Quantitative Temporal Viromics of HSV-1 infected i3Neurones

ABSTRACT: Herpes simplex virus (HSV)-1 invasion of the CNS can cause life-threatening herpes simplex encephalitis, the most common infectious encephalitis worldwide. The molecular consequences of lytic infection in CNS neurones are poorly understood, and many viral proteins remain functionally uncharacterised in this context. To investigate HSV-1 infection in human cortical neurones, a scalable induced pluripotent stem cell (i3 iPSC) system that generates human cortical glutamatergic neurones was used. Proteomic analysis in keratinocytes has previously identified proteins targeted for degradation by HSV-1 protein pUL56. Given the diversity of proteins present in neurones that are not found in keratinocytes, it was hypothesised that pUL56 and other viral proteins would have alternative functions in infected neurones. To determine changes in the abundance of neuronal proteins during HSV-1 infection, quantitative temporal viromics (QTV) was employed to describe changes in the proteome across a single replication cycle of HSV-1. This revealed changes to the microtubule architecture network and identified several new targets of pUL56, specifically PLCL2 and SCN2A.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cerebral Cortex Neuron, Cell Culture, Electrically Active Cell

SUBMITTER: Stephen Graham  

LAB HEAD: Stephen Charles Graham

PROVIDER: PXD076419 | Pride | 2026-10-16

REPOSITORIES: Pride