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Mucosal immune responses to microbes in genital tract
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
HSV-1 and HSV-2 enter the vaginal canal or the foreskin and first infect stratified squamous epithelial layers. HSV utilizes multiple cell-surface proteins for entry: heparan sulfate chains on cell-surface proteoglycans; a member of the tumor necrosis factor receptor family, herpesvirus entry mediator; and two members of the immunoglobulin superfamily related to the poliovirus receptor, nectin-1 and nectin-2. Primary replication in the keratinocytes results in the subsequent infection of sensory ganglia through nearby nerve endings. The de-enveloped virus migrates to the nerve cell body via retrograde axonal transport. Hiding in the ganglia, HSV establishes lifelong latent infection in the host. Immune suppression results in reactivation of the virus, causing lesions in the external genitalia. Notably, HSV virions are shed even in asymptomatic individuals, increasing the likelihood of transmission from carriers to uninfected partners.
Tea Polyphenolic Compounds against Herpes Simplex Viruses
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Tin-Chun Chu, Sandra D. Adams, Lee H. Lee
HSV infects epithelial cells during lytic infection and travels to sensory neurons in latent infections. Viruses stay in a dormant state within nerve cells during the latent infection until they are activated into the lytic cycle. This permits HSV to survive and replicate permanently for the HSV-infected patient (Kang et al. 2003). The lytic infection cycle of HSV begins when the virus attaches to, and then fuses with, a susceptible cell. Attachment and fusion take place when glycoproteins on the virus particle bind to suitable receptors on the plasma membrane of the host cell. Cell surface receptors bind specifically to the viral glycoproteins. Important HSV-1 glycoproteins (gs) extruding from the viral envelope include glycoproteins gB, gC, gD, gH, and gL, as well as gE, gI, and gK. Cell receptors to which these glycoproteins bind include heparan sulfate (HS), nectin-1, nectin-2, and herpesvirus entry mediator (HVEM). Although HS is found on many types of cells, nectin-1 and nectin-2 are found primarily at junctions of epithelial cells, as well as the synaptic junctions of neurons; HVEM is located on T lymphocytes and trabecular meshwork cells. The location of the receptors influences the tropism of HSV-1 and places a limit on the types of cells to which it can attach and thus infect (Akhtar and Shukla 2009; Garner 2003; O’Donnell et al. 2010).
Herpes Simplex Virus and Human CNS Infections
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Marcela Kúdelová, Július Rajčáni
In addition, the gD envelope gene, which is inevitable for adsorption to surface protein receptors, may be also important for the neural uptake; i.e., it may influence neurovirulence (Rajčáni et al. 1994). The latter assumption was confirmed by the finding that mice lacking the nectin receptor(s), the so-called herpesvirus entry mediator, are resistant to HSVE (Taylor et al. 2005; Kopp et al. 2009). Finally, an important factor for HSV neurovirulence is the protein ICP34.5, which may contribute to virion production and to cell-to-cell spread. In contrast to the wild-type virus, the ICP34.5 deletion mutants are neuroattenuated, though they can still replicate in the brain ependyma cells (Kesari et al. 1998). At in vitro experiments, the protein ICP34.5 redirects the interferon action, which is mediated by the increased activity of cellular RNA-dependent phosphokinase PKR pathway (Roizman and Knipe 2001).
Expression of herpesvirus entry mediator gene as a potential biomarker for disease severity in patients with persistent asthma
Published in Journal of Asthma, 2021
Yi Xiong, Binbin Li, Yidan Zhang, Fei Shi, Chen Qiu, Lingwei Wang, Jin Wang, Ying Le, Yujie Du, Can Yao, Sinian Li, Wenwen Liu, Dandan Chen, Mengjie Feng
In recent years, a newly discovered costimulatory molecule, herpesvirus entry mediator (HVEM), broadly expressed on immune cells including T cells, B cells, natural killer (NK) cells, polymorphonuclear cells (PMN), dendritic cells (DCs), and myeloid cells. Its biological ligand is the TNF superfamily member 14 (TNFSF14, also known as LIGHT), and the ligation by LIGHT provides a costimulatory signal for regulating T-cell activation. Previous studies have confirmed that HVEM plays an important role in the pathophysiology of asthma. Most of the effects of immunoregulation are mediated through HVEM-LIGHT signaling pathway, such as promoting pulmonary fibrosis (8,10,11), inducing inflammatory chemokine production, and developing airway remodeling (12,13). Based on these results, we suspect that HVEM expression is likely to be a relevant marker of airway inflammation and remodeling, further reflects the symptom severity of asthma. The aim of this work was to evaluate changes of HVEM expressions in patients with mild, moderate, and severe persistent asthma compared to healthy control subjects, and its association with disease severity in these patients.
Antibody-mediated delivery of LIGHT to the tumor boosts natural killer cells and delays tumor progression
Published in mAbs, 2021
Marco Stringhini, Jacqueline Mock, Vanessa Fontana, Patrizia Murer, Dario Neri
LIGHT, which is an acronym for Lymphotoxin-like, exhibits Inducible expression and competes with HSV Glycoprotein D for binding to Herpesvirus entry mediator, a receptor expressed on T lymphocytes, is a member of the tumor necrosis factor (TNF) superfamily expressed on a number of immune cells, including immature dendritic cells and activated T lymphocytes.18 The membrane-anchored form of LIGHT can be cleaved by proteases between residues L81 and I82, resulting in a functional soluble form.19 This cytokine binds to two receptors: Herpesvirus entry mediator (HVEM), which is expressed on T cells, NK cells and dendritic cells, and Lymphotoxin beta receptor (LTβR), which is expressed mainly on non-lymphoid cells.20 Upon homotrimerization and interaction with HVEM, LIGHT activates the NF-κB pathway leading to activation and stimulation of target lymphocytes, whereas signaling through LTβR leads to expression of chemokines and adhesion molecules involved in lymphoid organs organization and maintenance.18,21,22 Transgenic expression of LIGHT on tumor cells has been shown to mediate a potent anti-tumor effect in mice.19,23 In two independent studies, LIGHT expression resulted in a massive increase of CD8 + T cells infiltration, which played a central role in the tumor rejection process, as demonstrated by depletion experiments.19,23
Building on the anti-PD1/PD-L1 backbone: combination immunotherapy for cancer
Published in Expert Opinion on Investigational Drugs, 2019
Alvaro H Ingles Garces, Lewis Au, Robert Mason, Jennifer Thomas, James Larkin
The innate immune system plays an integral role in the immune-surveillance of tumor proliferation and migration. Many co-stimulatory receptors that belong to the TNF receptor family, including OX40, 41BB, CD27, and GITR are expressed on CD4 and CD8 T cells. Common features of these receptors are the downstream activation of nuclear factor kappa B, and c-Jun-N-terminal kinase signaling cascade signaling transcription factors that facilitate CD4 and CD8 T cell effector phenotype differentiation and survival. There is also interest in TNFR pathways as potential therapeutic targets including the Herpes virus entry mediator (HVEM).