Evidence map›Paper›PMID 42671474›Full record

ReviewApoptosis : an international journal on programmed cell death2026

Cell death network regulation in HSV infection: immune evasion versus host defense.

Jingjing Zhang, Siping Kuang, Zhiyang He, Junjie Chen, Tian Xu, Junfeng Yang, Shuli Li, Juntao Ding, Zhenghai Ma, Beibei Zhang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 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

10 authors.

Jingjing Zhang *Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Siping Kuang *Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Zhiyang HeXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Junjie ChenXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Tian XuXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Junfeng YangXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Shuli LiXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Juntao DingXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Zhenghai MaXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
Beibei ZhangXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China. zhangbeibei2022@xju.edu.cn.ORCID https://orcid.org/0000-0002-7022-5403

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Herpes simplex virus type 1 (HSV-1) causes prevalent infections ranging from orolabial lesions to keratitis and encephalitis, with virus-host interplay around cell death pathways critically determining disease outcomes. This review systematically examines how HSV-1 dynamically manipulates programmed cell death processes-including apoptosis, pyroptosis, necroptosis, autophagy, and ferroptosis-through multiple viral proteins to evade immune clearance, facilitate replication, or maintain latency. Concurrently, host DNA sensors such as AIM2 and IFI16 activate inflammasomes and the PANoptosome to trigger coordinated cell death that restricts viral spread; imbalances in this bidirectional regulation exacerbate tissue damage in skin, cornea, and central nervous system, driving neuroinflammation and blood-brain barrier disruption. Elucidating these mechanisms not only uncovers novel principles of HSV-1 pathogenesis and immune evasion but also informs antiviral therapies and the rational design of oncolytic HSV-1 vectors.

Indexed as

ApoptosisCell DeathHerpes SimplexHerpesvirus 1, HumanHost-Pathogen InteractionsImmune EvasionAnimalsAutophagyHumansInflammasomesNecroptosisPyroptosisInflammasomesApoptosisAutophagyCell deathHSVImmune evasionNecroptosisPyroptosisTherapeutic target

Identifiers

PMID42671474

What Socratic holds

Textmetadata
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.