming, and how virus infections are affected by the metabolic status. Here we report that phospholipase A2 inhibitor and LY6/PLAUR domain-containing protein (PINLYP) inhibits Kaposi's sarcoma-associated herpesvirus (KSHV) lytic reactivation by remodeling phospholipid metabolism and especially triacylglycerol (TAG) biosynthesis. PINLYP deficiency led to increased phospholipase cPLA2α activity, cPLA2α-mediated AKT phosphorylation, and KSHV lytic reactivation. Analyses of RNA-seq and lipidomics reveal that PINLYP regulates long-chain fatty acid CoA ligase ACSL5 expression and TAG production. The inhibition of ACSL5 activity or TAG biosynthesis suppresses AKT phosphorylation and KSHV lytic reactivation, restoring the phenotype of PINLYP deficiency. This finding underscores the pivotal role of PINLYP in remodeling phospholipid metabolism and promoting viral latency, which sheds new light on how phospholipid metabolism is regulated by herpesvirus and provides a potential target for controlling chronic herpesvirus infection.

Indexed as

Herpesviridae InfectionsHerpesvirus 8, HumanPhospholipidsHumansMetabolic ReprogrammingVirus ActivationVirus LatencyPhospholipids

Identifiers

PMID40373067
PMCPMC12080810

What OpenQuestion holds

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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.