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Josselin Houenou - One of the best experts on this subject based on the ideXlab platform.

  • Effects of Cumulative Herpesviridae and Toxoplasma gondii Infections on Cognitive Function in Healthy, Bipolar, and Schizophrenia Subjects.
    The Journal of clinical psychiatry, 2016
    Co-Authors: Nora Hamdani, Claire Daban-huard, Ophelia Godin, Hakim Laouamri, Stéphane Jamain, Dodji Attiba, Marine Delavest, Jean-pierre Lépine, Philippe Le Corvoisier, Josselin Houenou
    Abstract:

    Schizophrenia and bipolar disorder are associated with cognitive impairment leading to social disruption. While previous studies have focused on the effect of individual infectious exposure, namely, Herpesviridae viruses or Toxoplasma gondii (T gondii), on cognitive functioning, the objective of the present study was to examine the effect of multiple infections on cognitive functioning in patients with schizophrenia and bipolar disorder and in healthy controls. Seropositivity to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV), and T gondii was related to cognitive status among 423 participants (recruited between 2008 and 2014; 138 patients with bipolar disorder, 105 patients with schizophrenia [DSM-IV criteria], and 180 healthy controls) for episodic verbal memory (California Verbal Learning Test), working memory (Wechsler Adult Intelligence Scale, third edition), and premorbid intelligence quotient (National Adult Reading Test). Seropositivity to and antibody levels of HSV-1 were significantly associated with working memory, which persisted after correction (backward digit span: β = -0.10 [0.05], χ² = 33.89, P = .0001) in the overall sample. This association was particularly strong in the control group (β = -0.18 [0.08], P = .04, Z = -3.55, P = .0008; corrected P = .012). Further, cumulative exposure to HSV-1, HSV-2, and CMV viruses and T gondii parasite was also associated with lower scores on working memory as measured by backward digit span in the overall sample (Z = 2.86, P = .004; Z = 2.47, P = .01; and Z = 3.35, P = .01, respectively). Exposures to Herpesviridae and T gondii parasite seem to impact cognitive functioning. Because infections caused by Herpesviridae and/or T gondii parasite are quite common in the (general) population, assessing and confirming the cognitive impairment among those who have cumulative exposures is useful and of interest. © Copyright 2016 Physicians Postgraduate Press, Inc.

  • Effects of Cumulative Herpesviridae and Toxoplasma gondii Infections on Cognitive Function in Healthy, Bipolar, and Schizophrenia Subjects.
    The Journal of Clinical Psychiatry, 2016
    Co-Authors: Nora Hamdani, Claire Daban-huard, Ophelia Godin, Hakim Laouamri, Stéphane Jamain, Dodji Attiba, Marine Delavest, Jean-pierre Lépine, Philippe Le Corvoisier, Josselin Houenou
    Abstract:

    OBJECTIVE Schizophrenia and bipolar disorder are associated with cognitive impairment leading to social disruption. While previous studies have focused on the effect of individual infectious exposure, namely, Herpesviridae viruses or Toxoplasma gondii (T gondii), on cognitive functioning, the objective of the present study was to examine the effect of multiple infections on cognitive functioning in patients with schizophrenia and bipolar disorder and in healthy controls. METHODS Seropositivity to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV), and T gondii was related to cognitive status among 423 participants (recruited between 2008 and 2014; 138 patients with bipolar disorder, 105 patients with schizophrenia [DSM-IV criteria], and 180 healthy controls) for episodic verbal memory (California Verbal Learning Test), working memory (Wechsler Adult Intelligence Scale, third edition), and premorbid intelligence quotient (National Adult Reading Test). RESULTS Seropositivity to and antibody levels of HSV-1 were significantly associated with working memory, which persisted after correction (backward digit span: β = -0.10 [0.05], χ² = 33.89, P = .0001) in the overall sample. This association was particularly strong in the control group (β = -0.18 [0.08], P = .04, Z = -3.55, P = .0008; corrected P = .012). Further, cumulative exposure to HSV-1, HSV-2, and CMV viruses and T gondii parasite was also associated with lower scores on working memory as measured by backward digit span in the overall sample (Z = 2.86, P = .004; Z = 2.47, P = .01; and Z = 3.35, P = .01, respectively). CONCLUSIONS Exposures to Herpesviridae and T gondii parasite seem to impact cognitive functioning. Because infections caused by Herpesviridae and/or T gondii parasite are quite common in the (general) population, assessing and confirming the cognitive impairment among those who have cumulative exposures is useful and of interest.

Zhijun Liu - One of the best experts on this subject based on the ideXlab platform.

  • Toll-like receptor-mediated innate immunity against Herpesviridae infection: a current perspective on viral infection signaling pathways.
    Virology journal, 2020
    Co-Authors: Wenjin Zheng, Yiyuan Zhang, E Xiaofei, Wei Gao, Mogen Zhang, Weijie Zhai, Ronaldjit Singh Rajkumar, Zhijun Liu
    Abstract:

    In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against Herpesviridae, and systematically describes the processes of TLR actions and Herpesviridae recognition as well as the signal transduction pathways involved. Future studies of the interactions between TLRs and Herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.

  • correction to toll like receptor mediated innate immunity against Herpesviridae infection a current perspective on viral infection signaling pathways
    Virology Journal, 2020
    Co-Authors: Wenjin Zheng, Yiyuan Zhang, E Xiaofei, Wei Gao, Mogen Zhang, Weijie Zhai, Ronaldjit Singh Rajkumar, Zhijun Liu
    Abstract:

    BACKGROUND In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. MAIN BODY Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against Herpesviridae, and systematically describes the processes of TLR actions and Herpesviridae recognition as well as the signal transduction pathways involved. CONCLUSIONS Future studies of the interactions between TLRs and Herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.

Nora Hamdani - One of the best experts on this subject based on the ideXlab platform.

  • Effects of Cumulative Herpesviridae and Toxoplasma gondii Infections on Cognitive Function in Healthy, Bipolar, and Schizophrenia Subjects.
    The Journal of clinical psychiatry, 2016
    Co-Authors: Nora Hamdani, Claire Daban-huard, Ophelia Godin, Hakim Laouamri, Stéphane Jamain, Dodji Attiba, Marine Delavest, Jean-pierre Lépine, Philippe Le Corvoisier, Josselin Houenou
    Abstract:

    Schizophrenia and bipolar disorder are associated with cognitive impairment leading to social disruption. While previous studies have focused on the effect of individual infectious exposure, namely, Herpesviridae viruses or Toxoplasma gondii (T gondii), on cognitive functioning, the objective of the present study was to examine the effect of multiple infections on cognitive functioning in patients with schizophrenia and bipolar disorder and in healthy controls. Seropositivity to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV), and T gondii was related to cognitive status among 423 participants (recruited between 2008 and 2014; 138 patients with bipolar disorder, 105 patients with schizophrenia [DSM-IV criteria], and 180 healthy controls) for episodic verbal memory (California Verbal Learning Test), working memory (Wechsler Adult Intelligence Scale, third edition), and premorbid intelligence quotient (National Adult Reading Test). Seropositivity to and antibody levels of HSV-1 were significantly associated with working memory, which persisted after correction (backward digit span: β = -0.10 [0.05], χ² = 33.89, P = .0001) in the overall sample. This association was particularly strong in the control group (β = -0.18 [0.08], P = .04, Z = -3.55, P = .0008; corrected P = .012). Further, cumulative exposure to HSV-1, HSV-2, and CMV viruses and T gondii parasite was also associated with lower scores on working memory as measured by backward digit span in the overall sample (Z = 2.86, P = .004; Z = 2.47, P = .01; and Z = 3.35, P = .01, respectively). Exposures to Herpesviridae and T gondii parasite seem to impact cognitive functioning. Because infections caused by Herpesviridae and/or T gondii parasite are quite common in the (general) population, assessing and confirming the cognitive impairment among those who have cumulative exposures is useful and of interest. © Copyright 2016 Physicians Postgraduate Press, Inc.

  • Effects of Cumulative Herpesviridae and Toxoplasma gondii Infections on Cognitive Function in Healthy, Bipolar, and Schizophrenia Subjects.
    The Journal of Clinical Psychiatry, 2016
    Co-Authors: Nora Hamdani, Claire Daban-huard, Ophelia Godin, Hakim Laouamri, Stéphane Jamain, Dodji Attiba, Marine Delavest, Jean-pierre Lépine, Philippe Le Corvoisier, Josselin Houenou
    Abstract:

    OBJECTIVE Schizophrenia and bipolar disorder are associated with cognitive impairment leading to social disruption. While previous studies have focused on the effect of individual infectious exposure, namely, Herpesviridae viruses or Toxoplasma gondii (T gondii), on cognitive functioning, the objective of the present study was to examine the effect of multiple infections on cognitive functioning in patients with schizophrenia and bipolar disorder and in healthy controls. METHODS Seropositivity to herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV), and T gondii was related to cognitive status among 423 participants (recruited between 2008 and 2014; 138 patients with bipolar disorder, 105 patients with schizophrenia [DSM-IV criteria], and 180 healthy controls) for episodic verbal memory (California Verbal Learning Test), working memory (Wechsler Adult Intelligence Scale, third edition), and premorbid intelligence quotient (National Adult Reading Test). RESULTS Seropositivity to and antibody levels of HSV-1 were significantly associated with working memory, which persisted after correction (backward digit span: β = -0.10 [0.05], χ² = 33.89, P = .0001) in the overall sample. This association was particularly strong in the control group (β = -0.18 [0.08], P = .04, Z = -3.55, P = .0008; corrected P = .012). Further, cumulative exposure to HSV-1, HSV-2, and CMV viruses and T gondii parasite was also associated with lower scores on working memory as measured by backward digit span in the overall sample (Z = 2.86, P = .004; Z = 2.47, P = .01; and Z = 3.35, P = .01, respectively). CONCLUSIONS Exposures to Herpesviridae and T gondii parasite seem to impact cognitive functioning. Because infections caused by Herpesviridae and/or T gondii parasite are quite common in the (general) population, assessing and confirming the cognitive impairment among those who have cumulative exposures is useful and of interest.

Arjen Nikkels - One of the best experts on this subject based on the ideXlab platform.

  • alpha Herpesviridae in der dermatologie
    Hautarzt, 2017
    Co-Authors: El L Hayderi, Albert Rubben, Arjen Nikkels
    Abstract:

    Der zweite Teil der vorliegenden Ubersichtsarbeit befasst sich mit dem Varicella-Zoster-Virus (VZV) und bietet einen Uberblick uber neue, seltene und atypische klinische Symptome: fotolokalisierte Varizellen (an lichtexponierten Stellen), hamorrhagische Bullae wahrend der Varizelleninfektion, die Bedeutung des VZV bei Immunglobulin-A-Vaskulitis, VZV-bedingte Alopezie, ulcerative Varizellen-Hautlasionen, kindlicher Herpes zoster (HZ), anhaltende Prodromalschmerzen, rezidivierender HZ, Bedeutung des VZV beim „burning mouth syndrome“, warzenahnliche VZV-Lasionen, Bedeutung von Satellitenlasionen bei HZ und neurologische oder internistische Spatkomplikationen des HZ. Daruber hinaus werden bestimmte Zusammenhange zwischen dem Auftreten des HZ und nachfolgenden internistischen Erkrankungen, Risikofaktoren fur HZ und neue Entwicklungen bei der Impfung gegen HZ dargestellt.

  • The alpha-Herpesviridae in dermatology : Varicella zoster virus.
    Der Hautarzt; Zeitschrift fur Dermatologie Venerologie und verwandte Gebiete, 2017
    Co-Authors: L. El Hayderi, Albert Rubben, Arjen Nikkels
    Abstract:

    The second part of this publication deals with varicella zoster virus (VZV) and presents an overview of new, rare, and atypical clinical manifestations, including photolocalized varicella, hemorrhagic bullae during varicella, the implication of VZV in immunoglobulin A vasculitis, VZV-related alopecia, ulcerative varicella skin lesions, childhood herpes zoster (HZ), prolonged prodromal pains, recurrent HZ, VZV implication in burning mouth syndrome, verruciform VZV lesions, the significance of satellite lesions during HZ, and late HZ complications, either neurological or internal. Furthermore, certain associations between the occurrence of HZ and subsequent internal pathologies, as well as risk factors for HZ and new developments in vaccination against HZ will be addressed.

  • Simultaneous Reactivation of Herpes simplex Virus and Varicella-Zoster Virus in a Patient with Idiopathic Thrombocytopenic Purpura
    Dermatology (Basel Switzerland), 1999
    Co-Authors: Arjen Nikkels, Pascale Frere, L. Rakic, M. F. Fassotte, Béatrice Evrard, P. De Mol, Gérald Pierard
    Abstract:

    Simultaneous reactivation of distinct Herpesviridae with development of clinical manifestations is exceptional. We report a 48-year-old woman suffering from idiopathic thrombocytopenic purpura. As the

  • distribution of varicella zoster virus and herpes simplex virus in disseminated fatal infections
    Journal of Clinical Pathology, 1996
    Co-Authors: Arjen Nikkels, Serge Debrus, Philippe Delvenne, Jacques Piette, Bernard Rentier, Catherine Sadzotdelvaux, G Lipcsei, Pascale Quatresooz, Gérald Pierard
    Abstract:

    AIMS: To study the cutaneous and visceral distribution of herpes simplex virus (HSV) and varicella zoster virus (VZV) in fatal infections. METHODS: Standard histology, immunohistochemistry (monoclonal antibodies VL8 and VL2 and polyclonal antibody IE63 directed against VZV; monoclonal antibodies IBD4 and HH2 and polyclonal antibodies directed against HSVI and HSVII) and in situ hybridisation (anti-HSV and anti-VZV probes) were applied to formalin fixed, paraffin wax sections. RESULTS: On histological examination, Herpesviridae infection was evident in various organs including the lungs, liver and skin. In addition, immunohistochemistry and in situ hybridisation revealed the presence of HSV and VZV antigens and nucleic acids in several cell types and tissues showing no cytopathological alterations suggestive of Herpesviridae infection. The organs with histological evidence of infection also contained VZV or HSV antigens and their genes. CONCLUSIONS: These findings suggest that organ failure in disseminated VZV and HSV infections is primarily caused by HSV or VZV induced cell damage and lysis. They also indicate that immunohistochemistry and in situ hybridisation can provide an accurate, type-specific diagnosis on formalin fixed, paraffin wax embedded tissue even when classic histological and cytological characteristics are lacking.

  • Viral glycoproteins in Herpesviridae granulomas
    The American Journal of dermatopathology, 1994
    Co-Authors: Arjen Nikkels, Serge Debrus, Philippe Delvenne, Catherine Sadzot-delvaux, Jacques Piette, Bernard Rentier, Gérald Pierard
    Abstract:

    Granulomatous reactions after varicella zoster virus (VZV) and herpes simplex virus (HSV) infections are rare, and their pathogenesis remains unclear. We studied by immunohistochemistry and in situ hybridization early granulomatous reactions after VZV and HSV infections. In the five cases studied, the VZV glycoproteins gp I and gp II were present in cells abutted to altered vessels, but the corresponding genome sequences were disclosed in similar locations in only one of these cases. In an immunocompromised patient with diffuse HSV eruption, HSV 1 antigens were present in cells of the reticular dermis, while viral nucleic acids were not evident. Immunophe-notyping of the granulomas showed strong Mac 387 and CD68 positive labelings of macrophages/monocytes, without any involvement of Factor XIlla-positive cells. These findings suggest that the major viral envelope glycoproteins, rather than complete viral particles could trigger granuloma formation following HSV and VZV skin infections.

Wenjin Zheng - One of the best experts on this subject based on the ideXlab platform.

  • Toll-like receptor-mediated innate immunity against Herpesviridae infection: a current perspective on viral infection signaling pathways.
    Virology journal, 2020
    Co-Authors: Wenjin Zheng, Yiyuan Zhang, E Xiaofei, Wei Gao, Mogen Zhang, Weijie Zhai, Ronaldjit Singh Rajkumar, Zhijun Liu
    Abstract:

    In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against Herpesviridae, and systematically describes the processes of TLR actions and Herpesviridae recognition as well as the signal transduction pathways involved. Future studies of the interactions between TLRs and Herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.

  • correction to toll like receptor mediated innate immunity against Herpesviridae infection a current perspective on viral infection signaling pathways
    Virology Journal, 2020
    Co-Authors: Wenjin Zheng, Yiyuan Zhang, E Xiaofei, Wei Gao, Mogen Zhang, Weijie Zhai, Ronaldjit Singh Rajkumar, Zhijun Liu
    Abstract:

    BACKGROUND In the past decades, researchers have demonstrated the critical role of Toll-like receptors (TLRs) in the innate immune system. They recognize viral components and trigger immune signal cascades to subsequently promote the activation of the immune system. MAIN BODY Herpesviridae family members trigger TLRs to elicit cytokines in the process of infection to activate antiviral innate immune responses in host cells. This review aims to clarify the role of TLRs in the innate immunity defense against Herpesviridae, and systematically describes the processes of TLR actions and Herpesviridae recognition as well as the signal transduction pathways involved. CONCLUSIONS Future studies of the interactions between TLRs and Herpesviridae infections, especially the subsequent signaling pathways, will not only contribute to the planning of effective antiviral therapies but also provide new molecular targets for the development of antiviral drugs.