Neuroendocrine-mediated alteration of CD8+ T cell and microglia immune function during the development of stress-induced herpes simplex virus type-1 (HSV-1) encephalitis

2006 ◽  
Vol 20 (3) ◽  
pp. 50
Author(s):  
Aji Nair ◽  
John Hunzeker ◽  
Robert H. Bonneau
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Immune Function ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cd8 T Cell ◽  
Simplex Virus ◽  
Hsv 1

scholarly journals Psychological Stress Compromises CD8+T Cell Control of Latent Herpes Simplex Virus Type 1 Infections

2007 ◽  
Vol 179 (1) ◽  
pp. 322-328 ◽  
Author(s):  
Michael L. Freeman ◽  
Brian S. Sheridan ◽  
Robert H. Bonneau ◽  
Robert L. Hendricks
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Psychological Stress ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cd8 T Cell ◽  
Cell Control ◽  
Simplex Virus

scholarly journals T Cell Receptor–γ/δ Cells Protect Mice from Herpes Simplex Virus Type 1–induced Lethal Encephalitis

1997 ◽  
Vol 185 (11) ◽  
pp. 1969-1975 ◽  
Author(s):  
Roger Sciammas ◽  
P. Kodukula ◽  
Q. Tang ◽  
R.L. Hendricks ◽  
J.A. Bluestone
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
T Cell Receptor ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cell Receptor ◽  
Simplex Virus ◽  
Hsv 1

Increased numbers of T cell receptor (TCR)-γ/δ cells have been observed in animal models of influenza and sendai virus infections, as well as in patients infected with human immunodeficiency virus and herpes simplex virus type 1 (HSV-1). However, a direct role for TCR-γ/δ cells in protective immunity for pathogenic viral infection has not been demonstrated. To define the role of TCR-γ/δ cells in anti–HSV-1 immunity, TCR-α−/− mice treated with anti– TCR-γ/δ monoclonal antibodies or TCR-γ/δ × TCR-α/β double-deficient mice were infected with HSV-1 by footpad or ocular routes of infection. In both models of HSV-1 infection, TCR-γ/δ cells limited severe HSV-1–induced epithelial lesions and greatly reduced mortality by preventing the development of lethal viral encephalitis. The observed protection resulted from TCR-γ/δ cell–mediated arrest of both viral replication and neurovirulence. The demonstration that TCR-γ/δ cells play an important protective role in murine HSV-1 infections supports their potential contribution to the immune responses in human HSV-1 infection. Thus, this study demonstrates that TCR-γ/δ cells may play an important regulatory role in human HSV-1 infections.

scholarly journals In Vivo Ablation of CD11c-Positive Dendritic Cells Increases Susceptibility to Herpes Simplex Virus Type 1 Infection and Diminishes NK and T-Cell Responses

2006 ◽  
Vol 80 (8) ◽  
pp. 3985-3993 ◽  
Author(s):  
Sadik H. Kassim ◽  
Naveen K. Rajasagi ◽  
Xiangyi Zhao ◽  
Robert Chervenak ◽  
Stephen R. Jennings
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT The precise role of each of the seven individual CD11c+ dendritic cell subsets (DCs) identified to date in the response to viral infections is not known. DCs serve as critical links between the innate and adaptive immune responses against many pathogens, including herpes simplex virus type 1 (HSV-1). The role of DCs as mediators of resistance to HSV-1 infection was investigated using CD11c-diphtheria toxin (DT) receptor-green fluorescent protein transgenic mice, in which DCs can be transiently depleted in vivo by treatment with low doses of DT. We show that ablation of DCs led to enhanced susceptibility to HSV-1 infection in the highly resistant C57BL/6 mouse strain. Specifically, we showed that the depletion of DCs led to increased viral spread into the nervous system, resulting in an increased rate of morbidity and mortality. Furthermore, we showed that ablation of DCs impaired the optimal activation of NK cells and CD4+ and CD8+ T cells in response to HSV-1. These data demonstrated that DCs were essential not only in the optimal activation of the acquired T-cell response to HSV-1 but also that DCs were crucial for innate resistance to HSV-1 infection.

scholarly journals Upregulation of Multiple CD8+ T Cell Exhaustion Pathways Is Associated with Recurrent Ocular Herpes Simplex Virus Type 1 Infection

2020 ◽  
Vol 205 (2) ◽  
pp. 454-468
Author(s):  
Pierre-Grégoire Coulon ◽  
Soumyabrata Roy ◽  
Swayam Prakash ◽  
Ruchi Srivastava ◽  
Nisha Dhanushkodi ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cd8 T Cell ◽  
Cell Exhaustion ◽  
Ocular Herpes ◽  
Simplex Virus

scholarly journals Pharmacological Inhibition of IRE-1 Alpha Activity in Herpes Simplex Virus Type 1 and Type 2-Infected Dendritic Cells Enhances T Cell Activation

2022 ◽  
Vol 12 ◽  
Author(s):  
Eduardo I. Tognarelli ◽  
Angello Retamal-Díaz ◽  
Mónica A. Farías ◽  
Luisa F. Duarte ◽  
Tomás F. Palomino ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections are life-long and highly prevalent in the human population. These viruses persist in the host, eliciting either symptomatic or asymptomatic infections that may occur sporadically or in a recurrent manner through viral reactivations. Clinical manifestations due to symptomatic infection may be mild such as orofacial lesions, but may also translate into more severe diseases, such as ocular infections that may lead to blindness and life-threatening encephalitis. A key feature of herpes simplex viruses (HSVs) is that they have evolved molecular determinants that hamper numerous components of the host’s antiviral innate and adaptive immune system. Importantly, HSVs infect and negatively modulate the function of dendritic cells (DCs), by inhibiting their T cell-activating capacity and eliciting their apoptosis after infection. Previously, we reported that HSV-2 activates the splicing of the mRNA of XBP1, which is related to the activity of the unfolded protein response (UPR) factor Inositol-Requiring Enzyme 1 alpha (IRE-1α). Here, we sought to evaluate if the activation of the IRE-1α pathway in DCs upon HSV infection may be related to impaired DC function after infection with HSV-1 or HSV-2. Interestingly, the pharmacological inhibition of the endonuclease activity of IRE-1α in HSV-1- and HSV-2-infected DCs significantly reduced apoptosis in these cells and enhanced their capacity to migrate to lymph nodes and activate virus-specific CD4+ and CD8+ T cells. These findings suggest that the activation of the IRE-1α-dependent UPR pathway in HSV-infected DCs may play a significant role in the negative effects that these viruses exert over these cells and that the modulation of this signaling pathway may be relevant for enhancing the function of DCs upon infection with HSVs.

scholarly journals Cutting Edge: Priming of CD8 T Cell Immunity to Herpes Simplex Virus Type 1 Requires Cognate TLR3 Expression InVivo

2010 ◽  
Vol 184 (5) ◽  
pp. 2243-2246 ◽  
Author(s):  
Gayle M. Davey ◽  
Magdalena Wojtasiak ◽  
Anna I. Proietto ◽  
Francis R. Carbone ◽  
William R. Heath ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cd8 T Cell ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Simplex Virus

scholarly journals Interaction of ICP34.5 with Beclin 1 Modulates Herpes Simplex Virus Type 1 Pathogenesis through Control of CD4+ T-Cell Responses

2009 ◽  
Vol 83 (23) ◽  
pp. 12164-12171 ◽  
Author(s):  
David A. Leib ◽  
Diane E. Alexander ◽  
Douglas Cox ◽  
Jiyi Yin ◽  
Thomas A. Ferguson
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Antigen Presentation ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Beclin 1 ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT Autophagy is an important component of host innate and adaptive immunity to viruses. It is critical for the degradation of intracellular pathogens and for promoting antigen presentation. Herpes simplex virus type 1 (HSV-1) infection induces an autophagy response, but this response is antagonized by the HSV-1 neurovirulence gene product, ICP34.5. This is due, in part, to its interaction with the essential autophagy protein Beclin 1 (Atg6) via the Beclin-binding domain (BBD) of ICP34.5. Using a recombinant virus lacking the BBD, we examined pathogenesis and immune responses using mouse models of infection. The BBD-deficient virus (Δ68H) replicated equivalently to its marker-rescued counterpart (Δ68HR) at early times but was cleared more rapidly than Δ68HR from all tissues at late times following corneal infection. In addition, the infection of the cornea with Δ68H induced less ocular disease than Δ68HR. These results suggested that Δ68H was attenuated due to its failure to control adaptive rather than innate immunity. In support of this idea, Δ68H stimulated a significantly stronger CD4+ T-cell-mediated delayed-type hypersensitivity response and resulted in significantly more production of gamma interferon and interleukin-2 from HSV-specific CD4+ T cells than Δ68HR. Taken together, these data suggest a role for the BBD of ICP34.5 in precluding autophagy-mediated class II antigen presentation, thereby enhancing the virulence and pathogenesis of HSV-1.

Stepwise identification of HLA-A*0201-restricted CD8+ T-cell epitope peptides from herpes simplex virus type 1 genome boosted by a steprank scheme

Biopolymers ◽  
2010 ◽  
Vol 96 (3) ◽  
pp. 328-339 ◽  
Author(s):  
Jianjun Bi ◽  
Rengang Song ◽  
Huilan Yang ◽  
Bingling Li ◽  
Jianyong Fan ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Cell Epitope ◽  
Cd8 T Cell ◽  
T Cell Epitope ◽  
Simplex Virus

scholarly journals Medroxyprogesterone Acetate Inhibits CD8+T Cell Viral-Specific Effector Function and Induces Herpes Simplex Virus Type 1 Reactivation

2008 ◽  
Vol 181 (2) ◽  
pp. 969-975 ◽  
Author(s):  
Thomas L. Cherpes ◽  
James L. Busch ◽  
Brian S. Sheridan ◽  
Stephen A. K. Harvey ◽  
Robert L. Hendricks
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Medroxyprogesterone Acetate ◽  
Cd8 T Cell ◽  
Specific Effector ◽  
Simplex Virus
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