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Special Issue "Modulation of Apoptosis by Viral Infection"

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (31 January 2013)

Special Issue Editor

Guest Editor
Prof. Dr. John A. Blaho

Professor of Microbiology, Mount Sinai School of Medicine, Annenberg Building Room 16-23, 1468 Madison Avenue, New York, NY 10029, USA
Website | E-Mail
Fax: +212 534 1684
Interests: Molecular Virology; Regulation of Herpes Simplex Virus Replication; Apoptosis and Signal Transduction; Biotechnology; Oncoapoptosis for Cancer Therapy

Keywords

  • DNA / RNA, animal / insect viruses
  • virus replication / assembly
  • viral immune evasion
  • intrinsic (mitochondria) / extrinsic (death receptor) apoptosis
  • cell cycle / programmed cell death
  • viral / cellular pro/antagonists
  • viral oncotherapy
  • viral pathogenesis
  • host defenses
  • NF-kB
  • TNF /Fas
  • p53
  • Bcl-2 family members
  • caspases

Published Papers (6 papers)

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Research

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Open AccessArticle Dendritic Cell Apoptosis and the Pathogenesis of Dengue
Viruses 2012, 4(11), 2736-2753; doi:10.3390/v4112736
Received: 12 October 2012 / Revised: 30 October 2012 / Accepted: 31 October 2012 / Published: 1 November 2012
Cited by 11 | PDF Full-text (869 KB) | HTML Full-text | XML Full-text
Abstract
Dengue viruses and other members of the Flaviviridae family are emerging human pathogens. Dengue is transmitted to humans by Aedes aegypti female mosquitoes. Following infection through the bite, cells of the hematopoietic lineage, like dendritic cells, are the first targets of dengue virus
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Dengue viruses and other members of the Flaviviridae family are emerging human pathogens. Dengue is transmitted to humans by Aedes aegypti female mosquitoes. Following infection through the bite, cells of the hematopoietic lineage, like dendritic cells, are the first targets of dengue virus infection. Dendritic cells (DCs) are key antigen presenting cells, sensing pathogens, processing and presenting the antigens to T lymphocytes, and triggering an adaptive immune response. Infection of DCs by dengue virus may induce apoptosis, impairing their ability to present antigens to T cells, and thereby contributing to dengue pathogenesis. This review focuses on general mechanisms by which dengue virus triggers apoptosis, and possible influence of DC-apoptosis on dengue disease severity. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
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Review

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Open AccessReview HIV-1 Induced Bystander Apoptosis
Viruses 2012, 4(11), 3020-3043; doi:10.3390/v4113020
Received: 7 September 2012 / Revised: 19 October 2012 / Accepted: 2 November 2012 / Published: 9 November 2012
Cited by 18 | PDF Full-text (447 KB) | HTML Full-text | XML Full-text
Abstract
Apoptosis of uninfected bystander cells is a key element of HIV pathogenesis and believed to be the driving force behind the selective depletion of CD4+ T cells leading to immunodeficiency. While several viral proteins have been implicated in this process the complex interaction
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Apoptosis of uninfected bystander cells is a key element of HIV pathogenesis and believed to be the driving force behind the selective depletion of CD4+ T cells leading to immunodeficiency. While several viral proteins have been implicated in this process the complex interaction between Env glycoprotein expressed on the surface of infected cells and the receptor and co-receptor expressing bystander cells has been proposed as a major mechanism. HIV-1 utilizes CD4 as the primary receptor for entry into cells; however, it is the viral co-receptor usage that greatly influences CD4 decline and progression to AIDS. This phenomenon is relatively simple for X4 viruses, which arise later during the course of the disease, are considered to be highly fusogenic, and cause a rapid CD4+ T cell decline. However, in contrast, R5 viruses in general have a greater transmissibility, are encountered early during the disease and have a lesser pathogenic potential than the former. The above generalization gets complicated in numerous situations where R5 viruses persist throughout the disease and are capable of causing a rigorous CD4+ T cell decline. This review will discuss the multiple factors that are reported to influence HIV induced bystander apoptosis and pathogenesis including Env glycoprotein phenotype, virus tropism, disease stage, co-receptor expression on CD4+ T cells, immune activation and therapies targeting the viral envelope. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
Open AccessReview Modulation of Apoptotic Signaling by the Hepatitis B Virus X Protein
Viruses 2012, 4(11), 2945-2972; doi:10.3390/v4112945
Received: 5 September 2012 / Revised: 23 October 2012 / Accepted: 31 October 2012 / Published: 8 November 2012
Cited by 31 | PDF Full-text (764 KB) | HTML Full-text | XML Full-text
Abstract
Worldwide, an estimated 350 million people are chronically infected with the Hepatitis B Virus (HBV); chronic infection with HBV is associated with the development of severe liver diseases including hepatitis and cirrhosis. Individuals who are chronically infected with HBV also have a significantly
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Worldwide, an estimated 350 million people are chronically infected with the Hepatitis B Virus (HBV); chronic infection with HBV is associated with the development of severe liver diseases including hepatitis and cirrhosis. Individuals who are chronically infected with HBV also have a significantly higher risk of developing hepatocellular carcinoma (HCC) than uninfected individuals. The HBV X protein (HBx) is a key regulatory HBV protein that is important for HBV replication, and likely plays a cofactor role in the development of HCC in chronically HBV-infected individuals. Although some of the functions of HBx that may contribute to the development of HCC have been characterized, many HBx activities, and their putative roles during the development of HBV-associated HCC, remain incompletely understood. HBx is a multifunctional protein that localizes to the cytoplasm, nucleus, and mitochondria of HBV‑infected hepatocytes. HBx regulates numerous cellular signal transduction pathways and transcription factors as well as cell cycle progression and apoptosis. In this review, we will summarize reports in which the impact of HBx expression on cellular apoptotic pathways has been analyzed. Although various effects of HBx on apoptotic pathways have been observed in different model systems, studies of HBx activities in biologically relevant hepatocyte systems have begun to clarify apoptotic effects of HBx and suggest mechanisms that could link HBx modulation of apoptotic pathways to the development of HBV-associated HCC. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
Open AccessReview Prevention of Cellular Suicide by Cytomegaloviruses
Viruses 2012, 4(10), 1928-1949; doi:10.3390/v4101928
Received: 31 August 2012 / Revised: 21 September 2012 / Accepted: 25 September 2012 / Published: 2 October 2012
Cited by 12 | PDF Full-text (1211 KB) | HTML Full-text | XML Full-text
Abstract
As intracellular parasites, viruses rely on many host cell functions to ensure their replication. The early induction of programmed cell death (PCD) in infected cells constitutes an effective antiviral host mechanism to restrict viral spread within an organism. As a countermeasure, viruses have
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As intracellular parasites, viruses rely on many host cell functions to ensure their replication. The early induction of programmed cell death (PCD) in infected cells constitutes an effective antiviral host mechanism to restrict viral spread within an organism. As a countermeasure, viruses have evolved numerous strategies to interfere with the induction or execution of PCD. Slowly replicating viruses such as the cytomegaloviruses (CMVs) are particularly dependent on sustained cell viability. To preserve viability, the CMVs encode several viral cell death inhibitors that target different key regulators of the extrinsic and intrinsic apoptosis pathways. The best-characterized CMV-encoded inhibitors are the viral inhibitor of caspase-8-induced apoptosis (vICA), viral mitochondrial inhibitor of apoptosis (vMIA), and viral inhibitor of Bak oligomerization (vIBO). Moreover, a viral inhibitor of RIP-mediated signaling (vIRS) that blocks programmed necrosis has been identified in the genome of murine CMV (MCMV), indicating that this cell death mode is a particularly important part of the antiviral host response. This review provides an overview of the known cell death suppressors encoded by CMVs and their mechanisms of action. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
Open AccessReview Contributions of Epstein–Barr Nuclear Antigen 1 (EBNA1) to Cell Immortalization and Survival
Viruses 2012, 4(9), 1537-1547; doi:10.3390/v4091537
Received: 19 July 2012 / Revised: 14 August 2012 / Accepted: 27 August 2012 / Published: 13 September 2012
Cited by 28 | PDF Full-text (260 KB) | HTML Full-text | XML Full-text
Abstract
Epstein–Barr virus (EBV) immortalizes host cells as part of its latent mode of infection. As a result of this ability to promote cell proliferation and survival, EBV infection contributes to the development of several kinds of B-cell lymphomas and epithelial tumours. The EBV
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Epstein–Barr virus (EBV) immortalizes host cells as part of its latent mode of infection. As a result of this ability to promote cell proliferation and survival, EBV infection contributes to the development of several kinds of B-cell lymphomas and epithelial tumours. The EBV Epstein–Barr nuclear antigen 1 (EBNA1) protein is the only EBV protein expressed in all EBV-associated tumours and plays multiple important roles in EBV latency. In addition to its well-studied roles in viral DNA replication, segregation and transcriptional activation, several studies have identified roles of EBNA1 in manipulating cellular processes that result in reduced apoptosis and increased cell survival. This review discusses these cellular effects of EBNA1 and mechanisms by which they occur. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
Open AccessReview Does Apoptosis Play a Role in Varicella Zoster Virus Latency and Reactivation?
Viruses 2012, 4(9), 1509-1514; doi:10.3390/v4091509
Received: 13 August 2012 / Revised: 5 September 2012 / Accepted: 6 September 2012 / Published: 11 September 2012
Cited by 6 | PDF Full-text (227 KB) | HTML Full-text | XML Full-text
Abstract
Varicella zoster virus (VZV) is an exclusively human highly neurotropic alphaherpesvirus. To date, VZV has been shown to induce apoptosis, primarily through the intrinsic pathway in different cell types, except for neurons in which the virus becomes latent. This review summarizes current studies
[...] Read more.
Varicella zoster virus (VZV) is an exclusively human highly neurotropic alphaherpesvirus. To date, VZV has been shown to induce apoptosis, primarily through the intrinsic pathway in different cell types, except for neurons in which the virus becomes latent. This review summarizes current studies of varicella-induced apoptosis in non‑neuronal cells. Future studies are proposed to determine whether apoptosis is terminated prematurely or even begins in neurons that are non-productively infected with VZV. Full article
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)

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