BibTex format
@article{Nash:2026:10.1126/sciadv.aei1796,
author = {Nash, DA and Barrow, HG and Antrobus, PR and Nicholson, AS and Suberu, J and Johnston, HE and Potts, M and Almeida, MA and Lulla, V and Crump, CM and Enright, AJ and Weekes, MP and Deane, JE and Graham, SC},
doi = {10.1126/sciadv.aei1796},
journal = {Sci Adv},
title = {Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.},
url = {http://dx.doi.org/10.1126/sciadv.aei1796},
volume = {12},
year = {2026}
}
RIS format (EndNote, RefMan)
TY - JOUR
AB - Herpes simplex virus 1 (HSV-1) infections of the central nervous system cause encephalitis and are associated with increased risk of neurodegeneration, yet the molecular consequences of lytic infection in human neurons remain incompletely defined. We map the transcriptomic, proteomic, and surface-proteome changes induced by HSV-1 across the lytic infection cycle in human induced pluripotent stem cell-derived cortical glutamatergic neurons. HSV-1 drives extensive plasma-membrane remodeling, including the removal of voltage-gated sodium, potassium, and calcium channels, resulting in a profound loss of synchronous calcium signaling. We identify the viral ubiquitin-ligase adaptor pUL56 as the principal effector of this process: pUL56-dependent degradation of ion channels abolishes coordinated calcium signaling, whereas mutation of its E3-ligase-binding motifs preserves synchrony. Furthermore, expression of pUL56 alone is sufficient to abolish neuronal electrical activity. These findings establish pUL56 as a potent viral suppressor of neuronal excitability.
AU - Nash,DA
AU - Barrow,HG
AU - Antrobus,PR
AU - Nicholson,AS
AU - Suberu,J
AU - Johnston,HE
AU - Potts,M
AU - Almeida,MA
AU - Lulla,V
AU - Crump,CM
AU - Enright,AJ
AU - Weekes,MP
AU - Deane,JE
AU - Graham,SC
DO - 10.1126/sciadv.aei1796
PY - 2026///
TI - Herpes simplex virus pUL56 abolishes neuronal activity by removing voltage-gated ion channels from the plasma membrane.
T2 - Sci Adv
UR - http://dx.doi.org/10.1126/sciadv.aei1796
UR - https://www.ncbi.nlm.nih.gov/pubmed/42842648
VL - 12
ER -