Proteomics

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Interplay between nuclear tau phosphorylation and HSV-1 infection.

ABSTRACT: In this study, we investigated the effects of HSV-1 infection on tau phosphorylation in human brain cortical organoids. Our findings demonstrate that HSV-1 triggers nuclear accumulation of phosphorylated tau in neurons within the developing cortical plate as well as in neural precursor cells (NPCs) in the ventricular/subventricular-like zones of these differentiating cortical structures. Antiviral treatment effectively inhibited nuclear tau accumulation in both KOS- and 17syn+-infected organoids. Importantly, for the first time we provide evidence of a potential interaction of phosphorylated tau with HSV-1 genome. Furthermore, we ruled out the involvement of the Cyclin-dependent kinase 5 (Cdk5) in the nuclear phosphorylation of tau. Finally, we show that HSV-1 causes a significant alteration in the abundance of components of nuclear speckles and proteins known to be associated with neurodegenerative diseases.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Hipsc Cell

DISEASE(S): Neurodegenerative Disease

SUBMITTER: Matthew MacDonald  

LAB HEAD: Matthew L. MacDonald

PROVIDER: PXD047281 | Pride | 2025-05-06

REPOSITORIES: Pride

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Dino_Peptide_Norm.mzid.gz Mzid
MM000056.raw Raw
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Publications

Phosphorylated-tau associates with HSV-1 chromatin and correlates with nuclear speckles decondensation in low-density host chromatin regions.

D'Aiuto Leonardo L   Caldwell Jill K JK   Edwards Terri G TG   Zhou Chaoming C   McDonald Matthew L ML   Di Maio Roberto R   Joel Wood A WA   Hyde Vanesa R VR   Wallace Callen T CT   Watkins Simon C SC   Wesesky Maribeth A MA   Shemesh Or A OA   Nimgaonkar Vishwajit L VL   Bloom David C DC  

Neurobiology of disease 20250114

Abnormal tau phosphorylation is a key mechanism in neurodegenerative diseases. Evidence implicates infectious agents, such as Herpes Simplex Virus 1 (HSV-1), as co-factors in the onset or the progression of neurodegenerative diseases, including Alzheimer's disease. This has led to divergence in the field regarding the contribution of viruses in the etiology of neurodegenerative diseases. Research indicates that viruses may function as risk factors driving neurodegenerative disease rather than pl  ...[more]

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