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Results: 1 to 10 of 12

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Recent advances in the understanding of severe cutaneous adverse reactions.
Adler NR, Aung AK, Ergen EN, Trubiano J, Goh MSY, Phillips EJ
(2017) Br J Dermatol 177: 1234-1247
MeSH Terms: Allopurinol, Anticonvulsants, Carbamazepine, Cephalosporins, Dideoxynucleosides, Drug Eruptions, Drug Interactions, Herpesviridae Infections, Humans, Leukocytes, Mononuclear, Pharmacogenetics, Prospective Studies, Skin Tests, T-Lymphocytes, Virus Activation, Virus Latency, beta-Lactams
Show Abstract · Added March 30, 2020
Severe cutaneous adverse reactions (SCARs) encompass a heterogeneous group of delayed hypersensitivity reactions, which are most frequently caused by drugs. Our understanding of several aspects of SCAR syndromes has evolved considerably over the last decade. This review explores evolving knowledge of the immunopathogenic mechanisms, pharmacogenomic associations, in vivo and ex vivo diagnostics for causality assessment, and medication cross-reactivity data related to SCAR syndromes. Given the rarity and severity of these diseases, multidisciplinary collaboration through large international, national and/or multicentre networks to collect prospective data on patients with SCAR syndromes should be prioritized. This will further enhance a systematized framework for translating epidemiological, clinical and immunopathogenetic advances into preventive efforts and improved outcomes for patients.
© 2017 British Association of Dermatologists.
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Extensive CD4 and CD8 T Cell Cross-Reactivity between Alphaherpesviruses.
Jing L, Laing KJ, Dong L, Russell RM, Barlow RS, Haas JG, Ramchandani MS, Johnston C, Buus S, Redwood AJ, White KD, Mallal SA, Phillips EJ, Posavad CM, Wald A, Koelle DM
(2016) J Immunol 196: 2205-2218
MeSH Terms: Alphaherpesvirinae, Antigen Presentation, Antigens, Viral, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Cross Reactions, Cytokines, Epitopes, T-Lymphocyte, Herpesviridae Infections, Herpesvirus 1, Human, Herpesvirus 2, Human, Humans, Peptides, Receptors, Antigen, T-Cell, T-Lymphocyte Subsets, Viral Proteins
Show Abstract · Added March 30, 2020
The Alphaherpesvirinae subfamily includes HSV types 1 and 2 and the sequence-divergent pathogen varicella zoster virus (VZV). T cells, controlled by TCR and HLA molecules that tolerate limited epitope amino acid variation, might cross-react between these microbes. We show that memory PBMC expansion with either HSV or VZV enriches for CD4 T cell lines that recognize the other agent at the whole-virus, protein, and peptide levels, consistent with bidirectional cross-reactivity. HSV-specific CD4 T cells recovered from HSV-seronegative persons can be explained, in part, by such VZV cross-reactivity. HSV-1-reactive CD8 T cells also cross-react with VZV-infected cells, full-length VZV proteins, and VZV peptides, as well as kill VZV-infected dermal fibroblasts. Mono- and cross-reactive CD8 T cells use distinct TCRB CDR3 sequences. Cross-reactivity to VZV is reconstituted by cloning and expressing TCRA/TCRB receptors from T cells that are initially isolated using HSV reagents. Overall, we define 13 novel CD4 and CD8 HSV-VZV cross-reactive epitopes and strongly imply additional cross-reactive peptide sets. Viral proteins can harbor both CD4 and CD8 HSV/VZV cross-reactive epitopes. Quantitative estimates of HSV/VZV cross-reactivity for both CD4 and CD8 T cells vary from 10 to 50%. Based on these findings, we hypothesize that host herpesvirus immune history may influence the pathogenesis and clinical outcome of subsequent infections or vaccinations for related pathogens and that cross-reactive epitopes and TCRs may be useful for multi-alphaherpesvirus vaccine design and adoptive cellular therapy.
Copyright © 2016 by The American Association of Immunologists, Inc.
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Right place, right time: the evolving role of herpesvirus infection as a "second hit" in idiopathic pulmonary fibrosis.
Kropski JA, Lawson WE, Blackwell TS
(2012) Am J Physiol Lung Cell Mol Physiol 302: L441-4
MeSH Terms: Animals, Cytokines, Endoplasmic Reticulum Stress, Epithelial-Mesenchymal Transition, Herpesviridae Infections, Humans, Idiopathic Pulmonary Fibrosis, Inflammation, Lung, Respiratory Mucosa
Show Abstract · Added March 5, 2014
Over the course of the past decade, increasing evidence has implicated alveolar epithelial cell injury and dysfunction in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Genetic factors, cigarette smoking, and other environmental exposures have been identified as potential factors leading to a population of vulnerable alveolar epithelial cells. In addition, molecular techniques have demonstrated herpesviruses are commonly detectable in the lungs of patients with IPF, raising suspicion that, in the setting of a vulnerable alveolar epithelium, lytic (or latent) herpesvirus infection may act as a "second hit" leading to the development of pulmonary fibrosis. Intriguingly, in vivo modeling has shown that herpesvirus infection induces or worsens lung fibrosis when combined with immunodeficiency or other injurious stimuli. Here, we discuss potential mechanisms through which herpesvirus infection may contribute to the pathogenesis of IPF. Ultimately, antiviral therapy may hold promise for halting the progression of this deadly disease.
1 Communities
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10 MeSH Terms
Human herpesvirus-8 infection of primary pulmonary microvascular endothelial cells.
Bull TM, Meadows CA, Coldren CD, Moore M, Sotto-Santiago SM, Nana-Sinkam SP, Campbell TB, Geraci MW
(2008) Am J Respir Cell Mol Biol 39: 706-16
MeSH Terms: Apoptosis, Blood Vessels, Bone Morphogenetic Protein 4, Carrier Proteins, Caspase 3, Caspase 7, Cells, Cultured, Culture Media, Conditioned, Endothelial Cells, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Gene Expression Regulation, Herpesviridae Infections, Herpesvirus 8, Human, In Situ Nick-End Labeling, Interleukin-6, Oligonucleotide Array Sequence Analysis, Phenotype, Polymerase Chain Reaction, Reproducibility of Results
Show Abstract · Added November 17, 2011
Human herpesvirus-8 (HHV-8) is the causative agent of Kaposi's sarcoma and is associated with the angioproliferative disorders primary effusion lymphoma and multicentric Castleman's disease. Evidence of HHV-8 infection within the pulmonary vasculature of patients with idiopathic pulmonary arterial hypertension (IPAH) has been described. We hypothesize that HHV-8 infection of pulmonary microvascular endothelial cells results in an apoptotic-resistant phenotype characteristic of severe pulmonary arterial hypertension. Our objective was to investigate the ability of HHV-8 to infect human pulmonary microvascular endothelial cells in vitro and characterize the phenotypic effect of this infection. Human pulmonary microvascular endothelial cells were exposed to HHV-8 using two methods (direct virus and co-culture technique). The presence of lytic and latent infection was confirmed. Changes in endothelial cell gene and protein expression and effects on cellular apoptosis were measured. HHV-8 can both lytically and latently infect primary human pulmonary microvascular endothelial cells in vitro. HHV-8 infection results in significant changes in gene expression, including alterations of pathways important to cellular apoptosis. HHV-8 infection also alters expression of genes integral to the bone morphogenic protein pathway, including down-regulation of bone morphogenic protein-4. Other genes previously implicated in the development of PAH are affected by HHV-8 infection, and cells infected with HHV-8 are resistant to apoptosis.
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20 MeSH Terms
Endoplasmic reticulum stress in alveolar epithelial cells is prominent in IPF: association with altered surfactant protein processing and herpesvirus infection.
Lawson WE, Crossno PF, Polosukhin VV, Roldan J, Cheng DS, Lane KB, Blackwell TR, Xu C, Markin C, Ware LB, Miller GG, Loyd JE, Blackwell TS
(2008) Am J Physiol Lung Cell Mol Physiol 294: L1119-26
MeSH Terms: Antigens, Viral, Cells, Cultured, DNA-Binding Proteins, Endoplasmic Reticulum, Glycoproteins, Heat-Shock Proteins, Herpesviridae Infections, Humans, Immunohistochemistry, Molecular Chaperones, Nuclear Proteins, Protein Folding, Pulmonary Alveoli, Pulmonary Fibrosis, Pulmonary Surfactant-Associated Protein C, Regulatory Factor X Transcription Factors, Stress, Physiological, Transcription Factors, alpha-Mannosidase
Show Abstract · Added March 5, 2014
Recent evidence suggests that dysfunctional type II alveolar epithelial cells (AECs) contribute to the pathogenesis of idiopathic pulmonary fibrosis (IPF). Based on the hypothesis that disease-causing mutations in surfactant protein C (SFTPC) provide an important paradigm for studying IPF, we investigated a potential mechanism of AEC dysfunction suggested to result from mutant SFTPC expression: induction of endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). We evaluated biopsies from 23 IPF patients (including 3 family members with L188Q SFTPC mutations, 10 individuals with familial interstitial pneumonia without SFTPC mutations, and 10 individuals with sporadic IPF) and sections from 10 control lungs. After demonstrating UPR activation in cultured A549 cells expressing mutant SFTPC, we identified prominent expression of UPR markers in AECs in the lungs of patients with SFTPC mutation-associated fibrosis. In individuals with familial interstitial pneumonia without SFTPC mutations and patients with sporadic IPF, we also found UPR activation selectively in AECs lining areas of fibrotic remodeling. Because herpesviruses are found frequently in IPF lungs and can induce ER stress, we investigated expression of viral proteins in lung biopsies. Herpesvirus protein expression was found in AECs from 15/23 IPF patients and colocalized with UPR markers in AECs from these patients. ER stress and UPR activation are found in the alveolar epithelium in patients with IPF and could contribute to disease progression. Activation of these pathways may result from altered surfactant protein processing or chronic herpesvirus infection.
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19 MeSH Terms
Proteins of the secretory pathway govern virus productivity during lytic gammaherpesvirus infection.
Mages J, Freimüller K, Lang R, Hatzopoulos AK, Guggemoos S, Koszinowski UH, Adler H
(2008) J Cell Mol Med 12: 1974-89
MeSH Terms: Cell Line, Gammaherpesvirinae, Gene Expression Regulation, Viral, Herpesviridae Infections, Humans, Oligonucleotide Array Sequence Analysis, Proteins, RNA, Small Interfering, RNA, Viral, Secretory Pathway, Viral Proteins, Virus Physiological Phenomena, Virus Replication, Viruses
Show Abstract · Added November 18, 2010
BACKGROUND - Diseases caused by gammaherpesviruses continue to be a challenge for human health and antiviral treatment. Most of the commonly used antiviral drugs are directed against viral gene products. However, the emergence of drug-resistant mutations ma limit the effectiveness of these drugs. Since viruses require a host cell to propagate, the search for host cell targets is an interesting alternative.
METHODS - In this study, we infected three different cell types (fibroblasts, endothelial precursor cells and macrophages with a murine gammaherpesvirus and analysed the host cell response for changes either common to all or unique to a particular cell type using oligonucleotide microarrays.
RESULTS - The analysis revealed a number of genes whose transcription was significantly up- or down-regulated in either one or two of the cell types tested. After infection, only two genes, Lman1 (also known as ERGIC53) an synaptobrevin-like 1 (sybl1) were significantly up-regulated in all three cell types, suggestive for a general role for the virus life cycl independent of the cell type. Both proteins have been implicated in cellular exocytosis and transport of glycoproteins through the secretory pathway. To test the significance of the observed up-regulation, the functionality of these proteins was modulated, and the effect on virus replication was monitored. Inhibition of either Lman1 or sybl1 resulted in a significant reduction in virus production.
CONCLUSIONS - This suggests that proteins of the secretory pathway which appear to be rate limiting for virus production may represent new targets for intervention.
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14 MeSH Terms
Cytopathic herpesvirus infection in a green iguana (Iguana iguana).
Wilkinson M, Cline M, Jerome WG
(2005) J Zoo Wildl Med 36: 724-6
MeSH Terms: Animals, Hepatitis, Viral, Animal, Herpesviridae Infections, Iguanas, Inclusion Bodies, Viral, Male
Show Abstract · Added December 10, 2013
A juvenile male green iguana (Iguana iguana) died 5 days following movement to a room 3-5 degrees C cooler than its previous housing. Gross necropsy lesions were limited to thin body condition. Histologically the animal had multifocal, random, moderate to severe, acute hepatocellular necrosis with intranuclear inclusion bodies at the periphery of the necrotic areas. Electron microscopy of the liver revealed icosahedral viral particles approximately 110 nm in diameter, consistent with a herpesvirus infection. Characteristics of the herpesvirus are similar to those described for iguanid herpesvirus 1.
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6 MeSH Terms
Update on post-liver transplantation infections, malignancies, and surgical complications.
Washington K
(2005) Adv Anat Pathol 12: 221-6
MeSH Terms: Animals, Candidiasis, Cytomegalovirus Infections, Diagnosis, Differential, Graft Occlusion, Vascular, Graft Rejection, Hepatic Artery, Herpesviridae Infections, Humans, Ischemia, Liver, Liver Transplantation, Neoplasms, Organ Preservation, Postoperative Complications, Reperfusion Injury, Thrombosis, Time Factors
Show Abstract · Added March 5, 2014
Complications of liver transplantation are not limited to acute and chronic rejection, and recurrence of original disease, but include surgical complications, most commonly hepatic artery occlusion, infections, and development of de novo malignancies. In the early posttransplantation period, procurement/preservation injury, non-immunologic injury to the graft during harvesting and implantation, is manifested by centrilobular hepatocyte pallor and cholestasis but rarely leads to significant graft dysfunction. Ischemic complications, such as hepatic artery thrombosis, are more serious complications and may lead to early graft loss or biliary stricture. Infectious complications generally occur in the mid-to-late period after transplantation; cytomegalovirus (CMV) remains a common pathogen. Human herpes 6 virus infection has been implicated in allograft dysfunction, but is usually seen in the setting of co-infection with CMV. De novo malignancies are emerging as a significant cause of mortality after liver transplantation; risk is cumulative, and increases with time posttransplantation. Development of such malignancies in the setting of solid organ transplantation is multifactorial, and is related to individual and regional predispositions to malignancy, pre-transplantation disease states, recipient viral status, and use and intensity of immunosuppression regimens.
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18 MeSH Terms
Constitutively active K-cyclin/cdk6 kinase in Kaposi sarcoma-associated herpesvirus-infected cells.
Van Dross R, Yao S, Asad S, Westlake G, Mays DJ, Barquero L, Duell S, Pietenpol JA, Browning PJ
(2005) J Natl Cancer Inst 97: 656-66
MeSH Terms: Blotting, Western, CDC2-CDC28 Kinases, Cell Cycle Proteins, Cell Line, Tumor, Cyclin D, Cyclin-Dependent Kinase 2, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinase 6, Cyclin-Dependent Kinase Inhibitor p21, Cyclin-Dependent Kinase Inhibitor p27, Cyclin-Dependent Kinases, Cyclins, Enzyme Inhibitors, Half-Life, Herpesviridae Infections, Herpesvirus 8, Human, Humans, Immunoprecipitation, Lymphoma, Phosphorylation, Proto-Oncogene Proteins, Recombinant Fusion Proteins, Tumor Suppressor Proteins
Show Abstract · Added February 15, 2016
BACKGROUND - Kaposi sarcoma-associated human herpesvirus (KSHV) encodes K-cyclin, a homologue of D-type cellular cyclins, which binds cyclin-dependent kinases to phosphorylate various substrates. K-cyclin/cdk phosphorylates a subset of substrates normally targeted by cyclins D, E, and A. We used cells naturally infected with KSHV to further characterize the biochemical features of K-cyclin.
METHODS - We used immunoprecipitation with K-cyclin antibodies to examine the association of K-cyclin with cdk2, cdk6, p21Cip1, and p27Kip1 proteins in BC3 cells. We separated populations of BC3 cells enriched in cells in G1, S, or G2/M phases by elutriation and measured K-cyclin protein and the kinase activity of K-cyclin/cdk6 complexes. The half-life of K-cyclin and cyclin D2 proteins was determined by blocking protein synthesis with cycloheximide and measuring proteins in cell lysates by western blot analysis. We fused the entire K-cyclin sequence to the carboxyl-terminal sequence of cellular cyclin D that contains the PEST degradation sequence to produce K-cyclin/D2 and transfected K-cyclin/D2 into K-cyclin-negative cells to investigate the effect of the PEST sequence on K-cyclin's stability.
RESULTS - Viral K-cyclin interacted with cyclin-dependent kinases cdk2, cdk4, and cdk6 and with the cyclin/cdk inhibitory proteins p21Cip1 and p27Kip1 in BC3 cell lysates. Unlike D-type cyclins, whose expression is cell cycle dependent, the level of K-cyclin was stable throughout the cell cycle, and the kinase associated with the K-cyclin/cdk6 complex was constitutively active. The half-life of K-cyclin (6.9 hours) was much longer than that of cellular cyclin D2 (0.6 hour) and that of K-cyclin/D2 (0.5 hour), probably because K-cyclin lacks the PEST degradation sequence present in D-type cyclins.
CONCLUSION - The constitutive activation of K-cyclin/cdk complexes in KSHV-infected cells appears to result from the extended half-life of K-cyclin and may explain its role in Kaposi sarcoma.
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23 MeSH Terms
Herpesvirus DNA is consistently detected in lungs of patients with idiopathic pulmonary fibrosis.
Tang YW, Johnson JE, Browning PJ, Cruz-Gervis RA, Davis A, Graham BS, Brigham KL, Oates JA, Loyd JE, Stecenko AA
(2003) J Clin Microbiol 41: 2633-40
MeSH Terms: Adult, Aged, DNA, Viral, Female, Herpesviridae, Herpesviridae Infections, Humans, Lung, Male, Middle Aged, Polymerase Chain Reaction, Pulmonary Fibrosis
Show Abstract · Added December 10, 2013
On the basis of earlier reports associating Epstein-Barr Virus (EBV) with half of the cases of idiopathic pulmonary fibrosis (IPF), we hypothesized that chronic infection with EBV or a closely related herpesvirus would be detected in all cases of IPF. We tested lung specimens from 33 IPF patients (8 patients with familial IPF and 25 patients with sporadic IPF) and 25 patients with other diseases as controls for the presence of eight herpesviruses using PCR-based techniques. One or more of four herpesviruses (cytomegalovirus [CMV], EBV, human herpesvirus 7 [HHV-7], and HHV-8) were detected in 32 of 33 (97%) subjects with IPF and in 9 of 25 (36%) controls (P < 0.0001). CMV, EBV, and HHV-8 were found more frequently in IPF patients than in controls (P < 0.05, P < 0.001, and P < 0.01 respectively). Two or more herpesviruses were detected in 19 of 33 (57%) IPF patients and in 2 of 25 (8%) controls (P < 0.001). Two or more herpesviruses and HHV-8 were found more frequently in patients with sporadic IPF than in patients with familial IPF (P < 0.05 for both comparisons), and CMV was found less frequently in patients with sporadic IPF than in patients with familial IPF (P < 0.05). Immunohistochemistry for EBV or HHV-8 antigen showed viral antigen primarily in airway epithelial cells. These data support the concept that a herpesvirus could be a source of chronic antigenic stimulation in IPF.
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12 MeSH Terms