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Glutamine supplementation suppresses herpes simplex virus reactivation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE95716 | GEO | 2017/08/30

SECONDARY ACCESSION(S): PRJNA378202

REPOSITORIES: GEO

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Glutamine supplementation suppresses herpes simplex virus reactivation.

Project description:Chronic viral infections are difficult to treat, and new approaches are needed, particularly those aimed at reducing reactivation by enhancing immune responses. Herpes simplex virus (HSV) establishes latency and reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and proliferation of activated T cells requires increased metabolism of glutamine. Here, we found that supplementation with oral glutamine reduced virus reactivation in latently HSV-1-infected mice and HSV-2-infected guinea pigs. Transcriptome analysis of trigeminal ganglia from latently HSV-1-infected, glutamine-treated WT mice showed upregulation of several IFN-γ-inducible genes. In contrast to WT mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in latently HSV-1-infected IFN-γ-KO mice. Mice treated with glutamine also had higher numbers of HSV-specific IFN-γ-producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.

| S-EPMC5490748 | biostudies-literature

Glutamine supplementation suppresses herpes simplex virus reactivation III

Project description:Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)-γ inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN-γ knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN-γ producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN-γ-associated immune response and reduce the rate of reactivation of latent virus infection.

2017-08-30 | GSE95715 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation II

2017-08-30 | GSE95714 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation I

2017-08-30 | GSE95713 | GEO

Glutamine supplementation suppresses herpes simplex virus reactivation

Project description:Glutamine supplementation suppresses herpes simplex virus reactivation

| PRJNA378202 | ENA

Induced pluripotent stem cell derived neuronal lineages as human cellular models for Herpes Simplex Virus, type 1 (HSV-1) infections

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-05-02 | E-GEOD-46043 | biostudies-arrayexpress

Activation of alpha7 nicotinic receptor regulates herpes simplex virus infection in the central nervous system.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-06-24 | GSE252931 | GEO

Identification of herpes simplex virus 1 and host targets of miR-138 by combined RNAseq/PARCLIP

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-04-27 | GSE127504 | GEO

Gene expression in human recurrent glioblastoma before and after inoculation with the oncolytic herpes simplex virus G207

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-31 | GSE164105 | GEO

Herpes simplex virus suppresses necroptosis in human cells.

Project description:Herpes simplex virus (HSV)-1 and HSV-2 are significant human pathogens causing recurrent disease. During infection, HSV modulates cell death pathways using the large subunit (R1) of ribonucleotide reductase (RR) to suppress apoptosis by binding to and blocking caspase-8. Here, we demonstrate that HSV-1 and HSV-2 R1 proteins (ICP6 and ICP10, respectively) also prevent necroptosis in human cells by inhibiting the interaction between receptor-interacting protein kinase 1 (RIP1) and RIP3, a key step in tumor necrosis factor (TNF)-induced necroptosis. We show that suppression of this cell death pathway requires an N-terminal RIP homotypic interaction motif (RHIM) within R1, acting in concert with the caspase-8-binding domain, which unleashes necroptosis independent of RHIM function. Thus, necroptosis is a human host defense pathway against two important viral pathogens that naturally subvert multiple death pathways via a single evolutionarily conserved gene product.

| S-EPMC4382104 | biostudies-literature

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