Evidence map›Paper›PMID 40832295›Full record

ArticlebioRxiv : the preprint server for biology2025

HSV-1 infection induces brain cofilin hyperphosphorylation in the 5×FAD Alzheimer's Disease mouse model.

Laia Gharavi-Naeini, Zhenfeng Shu, Farhang Alem, Shu Feng, Linda D Chilin, Pinghui Feng, Yuntao Wu

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

7 authors.

Laia Gharavi-NaeiniGeorge Mason University, Center for Infectious Disease Research, School of Systems Biology, Manassas, VA.
Zhenfeng ShuSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Farhang AlemGeorge Mason University, Center for Infectious Disease Research, School of Systems Biology, Manassas, VA.
Shu FengSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Linda D ChilinGeorge Mason University, Center for Infectious Disease Research, School of Systems Biology, Manassas, VA.
Pinghui FengSection of Infection and Immunity, Herman Ostrow School of Dentistry, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA.
Yuntao WuGeorge Mason University, Center for Infectious Disease Research, School of Systems Biology, Manassas, VA.

Funding

Mechanisms of PSGL-1 restriction of HIV virion infectivityR01AI148012 · NIAID · GEORGE MASON UNIVERSITY · PI YUNTAO WU · 2020 to 2026
$5.0M
Explore roles of HSV-1 in Alzheimer's disease using mouse modelsR01AG070904 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHEN, CASEY, FENG, PINGHUI · 2021 to 2025
$3.9M
Molecular Modeling of the DR domain of an HIV restriction factor PSGL-1R56AI183995 · NIAID · GEORGE MASON UNIVERSITY · PI JAFRI, MOHSIN SALEET, KLIMOV, DMITRI KONSTANTINOVICH · 2024 to 2024
$760k
NIAID NIH HHS R01 AI148012NIAID NIH HHS R56 AI183995NIA NIH HHS R01 AG070904
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a degenerative neurological disease characterized by various biological signatures, including synaptic dysfunction, β-amyloid plaques, hyperphosphorylated Tau, cofilin-actin rods, and Hirano bodies, all of which are linked to the actin cytoskeleton and its regulators. Additionally, the presence of herpes simplex virus type 1 (HSV-1) in the brains of AD patients has long been suggested as a contributing factor for AD. However, mechanisms by which HSV-1 accelerates AD pathogenesis remain poorly understood. Here we report that HSV-1 infection induces hyperphosphorylation of cofilin in the brains of 5×FAD mice. Cofilin is an actin depolymerizing factor, and its S3 phosphorylation inactivates cofilin's activity to depolymerize actin filaments. These findings facilitate the understanding of impacts of HSV-1 infection on the development of Alzheimer's disease and have implications in AD therapeutics.

Indexed as

actinAlzheimer’s diseaseBiological SciencesCofilincofilin-actin rodsHSV-1LIM kinaseMicrobiologyβ-amyloid

Identifiers

PMID40832295
PMCPMC12363793

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.