Rezeptor «herpes virus entry mediator» moduliert in humanen Hornhaut-Epithelzellen die Produktion inflammatorischer Zytokine in Reaktion auf Stimulation mit HSV Typ 1

2016 ◽  
Vol 2 (1) ◽  
pp. 14-15
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Virus ◽  
Virus Entry ◽  
Herpes Virus Entry Mediator ◽  
Tnf Α ◽  
Ifn Γ ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

Ziele: Beurteilung der Rolle des «herpes virus entry mediator» (HVEM) beim Viruseintritt und der Produktion inflammatorischer Zytokine in Reaktion auf eine Stimulation mit dem Herpes-simplex-Virus Typ 1 (HSV-1) in humanen Hornhaut-Epithelzellen. Methoden: Die HVEM-Expression in humanen Hornhaut-Epithelzellen wurde mittels Immunfluoreszenz und Durchflusszytometrie bestimmt. Mit β-Galaktosidase-exprimierendem HSV-1 wurden die Hornhaut-Epithelzellen stimuliert, und Viruseintrittstests wurden durchgeführt, um den Eintritt von HSV-1 in die Zellen zu überprüfen. Die Konzentrationen der Zytokine TNF-α, IL-6, IFN-γ, IL-12 und IL-18 sowie der Chemokine MIP-1α, MIP-1β und MIP-2 in Reaktion auf die HSV-1-Stimulation wurden in mit Kontrollsubstanz oder HVEM-siRNA behandelten Hornhaut-Epithelzellen untersucht. Ergebnisse: Die humanen Hornhaut-Epithelzellen waren positiv für HVEM-Expression und zeigten eine hohe Suszeptibilität für den Eintritt von HSV-1. Ein HVEM-«Silencing» bewirkte keine wesentliche Veränderung des Viruseintritts. Allerdings wurden nach der HSV-1-Stimulation in den mit HVEM-siRNA behandelten Zellen im Vergleich zu den Kontrollzellen höhere Konzentrationen des Zytokins IFN-γ sowie der Chemokine MIP-1α und MIP-1β gemessen. Schlussfolgerungen: HVEM in menschlichen Hornhaut-Epithelzellen kann die Produktion bestimmter Zytokine und Chemokine dämpfen und dadurch die angeborene Immunreaktion gegen HSV-1 modulieren. Dies könnte ein bisher unbekannter Mechanismus in der Pathogenese der HSV-1-Infektion der Hornhaut sein. Übersetzung aus Ophthalmic Res 2015;54:128-134 (DOI: 10.1159/000437209)

scholarly journals Pathological processes of immunological decontamination of herpes simplex virus type 1 from the cornea

2020 ◽  
pp. 4-11
Author(s):  
Т.З. Керимов ◽  
В.П. Соболев ◽  
М.А. Соболева ◽  
Н.А. Гаврилова ◽  
С.А. Борзенок
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Herpes Virus ◽  
Toll Like Receptors ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

В обзоре представлено описание патофизиологических механизмов герпесвирусной инфекции. Согласно данным медицинской статистики, вирусом простого герпеса 1 типа инфицировано большинство населения планеты. В развивающихся странах данный вирус является ведущей инфекционной причиной поражения роговицы. Также вирусу простого герпеса 1 типа отводится роль одного из факторов, приводящих к отторжению трансплантата роговицы. Вышеописанные патологические явления сопряжены с перестройкой клеточных систем в ответ на вирусное воздействие. Недавние открытия в данной области обнаружили значительный вклад трансмембранных и эндосомальных Toll-подобных рецепторов во врожденный противовирусный клеточный ответ. Показано, что эндосомальные Toll-подобные рецепторы 3 типа экспрессируются в кератоцитах только после их фенотипического перехода в фибробласты. Данная трансформация обычно происходит в результате механических и патогенных воздействий на роговицу. Изменение рецепторного состава клеток в ответ на герпесвирусную инвазию вызывает выработку интерферонов 1 типа - интерферона-альфа, интерферона-бета, и синтезу провоспалительных цитокинов, что приводит к вирусной деконтаминации. This review describes pathophysiological mechanisms of herpes virus infection in cornea cells. It has been previously reported that herpes simplex virus type 1 (HSV-1) infects most of the world’s population. In developing countries, HSV-1 is the leading infectious cause of corneal damage. Also, herpes simplex virus type 1 was assigned the role of one of the factors leading to rejection of the corneal transplant. These pathological phenomena are associated with restructuring of cellular systems in response to viral exposure. Recent discoveries have revealed a significant contribution of transmembrane and endosomal Toll-like receptors to the innate antiviral cell response. It is well known that endosomal Toll-like receptors-3 are expressed in keratocytes only after their phenotypic transformation to fibroblasts. This transformation usually occurs as a result of mechanical or infectious impact on the cornea. Changes in the receptor composition of cells as a response to herpes virus invasion is the main cause of type 1 interferons (interferon-alpha and interferon-beta) production and expression of proinflammatory cytokines, which leads to viral decontamination.

scholarly journals Characterization of heterosubunit complexes formed by the R1 and R2 subunits of herpes simplex virus 1 and equine herpes virus 4 ribonucleotide reductase

2000 ◽  
Vol 347 (1) ◽  
pp. 97-104
Author(s):  
Yunming SUN ◽  
Joe CONNER
Keyword(s):  
Enzyme Activity ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Ribonucleotide Reductase ◽  
Herpes Virus ◽  
Subunit Interaction ◽  
Herpes Simplex Virus 1 ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

We report on the separate PCR cloning and subsequent expression and purification of the large (R1) and small (R2) subunits from equine herpes virus type 4 (EHV-4) ribonucleotide reductase. The EHV-4 R1 and R2 subunits reconstituted an active enzyme and their abilities to complement the R1 and R2 subunits from the closely related herpes simplex virus 1 (HSV-1) ribonucleotide reductase, with the use of subunit interaction and enzyme activity assays, were analysed. Both EHV-4 R1/HSV-1 R2 and HSV-1 R1/EHV-4 R2 were able to assemble heterosubunit complexes but, surprisingly, neither of these complexes was fully active in enzyme activity assays; the EHV-4 R1/HSV-1 R2 and HSV-1 R1/EHV-4 R2 enzymes had 50% and 5% of their respective wild-type activities. Site-directed mutagenesis was used to alter two non-conserved residues located within the highly conserved and functionally important C-termini of the EHV-4 and HSV-1 R1 proteins. Mutation of Pro-737 to Lys and Lys-1084 to Pro in EHV-4 and HSV-1 R1 respectively had no effects on subunit assembly. Mutation of Pro-737 to Lys in EHV-4 R1 decreased enzyme activity by 50%; replacement of Lys-1084 by Pro in HSV-1 R1 had no effect on enzyme activity. Both alterations failed to restore full enzyme activities to the heterosubunit enzymes. Therefore probably neither of these amino acids has a direct role in catalysis. However, mutation of the highly conserved Tyr-1111 to Phe in HSV-1 R1 inactivated enzyme activity without affecting subunit interaction.

scholarly journals Immunological Signaling During Herpes Simplex Virus-2 and Cytomegalovirus Vaginal Shedding After Initiation of Antiretroviral Treatment

2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Martha C. Nason ◽  
Eshan U. Patel ◽  
Allison R. Kirkpatrick ◽  
Jessica L. Prodger ◽  
Kamnoosh Shahabi ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Virus ◽  
Interferon Γ ◽  
Virus Reactivation ◽  
Viral Shedding ◽  
Tnf Α ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2

Abstract Vaginal proinflammatory cytokine expression during herpes virus reactivation was examined in human immunodeficiency virus-infected women before and after initiation of antiretroviral therapy (ART). Vaginal swabs were screened for levels of cytokines interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, tumor necrosis factor (TNF)-α, and interferon-γ. The relative risk (RR) of herpes simplex virus-2 or cytomegalovirus (CMV) shedding being associated with cytokine levels above the median were estimated. Herpes simplex virus-2 shedding was significantly associated with higher levels of IL-6 (RR = 1.4, P = .003) and TNF-α (RR = 1.3, P = .010), whereas CMV shedding was associated with higher IL-6 (RR = 1.3, P = .006) and IL-2 (RR = 1.4, P = .01). The association of viral shedding with higher IL-6 levels suggests that herpes virus reactivation may be playing a role in immune activation after ART initiation.

scholarly journals Detection of Herpes Simplex Virus in Chronic Generalized Periodontitis via Polymerase Chain Reaction: A Pilot Study

2017 ◽  
Vol 9 (1) ◽  
pp. 7-11
Author(s):  
Thomas George Veliyaveetil
Keyword(s):  
Polymerase Chain Reaction ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Virus ◽  
Chain Reaction ◽  
Periodontal Destruction ◽  
Polymerase Chain ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

Background. As bacterial etiology could not support and explain various aspects of periodontal disease, herpes virus is now proposed to be one of the factors responsible for the periodontal destruction. The aim of the present study was to detect the presence of Herpes simplex virus (HSV) in patients with chronic generalized periodontitis. Methods. Eleven patients were consecutively selected for the study, of which 3 were diagnosed with moderate chronic generalized periodontitis and 8 with severe chronic generalized periodontitis. Subgingival material was taken from the deepest pocket of the dentition from every study subject, before the commencement of any procedure and polymerase chain reaction (PCR) assay was used to detect the presence of HSV-1 and -2. Results. HSV-1 and -2 DNA was not detected in any of the samples. Conclusion. This study is in contrast with previous studies and questions the proposed pathogenic role and clinical relevance of herpes virus in periodontitis.

scholarly journals Harringtonine Inhibits Herpes Simplex Virus Type 1 Infection by Reducing Herpes Virus Entry Mediator Expression

2021 ◽  
Vol 12 ◽  
Author(s):  
Ye Liu ◽  
Qiao You ◽  
Fang Zhang ◽  
Deyan Chen ◽  
Zhenping Huang ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Virus Entry ◽  
Resistant Strains ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

Herpes simplex virus type 1 (HSV-1) infection induces various clinical disorders, such as herpes simplex encephalitis (HSE), herpes simplex keratitis (HSK), and genital herpes. In clinical intervention, acyclovir (ACV) is the major therapeutic drug used to suppress HSV-1; however, ACV-resistant strains have gradually increased. In the present study, harringtonine (HT) significantly inhibited infection of HSV-1 as well as two ACV-resistant strains, including HSV-1 blue and HSV-1 153. Time-of-drug addition assay further revealed that HT mainly reduced the early stage of HSV-1 infection. We also demonstrated that HT mainly affected herpes virus entry mediator (HVEM) expression as shown by qPCR, Western Blot, and Immunofluorescence. Collectively, HT showed antiviral activity against HSV-1 and ACV-resistant strains by targeting HVEM and could be a promising therapeutic candidate for mitigating HSV-1-induced-pathogenesis.

Réactivations à herpès virus (HSV, CMV) en réanimation : qui et quand traiter ?

2019 ◽  
Vol 28 (3) ◽  
pp. 232-238
Author(s):  
C.-E. Luyt ◽  
G. Hékimian ◽  
N. Bréchot
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Virus ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Charge Virale

Les réactivations à herpès simplex virus (HSV) et à cytomégalovirus (CMV) sont fréquentes chez le patient non immunodéprimé de réanimation. La réactivation HSV est localisée aux voies aériennes ; elle débute au niveau oropharyngé, progresse de façon descendante avec la contamination des voies aériennes distales et peut aboutir, chez certains malades, à une véritable bronchopneumonie herpétique. Elle est en outre associée à un pronostic défavorable. Le traitement prophylactique et préemptif des réactivations HSV ne peut pas être préconisé à l’heure actuelle. Le traitement curatif repose sur un avis d’experts, chez des malades présentant soit une charge virale élevée dans les voies aériennes distales, soit des signes cytologiques d’atteinte parenchymateuse pulmonaire sur les cellules recueillies lors du lavage bronchoalvéolaire. La réactivation CMV sanguine est fréquente et peut être isolée ou associée à une réactivation/atteinte pulmonaire et est aussi associée à un pronostic défavorable. Le traitement prophylactique de la réactivation CMV ne peut pas être préconisé, et le traitement préemptif est en cours d’évaluation. À l’heure actuelle, le traitement curatif des maladies pulmonaires à CMV repose soit sur des signes histologiques d’atteinte pulmonaire, soit sur un faisceau d’arguments clinicobiologiques évoquant une possible maladie à CMV.

scholarly journals Alpha herpes virus type and viral load in intraocular fluids in patients with acute retinal necrosis

2019 ◽  
Vol 4 (1) ◽  
pp. e000247 ◽  
Author(s):  
Joanna von Hofsten ◽  
Tomas Bergström ◽  
Madeleine Zetterberg
Keyword(s):  
Herpes Simplex Virus ◽  
Viral Load ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Virus ◽  
Visual Outcome ◽  
High Viral Load ◽  
Acute Retinal Necrosis ◽  
Herpès Virus ◽  
Simplex Virus

ObjectivesTo identify all patients tested positive for herpes viruses in intraocular samples between 2007 and 2016 in South-Western Sweden and evaluate which of these met the criteria of acute retinal necrosis (ARN). To compare viral load in intraocular samples and virus type with clinical outcome.Method and analysisRetrospective case series. Intraocular samples and serum were analysed with quantitative real-time PCR (qPCR) and presence of antibodies (IgG and IgM) were detected by ELISA in serum.ResultsBetween 2007 and 2016, 13 patients met the clinical criteria of ARN and were PCR-positive in aqueous or vitreous for herpes simplex virus 1 (HSV1; n=4), herpes simplex virus 2 (HSV2; n=3) and varicella zoster virus (VZV; n=6). None of the patients tested positive for cytomegalovirus (n=13) or Epstein Barr virus (n=2) met the criteria of ARN. All ARN patients had specific serum IgG and three patients exhibited virus DNA in serum. There was no correlation between high viral load and worse visual outcome. However, higher viral loads were seen in samples taken earlier in the disease process. Median age was higher (p=0.049) in VZV-ARN than for HSV-ARN patients (60.5 and 45.4 years, respectively) with a tendency of worse best corrected visual acuity at presentation (1.62 and 0.79 log MAR, respectively; p=0.079).ConclusionARN is a reactivation of alpha herpes virus and presence of herpes DNA in serum may occur. VZV-ARN are older than HSV-ARN patients. High viral load does not appear to be a predictor of worse visual outcome, but rather indicates earlier sampling.

scholarly journals Cell-to-Cell Spread Blocking Activity Is Extremely Limited in the Sera of Herpes Simplex Virus 1 (HSV-1)- and HSV-2-Infected Subjects

2019 ◽  
Vol 93 (11) ◽  
Author(s):  
Elena Criscuolo ◽  
Matteo Castelli ◽  
Roberta A. Diotti ◽  
Virginia Amato ◽  
Roberto Burioni ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Humoral Immunity ◽  
Virus Entry ◽  
Serum Antibody ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTHerpes simplex virus 1 (HSV-1) and HSV-2 can evade serum antibody-mediated neutralization through cell-to-cell transmission mechanisms, which represent one of the central steps in disease reactivation. To address the role of humoral immunity in controlling HSV-1 and HSV-2 replication, we analyzed serum samples from 44 HSV-1 and HSV-2 seropositive subjects by evaluating (i) their efficiency in binding both the purified viral particles and recombinant gD and gB viral glycoproteins, (ii) their neutralizing activity, and (iii) their capacity to inhibit the cell-to-cell virus passagein vitro. All of the sera were capable of binding gD, gB, and whole virions, and all sera significantly neutralized cell-free virus. However, neither whole sera nor purified serum IgG fraction was able to inhibit significantly cell-to-cell virus spreading inin vitropost-virus-entry infectious assays. Conversely, when spiked with an already described anti-gD human monoclonal neutralizing antibody capable of inhibiting HSV-1 and -2 cell-to-cell transmission, each serum boosted both its neutralizing and post-virus-entry inhibitory activity, with no interference exerted by serum antibody subpopulations.IMPORTANCEDespite its importance in the physiopathology of HSV-1 and -2 infections, the cell-to-cell spreading mechanism is still poorly understood. The data shown here suggest that infection-elicited neutralizing antibodies capable of inhibiting cell-to-cell virus spread can be underrepresented in most infected subjects. These observations can be of great help in better understanding the role of humoral immunity in controlling virus reactivation and in the perspective of developing novel therapeutic strategies, studying novel correlates of protection, and designing effective vaccines.

Effect of a combination therapy between IL-12 and soluble IL-4 receptor (sIL-4R) onCandida albicansand herpes simplex virus type 1 infections in thermally injured mice

2002 ◽  
Vol 48 (10) ◽  
pp. 886-894 ◽  
Author(s):  
Makiko Kobayashi ◽  
Hitoshi Takahashi ◽  
David N Herndon ◽  
Richard B Pollard ◽  
Fujio Suzuki
Keyword(s):  
T Cells ◽  
Candida Albicans ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Herpes Simplex Virus Type ◽  
Cell Responses ◽  
Ifn Γ ◽  
Simplex Virus ◽  
Hsv 1

The effectiveness of a combination using IL-12 and soluble IL-4 receptor (sIL-4R) to treat severe infections of herpes simplex virus type 1 (HSV-1) and Candida albicans in thermally injured mice was investigated. Although sIL-4R decreased burn-associated type 2 T-cell responses, the effect of sIL-4R was minimal on the morbidity and mortality of thermally injured mice exposed to 250 times LD50of HSV-1 or 10 times LD50of C. albicans. Compared with 100% mortality in control mice, mortality for HSV-1 and C. albicans was 40 and 20%, respectively, in thermally injured mice that received IL-12 and sIL-4R in combination. After stimulation with anti-CD3 monoclonal antibody, splenic T cells from thermally injured mice exposed to large amounts of HSV-1 or C. albicans did not produce gamma interferon (IFN-γ) into their culture fluids. However, IFN-γ was produced by splenic T cells from thermally injured and infected mice treated with IL-12 and sIL-4R in combination. These results suggest that therapeutic treatment with a combination of IL-12 and sIL-4R may be effective by inducing type 1 T-cell responses in thermally injured mice exposed to large amounts of HSV-1 or C. albicans.Key words: burn, IL-12, soluble IL-4 receptor, herpesvirus, Candida albicans.

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