Herpes Simplex Virus 2 Infection Impacts Stress Granule Accumulation

May 25, 2012Journal of virology

Herpes simplex virus 2 infection reduces stress-related cell structures

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Abstract

Stress granule (SG) accumulation does not occur in herpes simplex virus 2 (HSV-2)-infected cells.

Infection by HSV-2 interferes with the formation of SGs, which are typically induced by stress.
Despite increased phosphorylation of eIF2α, a key factor in stress response, SG accumulation is inhibited in HSV-2-infected cells.
Treatment with pateamine A allows SG accumulation in HSV-2-infected cells, indicating that HSV-2 alters typical stress response pathways.
SGs formed after pateamine A treatment contain G3BP and poly(A)-binding protein (PABP) but are mostly missing TIA-1.
Novel nuclear structures containing TIA-1 appear late in HSV-2 infection and associate with the protein Sam68.
These TIA-1 structures are absent in cells treated with viral DNA replication inhibitors, suggesting they are linked to late viral replication events.

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Interference with stress granule (SG) accumulation is gaining increased appreciation as a common strategy used by diverse viruses to facilitate their replication and to cope with translational arrest. Here, we examined the impact of infection by herpes simplex virus 2 (HSV-2) on SG accumulation by monitoring the localization of the SG components T cell internal antigen 1 (TIA-1), Ras-GTPase-activating SH3-domain-binding protein (G3BP), and poly(A)-binding protein (PABP). Our results indicate that SGs do not accumulate in HSV-2-infected cells and that HSV-2 can interfere with arsenite-induced SG accumulation early after infection. Surprisingly, SG accumulation was inhibited despite increased phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), implying that HSV-2 encodes previously unrecognized activities designed to maintain translation initiation downstream of eIF2α. SG accumulation was not inhibited in HSV-2-infected cells treated with pateamine A, an inducer that works independently of eIF2α phosphorylation. The SGs that accumulated following pateamine A treatment of infected cells contained G3BP and PABP but were largely devoid of TIA-1. We also identified novel nuclear structures containing TIA-1 that form late in infection. These structures contain the RNA binding protein 68-kDa Src-associated in mitosis (Sam68) and were noticeably absent in infected cells treated with inhibitors of viral DNA replication, suggesting that they arise as a result of late events in the virus replicative cycle.

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Herpes Simplex Virus 2 Infection Impacts Stress Granule Accumulation

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