scholarly journals The Intrinsic Antiviral Defense to Incoming HSV-1 Genomes Includes Specific DNA Repair Proteins and Is Counteracted by the Viral Protein ICP0

2011 ◽  
Vol 7 (6) ◽  
pp. e1002084 ◽  
Author(s):  
Caroline E. Lilley ◽  
Mira S. Chaurushiya ◽  
Chris Boutell ◽  
Roger D. Everett ◽  
Matthew D. Weitzman
Keyword(s):  
Dna Repair ◽  
Viral Protein ◽  
Antiviral Defense ◽  
Dna Repair Proteins ◽  
Protein Icp0 ◽  
Hsv 1

scholarly journals HSV-1 triggers paracrine fibroblast growth factor response from cortical brain cells via immediate-early protein ICP0

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Niko Hensel ◽  
Verena Raker ◽  
Benjamin Förthmann ◽  
Nora Tula Detering ◽  
Sabrina Kubinski ◽  
...  
Keyword(s):  
Glial Cells ◽  
Viral Protein ◽  
Tissue Response ◽  
Automated Image Analysis ◽  
Host Cells ◽  
Fibroblast Growth ◽  
Early Protein ◽  
Cortical Cultures ◽  
Protein Icp0 ◽  
Hsv 1

Abstract Background Herpes simplex virus-1 (HSV-1) infections of the central nervous system (CNS) can result in HSV-1 encephalitis (HSE) which is characterized by severe brain damage and long-term disabilities. Different cell types including neurons and astrocytes become infected in the course of an HSE which leads to an activation of glial cells. Activated glial cells change their neurotrophic factor profile and modulate inflammation and repair. The superfamily of fibroblast growth factors (FGFs) is one of the largest family of neurotrophic factors comprising 22 ligands. FGFs induce pro-survival signaling in neurons and an anti-inflammatory answer in glial cells thereby providing a coordinated tissue response which favors repair over inflammation. Here, we hypothesize that FGF expression is altered in HSV-1-infected CNS cells. Method We employed primary murine cortical cultures comprising a mixed cell population of astrocytes, neurons, microglia, and oligodendrocytes. Astrocyte reactivity was morphometrically monitored by an automated image analysis algorithm as well as by analyses of A1/A2 marker expression. Altered FGF expression was detected by quantitative real-time PCR and its paracrine FGF activity. In addition, HSV-1 mutants were employed to characterize viral factors important for FGF responses of infected host cells. Results Astrocytes in HSV-1-infected cortical cultures were transiently activated and became hypertrophic and expressed both A1- and A2-markers. Consistently, a number of FGFs were transiently upregulated inducing paracrine neurotrophic signaling in neighboring cells. Most prominently, FGF-4, FGF-8, FGF-9, and FGF-15 became upregulated in a switch-on like mechanism. This effect was specific for CNS cells and for a fully functional HSV-1. Moreover, the viral protein ICP0 critically mediated the FGF switch-on mechanism. Conclusions HSV-1 uses the viral protein ICP0 for the induction of FGF-expression in CNS cells. Thus, we propose that HSV-1 triggers FGF activity in the CNS for a modulation of tissue response upon infection.

scholarly journals DNA repair proteins may differentiate papillary thyroid cancer from chronic lymphocytic thyroiditis and nodular colloidal goiter

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Bahri Evren ◽  
Sami Yılmaz ◽  
Neşe Karadağ ◽  
Ayşe Çıkım Sertkaya ◽  
Ömercan Topaloğlu ◽  
...  
Keyword(s):  
Dna Repair ◽  
Thyroid Cancer ◽  
Papillary Carcinoma ◽  
Staining Intensity ◽  
Follicular Cell ◽  
Papillary Thyroid ◽  
Chronic Thyroiditis ◽  
Dna Repair Proteins ◽  
The Difference ◽  
Repair Genes

AbstractMalignant thyroid lesions are the most common malignancy of the endocrine glands with increasing rates in the last two decades. Papillary thyroid cancer is the most common thyroid malignancy. In our study, we aimed to quantitatively evaluate the levels of DNA repair proteins MSH2, MLH1, MGMT, which are representative blocks of patients diagnosed with papillary carcinoma, chronic thyroiditis, or colloidal goiter. Total or subtotal thyroidectomy material of 90 patients diagnosed with papillary carcinoma, nodular colloidal goiter, or chronic thyroiditis between 2009 and 2012 were retrospectively evaluated. Tissue samples obtained from paraffin blocks were stained with MGMT, MSH2, MLH1 proteins and their immunohistochemistry was evaluated. Prepared sections were examined qualitatively by an impartial pathologist and a clinician, taking into account the staining method under the trinocular light microscope. Although there was no statistically significant difference in MGMT, MSH2, MLH1, follicular cell positivity, staining intensity, and immunoreactivity values, papillary carcinoma cases showed a higher rate of follicular cell positivity, and this difference was more pronounced between papillary carcinoma and colloidal goiter. In the MSH2 follicular cell positivity evaluation, the difference between chronic thyroiditis and colloidal goiter was significant (p = 0.023). The difference between chronic thyroiditis and colloidal goiter was significant in the MSH2 staining intensity evaluation (p = 0.001). The difference between chronic thyroiditis and colloidal goiter was significant in MLH1 immunoreactivity evaluation (p = 0.012). Papillary carcinoma cases were demonstrated by nuclear staining only for MSH2 and MLH1 proteins as opposed to hyperplastic nodules. The higher levels of expression of DNA repair genes in malignant tumors compared to benign tumors are attributed to the functional activation of DNA repair genes. Further studies are needed for DNA repair proteins to be a potential test in the development and progression of thyroid cancer.

scholarly journals Host DNA Repair Proteins in Response toPseudomonas aeruginosain Lung Epithelial Cells and in Mice

2010 ◽  
Vol 79 (1) ◽  
pp. 75-87 ◽  
Author(s):  
Min Wu ◽  
Huang Huang ◽  
Weidong Zhang ◽  
Shibichakravarthy Kannan ◽  
Andrew Weaver ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Repair ◽  
Epithelial Cells ◽  
Critical Role ◽  
Lung Epithelial Cells ◽  
Host Cells ◽  
Myeloperoxidase Activity ◽  
Gram Negative ◽  
Lung Epithelial ◽  
Dna Repair Proteins

ABSTRACTAlthough DNA repair proteins in bacteria are critical for pathogens' genome stability and for subverting the host defense, the role of host DNA repair proteins in response to bacterial infection is poorly defined. Here, we demonstrate, for the first time, that infection with the Gram-negative bacteriumPseudomonas aeruginosasignificantly altered the expression and enzymatic activity of 8-oxoguanine DNA glycosylase (OGG1) in lung epithelial cells. Downregulation of OGG1 by a small interfering RNA strategy resulted in severe DNA damage and cell death. In addition, acetylation of OGG1 is required for host responses to bacterial genotoxicity, as mutations of OGG1 acetylation sites increased Cockayne syndrome group B (CSB) protein expression. These results also indicate that CSB may be involved in DNA repair activity during infection. Furthermore, OGG1 knockout mice exhibited increased lung injury after infection withP. aeruginosa, as demonstrated by higher myeloperoxidase activity and lipid peroxidation. Together, our studies indicate thatP. aeruginosainfection induces significant DNA damage in host cells and that DNA repair proteins play a critical role in the host response toP. aeruginosainfection, serving as promising targets for the treatment of this condition and perhaps more broadly Gram-negative bacterial infections.

Imaging techniques used for the detection of 8-oxoguanine adducts and DNA repair proteins in cells and tissues

2001 ◽  
Vol 36 (9) ◽  
pp. 1483-1494 ◽  
Author(s):  
Rebecca L. Persinger ◽  
Robert Melamede ◽  
Ivan Bespalov ◽  
Susan Wallace ◽  
Douglas J. Taatjes ◽  
...  
Keyword(s):  
Dna Repair ◽  
Imaging Techniques ◽  
Dna Repair Proteins ◽  
In Cells

scholarly journals Herpes Simplex Virus-Type1 (HSV-1) Impairs DNA Repair in Cortical Neurons

2016 ◽  
Vol 8 ◽  
Author(s):  
Giovanna De Chiara ◽  
Mauro Racaniello ◽  
Cristiana Mollinari ◽  
Maria Elena Marcocci ◽  
Giorgia Aversa ◽  
...  
Keyword(s):  
Dna Repair ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cortical Neurons ◽  
Simplex Virus ◽  
Hsv 1

Interference by toxic metal compounds with isolated zinc finger DNA repair proteins

2000 ◽  
Vol 112-113 ◽  
pp. 227-231 ◽  
Author(s):  
Monika Asmuß ◽  
Leon H.F. Mullenders ◽  
Andrea Hartwig
Keyword(s):  
Dna Repair ◽  
Zinc Finger ◽  
Toxic Metal ◽  
Metal Compounds ◽  
Dna Repair Proteins
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