The role of the immune system in establishment of herpes simplex virus latency ? studies using CD4+ T-cell depleted mice

1993 ◽  
Vol 133 (1-2) ◽  
pp. 179-187 ◽  
Author(s):  
Daniela Susi Schmidt ◽  
Anna Maria Eis-H�binger ◽  
K. E. Schneweis
Keyword(s):  
Herpes Simplex Virus ◽  
Immune System ◽  
Herpes Simplex ◽  
T Cell ◽  
Cd4 T Cell ◽  
Virus Latency ◽  
Simplex Virus

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 Herpes Simplex Virus-Induced Keratitis: Evaluation of the Role of Molecular Mimicry in Lesion Pathogenesis

2001 ◽  
Vol 75 (7) ◽  
pp. 3077-3088 ◽  
Author(s):  
Shilpa P. Deshpande ◽  
Sujin Lee ◽  
Mei Zheng ◽  
Byeongwoon Song ◽  
David Knipe ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Molecular Mimicry ◽  
T Cell Response ◽  
Activation Mechanism ◽  
Mouse Strains ◽  
Ocular Infection ◽  
Simplex Virus

ABSTRACT Viruses are suspected but usually unproven triggering factors in autoimmunity. One favored mechanism to explain the role of viruses in the genesis of autoimmunity is molecular mimicry. An immunoinflammatory blinding lesion called herpetic stromal keratitis (HSK) that follows ocular infection with herpes simplex virus (HSV) is suggested to result from a CD4+ T-cell response to a UL6 peptide of HSV that cross-reacts with a corneal autopeptide shared with the immunoglobulin G2ab (IgG2ab) isotype. The present report reevaluates the molecular mimicry hypothesis to explain HSK pathogenesis. Our results failed to reveal cross-reactivity between the UL6 and IgG2ab peptides or between peptide reactive T cells and HSV antigens. More importantly, animals infected with HSV failed to develop responses that reacted with either peptide, and infection with a recombinant vaccinia UL6 vector failed to cause HSK, in spite of generating UL6 reactivity. Other lines of evidence also failed to support the molecular mimicry hypothesis, such as the failure to affect HSK severity upon tolerization of susceptible BALB/c and B-cell-deficient mice with IgG2ab or UL6 peptides. An additional study system revealed that HSK could be induced in mouse strains, such as the OT2 × RAG1−/− mice (T cell receptor transgenic recognizing OVA323–339) that were unable to produce CD4+ T-cell responses to any detectable HSV antigens. Our results cast doubt on the molecular mimicry hypothesis as an explanation for the pathogenesis of HSK and indicate that if autoimmunity is involved its likely proceeds via a bystander activation mechanism.

Oncolytic therapy using a mutant type-1 herpes simplex virus and the role of the immune system

1999 ◽  
Vol 68 (5) ◽  
pp. 1756-1760 ◽  
Author(s):  
Eric S Lambright ◽  
David J Caparrelli ◽  
Abbas E Abbas ◽  
Takane Toyoizumi ◽  
George Coukos ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Immune System ◽  
Herpes Simplex ◽  
Mutant Type ◽  
Oncolytic Therapy ◽  
Simplex Virus

scholarly journals Peripheral Blood CD4 T-Cell and Plasmacytoid Dendritic Cell (pDC) Reactivity to Herpes Simplex Virus 2 and pDC Number Do Not Correlate with the Clinical or Virologic Severity of Recurrent Genital Herpes

2012 ◽  
Vol 86 (18) ◽  
pp. 9952-9963 ◽  
Author(s):  
Nicholas J. Moss ◽  
Amalia Magaret ◽  
Kerry J. Laing ◽  
Angela Shaulov Kask ◽  
Minna Wang ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Genital Herpes ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Functional Responses ◽  
Recurrent Genital Herpes ◽  
Cell Responses ◽  
Simplex Virus

Leukocytes participate in the immune control of herpes simplex virus (HSV). Data from HIV coinfections, germ line mutations, and case reports suggest involvement of CD4 T cells and plasmacytoid dendritic cells (pDC). We investigated the relationships between these cells and recurrent genital herpes disease severity in the general population. Circulating CD4 T-cell responses to HSV-2 were measured in specimens from 67 immunocompetent individuals with measured genital lesion and HSV shedding rates. Similarly, pDC number and functional responses to HSV-2 were analyzed in 40 persons. CD4 responses and pDC concentrations and responses ranged as much as 100-fold between persons while displaying moderate within-person consistency over time. No correlations were observed between these immune response parameters and genital HSV-2 severity. Cytomegalovirus (CMV) coinfection was not correlated with differences in HSV-2-specific CD4 T-cell responses. The CD4 T-cell response to HSV-2 was much more polyfunctional than was the response to CMV. These data suggest that other immune cell subsets with alternate phenotypes or anatomical locations may be responsible for genital herpes control in chronically infected individuals.

scholarly journals T Cell-Derived Lymphotoxin Is Essential for the Anti-Herpes Simplex Virus 1 Humoral Immune Response

2018 ◽  
Vol 92 (14) ◽  
Author(s):  
Kaiting Yang ◽  
Yong Liang ◽  
Zhichen Sun ◽  
Diyuan Xue ◽  
Hairong Xu ◽  
...  
Keyword(s):  
Immune Response ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Humoral Immune Response ◽  
Herpes Simplex Virus 1 ◽  
Humoral Immune ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTB cell-derived lymphotoxin (LT) is required for the development of follicular dendritic cell clusters for the formation of primary and secondary lymphoid follicles, but the role of T cell-derived LT in antibody response has not been well demonstrated. We observed that lymphotoxin β-receptor (LTβR) signaling is essential for optimal humoral immune response and protection against an acute herpes simplex virus 1 (HSV-1) infection. Blocking the LTβR pathway caused poor maintenance of germinal center B (GC-B) cells and follicular helper T (Tfh) cells. Using bone marrow chimeric mice and adoptive transplantation, we determined that T cell-derived LT played an indispensable role in the humoral immune response to HSV-1. Upregulation of gamma interferon by the LTβR-Ig blockade impairs the sustainability of Tfh-like cells, leading to an impaired humoral immune response. Our findings have identified a novel role of T cell-derived LT in the humoral immune response against HSV-1 infection.IMPORTANCEImmunocompromised people are susceptible to HSV-1 infection and lethal recurrence, which could be inhibited by anti-HSV-1 humoral immune response in the host. This study sought to explore the role of T cell-derived LT in the anti-HSV-1 humoral immune response using LT-LTβR signaling-deficient mice and the LTβR-Ig blockade. The data indicate that the T cell-derived LT may play an essential role in sustaining Tfh-like cells and ensure Tfh-like cells' migration into primary or secondary follicles for further maturation. This study provides insights for vaccine development against infectious diseases.

scholarly journals T Regulatory Cells Contribute to the Attenuated Primary CD8+and CD4+T Cell Responses to Herpes Simplex Virus Type 2 in Neonatal Mice

2008 ◽  
Vol 180 (3) ◽  
pp. 1556-1564 ◽  
Author(s):  
Marian A. Fernandez ◽  
Franz K. Puttur ◽  
Yuan M. Wang ◽  
Wade Howden ◽  
Stephen I. Alexander ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Herpes Simplex Virus Type ◽  
T Regulatory Cells ◽  
Cd4 T Cell ◽  
Regulatory Cells ◽  
Cell Responses ◽  
Simplex Virus

The Role of a Glycoprotein K (gK) CD8+T-Cell Epitope of Herpes Simplex Virus on Virus Replication and Pathogenicity

2009 ◽  
Vol 50 (6) ◽  
pp. 2903 ◽  
Author(s):  
Kevin R. Mott ◽  
Aziz A. Chentoufi ◽  
Dale Carpenter ◽  
Lbachir BenMohamed ◽  
Steven L. Wechsler ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Virus Replication ◽  
Cell Epitope ◽  
Cd8 T Cell ◽  
T Cell Epitope ◽  
Glycoprotein K ◽  
Simplex Virus

scholarly journals Role of CD28/CD80-86 and CD40/CD154 Costimulatory Interactions in Host Defense to Primary Herpes Simplex Virus Infection

2001 ◽  
Vol 75 (2) ◽  
pp. 612-621 ◽  
Author(s):  
Kurt H. Edelmann ◽  
Christopher B. Wilson
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
T Cell ◽  
Systemic Infection ◽  
T Cell Responses ◽  
Cd40 Ligand ◽  
Antiviral Immune Response ◽  
Cell Responses ◽  
Simplex Virus

ABSTRACT Dependence of the primary antiviral immune response on costimulatory interactions between CD28/CD80-86 and between CD40/CD154 (CD40 ligand) has been correlated with the extent of viral replication in two models of systemic infection, lymphocytic choriomeningitis virus and vesicular stomatitis virus. To determine the role of these costimulatory interactions in the context of an acute cytolytic, but locally replicating viral infection, herpes simplex virus (HSV) infection was assessed in mice that had the CD28/CD80-86 or CD40/CD154 interactions disrupted either genetically or with blocking reagents (CTLA4Ig and MR1, respectively). CTLA4Ig treatment greatly reduced paralysis-free survival during primary acute HSV infection. This reflected an almost total ablation of the anti-HSV CD4+ and CD8+ T-cell responses due to anergy and reduced cell numbers, respectively. Disruption of CD40/CD154 interactions impaired survival, but the effect was less severe than that observed in CTLA4Ig-treated mice, with reductions observed in the CD4+T-cell but not CD8+ T-cell responses. These two costimulatory pathways functioned in part independently, since disruption of both further impaired survival. The dependence on these costimulatory interactions for the control of primary HSV infection may represent a more widespread paradigm for nonsystemic viruses, which have restricted sites of replication and which employ immunoevasive measures.

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