Neuron-associated retroelement-derived protein Arc/Arg3.1 assists in the early stages of alphaherpesvirus infection in human neuronal cells
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View abstract on PubMed
Summary
This summary is machine-generated.Pseudorabies virus (PRV) and herpes simplex virus type 1 (HSV-1) infection upregulate Arc expression. Viral proteins ICP0 and VP5 interact with Arc, impacting the viral lifecycle and neurotropic disease pathogenesis.
Area Of Science
- Neurovirology
- Molecular Biology
- Genetics
Background
- Alphaherpesviruses like HSV-1 and PRV are neurotropic DNA viruses that manipulate host factors for propagation.
- Arc/Arg3.1 (Arc), a domesticated gene from retroelements, is implicated in neuronal plasticity and neurological disorders.
- The mechanisms by which alphaherpesviruses upregulate Arc and its role in infection are not fully understood.
Purpose Of The Study
- To investigate the mechanisms by which PRV and HSV-1 upregulate Arc expression.
- To identify viral factors involved in Arc regulation and interaction.
- To elucidate the role of Arc in the alphaherpesvirus lifecycle and pathogenesis.
Main Methods
- In vitro infection models using PRV.
- Identification of viral regulatory proteins (ICP0, EP0) and capsid protein (VP5).
- Mass spectrometry and co-immunoprecipitation assays.
- Arc knockdown experiments.
Main Results
- PRV infection upregulated Arc expression in vitro.
- HSV-1 and PRV ICP0 homologues (ICP0 and EP0) were identified as triggers for Arc upregulation.
- The major capsid protein VP5 of PRV and HSV-1 was found to interact with Arc.
- Arc knockdown delayed early viral infection stages but did not affect viral attachment or entry.
Conclusions
- Alphaherpesvirus ICP0 homologues regulate Arc expression.
- Arc interacts with the major capsid protein VP5 and plays a role post-entry in the viral lifecycle.
- This study provides insights into herpesvirus-Arc interactions, domesticated gene pathogenesis, and herpesvirus-induced neurological diseases.
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