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Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.

ABSTRACT: To determine changes in host gene expression in HSV-1 latent trigeminal ganglia (TG) after hyperthermic stress.Scarified corneas of 6-week-old female BALB/c mice were inoculated with either HSV-1 17Syn(+) (high phenotypic reactivator) or 17DeltaPst(LAT(-)) (low phenotypic reactivator) at 10(4) plaque-forming units/eye. At 28 days after infection, viral reactivation was induced in some of the infected mice with hyperthermic stress, and the mice were killed after 1 hour. Heat-treated uninfected mice served as the control. Labeled cRNA derived from TG-isolated total RNA was hybridized to 430 2.0 chips containing 14,000 mouse genes. Gene expression was confirmed by quantitative real-time PCR.There was no difference in gene expression in the non-heat-treated mice. Gene expression in the TG of each of the heat-treated mouse groups (17Syn(+), 17DeltaPst(LAT(-)) and uninfected) yielded upregulation of more than twofold of a group of the same genes, designated as heat stress-induced gene expression. Twenty-nine genes (0.2%) were significantly upregulated (2- to 17-fold) when the heat stress-induced gene expression was subtracted from the gene expression of 17Syn(+) latent TG relative to 17DeltaPst(LAT(-)) latent TG 1 hour after mouse hyperthermic stress. Nine host adaptive immunity genes comprising Ig molecules, CD83, CD8A, ADA, and CCL8 were the largest subset upregulated, and all were confirmed by real-time PCR. Others identified included genes involved in hypothalamic-pituitary gland functions.Hyperthermic stress-induced reactivation of the HSV-1 high phenotypic reactivator can upregulate gene expression involved in B-cell function and in T-cell function. CD83 is implicated in HSV-1 latency, suggesting it could also be involved in immune-mediated mechanisms of viral reactivation.

SUBMITTER: Clement C

PROVIDER: S-EPMC2702237 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature

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Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.

Clement Christian C Bhattacharjee Partha S PS Kaufman Herbert E HE Hill James M JM

Investigative ophthalmology & visual science 20090117 6

<h4>Purpose</h4>To determine changes in host gene expression in HSV-1 latent trigeminal ganglia (TG) after hyperthermic stress.<h4>Methods</h4>Scarified corneas of 6-week-old female BALB/c mice were inoculated with either HSV-1 17Syn(+) (high phenotypic reactivator) or 17DeltaPst(LAT(-)) (low phenotypic reactivator) at 10(4) plaque-forming units/eye. At 28 days after infection, viral reactivation was induced in some of the infected mice with hyperthermic stress, and the mice were killed after 1 ...[more]

PMID: 19151393

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Project description:Major human pathologies are caused by nuclear replicative viruses establishing life-long latent infection in their host. During latency the genomes of these viruses are intimately interacting with the cell nucleus environment. A hallmark of herpes simplex virus type 1 (HSV-1) latency establishment is the shutdown of lytic genes expression and the concomitant induction of the latency associated (LAT) transcripts. Although the setting up and the maintenance of the latent genetic program is most likely dependent on a subtle interplay between viral and nuclear factors, this remains uninvestigated. Combining the use of in situ fluorescent-based approaches and high-resolution microscopic analysis, we show that HSV-1 genomes adopt specific nuclear patterns in sensory neurons of latently infected mice (28 days post-inoculation, d.p.i.). Latent HSV-1 genomes display two major patterns, called "Single" and "Multiple", which associate with centromeres, and with promyelocytic leukemia nuclear bodies (PML-NBs) as viral DNA-containing PML-NBs (DCP-NBs). 3D-image reconstruction of DCP-NBs shows that PML forms a shell around viral genomes and associated Daxx and ATRX, two PML partners within PML-NBs. During latency establishment (6 d.p.i.), infected mouse TGs display, at the level of the whole TG and in individual cells, a substantial increase of PML amount consistent with the interferon-mediated antiviral role of PML. "Single" and "Multiple" patterns are reminiscent of low and high-viral genome copy-containing neurons. We show that LAT expression is significantly favored within the "Multiple" pattern, which underlines a heterogeneity of LAT expression dependent on the viral genome copy number, pattern acquisition, and association with nuclear domains. Infection of PML-knockout mice demonstrates that PML/PML-NBs are involved in virus nuclear pattern acquisition, and negatively regulate the expression of the LAT. This study demonstrates that nuclear domains including PML-NBs and centromeres are functionally involved in the control of HSV-1 latency, and represent a key level of host/virus interaction.

Dataset Information

Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.

Publications

Heat-induced reactivation of HSV-1 in latent mice: upregulation in the TG of CD83 and other immune response genes and their LAT-ICP0 locus.

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