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Special Issue "Immune Evasion"

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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 (30 November 2012)

Special Issue Editor

Guest Editor
Prof. Dr. Annette Oxenius

ETH Zürich, Institute of Microbiology HCI G, 401 Wolfgang-Pauli-Str. 10, 8093 Zuerich, Switzerland
Website | E-Mail

Keywords

  • immune evasion
  • antigen presentation
  • adaptive immunity
  • innate immunity
  • interference with host cell signaling
  • mutation

Published Papers (12 papers)

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Research

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Open AccessArticle Human Cytomegalovirus Encoded Homologs of Cytokines, Chemokines and their Receptors: Roles in Immunomodulation
Viruses 2012, 4(11), 2448-2470; doi:10.3390/v4112448
Received: 30 September 2012 / Revised: 24 October 2012 / Accepted: 24 October 2012 / Published: 25 October 2012
Cited by 23 | PDF Full-text (642 KB) | HTML Full-text | XML Full-text
Abstract
Human cytomegalovirus (HCMV), the largest human herpesvirus, infects a majority of the world’s population. Like all herpesviruses, following primary productive infection, HCMV establishes a life-long latent infection, from which it can reactivate years later to produce new, infectious virus. Despite the presence of
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Human cytomegalovirus (HCMV), the largest human herpesvirus, infects a majority of the world’s population. Like all herpesviruses, following primary productive infection, HCMV establishes a life-long latent infection, from which it can reactivate years later to produce new, infectious virus. Despite the presence of a massive and sustained anti-HCMV immune response, productively infected individuals can shed virus for extended periods of time, and once latent infection is established, it is never cleared from the host. It has been proposed that HCMV must therefore encode functions which help to evade immune mediated clearance during productive virus replication and latency. Molecular mimicry is a strategy used by many viruses to subvert and regulate anti-viral immunity and HCMV has hijacked/developed a range of functions that imitate host encoded immunomodulatory proteins. This review will focus on the HCMV encoded homologs of cellular cytokines/chemokines and their receptors, with an emphasis on how these virus encoded homologs may facilitate viral evasion of immune clearance. Full article
(This article belongs to the Special Issue Immune Evasion)

Review

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Open AccessReview Molecular Mechanisms of HIV Immune Evasion of the Innate Immune Response in Myeloid Cells
Viruses 2013, 5(1), 1-14; doi:10.3390/v5010001
Received: 7 November 2012 / Revised: 19 December 2012 / Accepted: 19 December 2012 / Published: 21 December 2012
Cited by 7 | PDF Full-text (352 KB) | HTML Full-text | XML Full-text
Abstract
The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of virally
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The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of virally encoded proteins that are necessary to infect myeloid cells, a better understanding of cellular intrinsic antiviral strategies has now been achieved. Recent findings have provided insight into how the lentiviral accessory proteins, Vpx, Vpr and Vif counteract antiviral factors found in myeloid cells including SAMHD1, APOBEC3G, APOBEC3A, UNG2 and uracil. Here we review our current understanding of the molecular basis of how cellular antiviral factors function and the viral countermeasures that antagonize them to promote viral transmission and spread. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Hiding Lipid Presentation: Viral Interference with CD1d-Restricted Invariant Natural Killer T (iNKT) Cell Activation
Viruses 2012, 4(10), 2379-2399; doi:10.3390/v4102379
Received: 2 September 2012 / Revised: 12 October 2012 / Accepted: 17 October 2012 / Published: 23 October 2012
Cited by 7 | PDF Full-text (1441 KB) | HTML Full-text | XML Full-text
Abstract
The immune system plays a major role in protecting the host against viral infection. Rapid initial protection is conveyed by innate immune cells, while adaptive immunity (including T lymphocytes) requires several days to develop, yet provides high specificity and long-lasting memory. Invariant natural
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The immune system plays a major role in protecting the host against viral infection. Rapid initial protection is conveyed by innate immune cells, while adaptive immunity (including T lymphocytes) requires several days to develop, yet provides high specificity and long-lasting memory. Invariant natural killer T (iNKT) cells are an unusual subset of T lymphocytes, expressing a semi-invariant T cell receptor together with markers of the innate NK cell lineage. Activated iNKT cells can exert direct cytolysis and can rapidly release a variety of immune-polarizing cytokines, thereby regulating the ensuing adaptive immune response. iNKT cells recognize lipids in the context of the antigen-presenting molecule CD1d. Intriguingly, CD1d-restricted iNKT cells appear to play a critical role in anti-viral defense: increased susceptibility to disseminated viral infections is observed both in patients with iNKT cell deficiency as well as in CD1d- and iNKT cell-deficient mice. Moreover, viruses have recently been found to use sophisticated strategies to withstand iNKT cell-mediated elimination. This review focuses on CD1d-restricted lipid presentation and the strategies viruses deploy to subvert this pathway. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Neutralizing Antibodies and Pathogenesis of Hepatitis C Virus Infection
Viruses 2012, 4(10), 2016-2030; doi:10.3390/v4102016
Received: 2 August 2012 / Revised: 28 September 2012 / Accepted: 28 September 2012 / Published: 9 October 2012
Cited by 12 | PDF Full-text (1116 KB) | HTML Full-text | XML Full-text
Abstract
Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. The interplay between the virus and host innate and adaptive immune responses determines the outcome of infection. There is increasing evidence that host neutralizing responses play a relevant role
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Hepatitis C virus (HCV) infection is a major cause of chronic liver disease worldwide. The interplay between the virus and host innate and adaptive immune responses determines the outcome of infection. There is increasing evidence that host neutralizing responses play a relevant role in the resulting pathogenesis. Furthermore, viral evasion from host neutralizing antibodies has been revealed to be an important contributor in leading both to viral persistence in acute liver graft infection following liver transplantation, and to chronic viral infection. The development of novel model systems to study HCV entry and neutralization has allowed a detailed understanding of the molecular mechanisms of virus-host interactions during antibody-mediated neutralization. The understanding of these mechanisms will ultimately contribute to the development of novel antiviral preventive strategies for liver graft infection and an urgently needed vaccine. This review summarizes recent concepts of the role of neutralizing antibodies in viral clearance and protection, and highlights consequences of viral escape from neutralizing antibodies in the pathogenesis of HCV infection. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Human Leukocyte Antigen (HLA) Class I Down-Regulation by Human Immunodeficiency Virus Type 1 Negative Factor (HIV-1 Nef): What Might We Learn From Natural Sequence Variants?
Viruses 2012, 4(9), 1711-1730; doi:10.3390/v4091711
Received: 31 August 2012 / Revised: 18 September 2012 / Accepted: 21 September 2012 / Published: 24 September 2012
Cited by 10 | PDF Full-text (3083 KB) | HTML Full-text | XML Full-text | Correction | Supplementary Files
Abstract
HIV-1 causes a chronic infection in humans that is characterized by high plasma viremia, progressive loss of CD4+ T lymphocytes, and severe immunodeficiency resulting in opportunistic disease and AIDS. Viral persistence is mediated in part by the ability of the Nef protein to
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HIV-1 causes a chronic infection in humans that is characterized by high plasma viremia, progressive loss of CD4+ T lymphocytes, and severe immunodeficiency resulting in opportunistic disease and AIDS. Viral persistence is mediated in part by the ability of the Nef protein to down-regulate HLA molecules on the infected cell surface, thereby allowing HIV-1 to evade recognition by antiviral CD8+ T lymphocytes. Extensive research has been conducted on Nef to determine protein domains that are required for its immune evasion activities and to identify critical cellular co-factors, and our mechanistic understanding of this process is becoming more complete. This review highlights our current knowledge of Nef-mediated HLA class I down-regulation and places this work in the context of naturally occurring sequence variation in this protein. We argue that efforts to fully understand the critical role of Nef for HIV-1 pathogenesis will require greater analysis of patient-derived sequences to elucidate subtle differences in immune evasion activity that may alter clinical outcome. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Neutralization Interfering Antibodies: A “Novel” Example of Humoral Immune Dysfunction Facilitating Viral Escape?
Viruses 2012, 4(9), 1731-1752; doi:10.3390/v4091731
Received: 2 August 2012 / Revised: 1 September 2012 / Accepted: 17 September 2012 / Published: 24 September 2012
Cited by 16 | PDF Full-text (825 KB) | HTML Full-text | XML Full-text
Abstract
The immune response against some viral pathogens, in particular those causing chronic infections, is often ineffective notwithstanding a robust humoral neutralizing response. Several evasion mechanisms capable of subverting the activity of neutralizing antibodies (nAbs) have been described. Among them, the elicitation of non-neutralizing
[...] Read more.
The immune response against some viral pathogens, in particular those causing chronic infections, is often ineffective notwithstanding a robust humoral neutralizing response. Several evasion mechanisms capable of subverting the activity of neutralizing antibodies (nAbs) have been described. Among them, the elicitation of non-neutralizing and interfering Abs has been hypothesized. Recently, this evasion mechanism has acquired an increasing interest given its possible impact on novel nAb-based antiviral therapeutic and prophylactic approaches. In this review, we illustrate the mechanisms of Ab-mediated interference and the viral pathogens described in literature as able to adopt this “novel” evasion strategy. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Evasion of Influenza A Viruses from Innate and Adaptive Immune Responses
Viruses 2012, 4(9), 1438-1476; doi:10.3390/v4091438
Received: 3 July 2012 / Revised: 10 August 2012 / Accepted: 22 August 2012 / Published: 3 September 2012
Cited by 40 | PDF Full-text (4444 KB) | HTML Full-text | XML Full-text
Abstract
The influenza A virus is one of the leading causes of respiratory tract infections in humans. Upon infection with an influenza A virus, both innate and adaptive immune responses are induced. Here we discuss various strategies used by influenza A viruses to evade
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The influenza A virus is one of the leading causes of respiratory tract infections in humans. Upon infection with an influenza A virus, both innate and adaptive immune responses are induced. Here we discuss various strategies used by influenza A viruses to evade innate immune responses and recognition by components of the humoral and cellular immune response, which consequently may result in reduced clearing of the virus and virus-infected cells. Finally, we discuss how the current knowledge about immune evasion can be used to improve influenza A vaccination strategies. Full article
(This article belongs to the Special Issue Immune Evasion)
Figures

Open AccessReview Herpesviruses Placating the Unwilling Host: Manipulation of the MHC Class II Antigen Presentation Pathway
Viruses 2012, 4(8), 1335-1353; doi:10.3390/v4081335
Received: 13 July 2012 / Revised: 14 August 2012 / Accepted: 15 August 2012 / Published: 22 August 2012
Cited by 10 | PDF Full-text (530 KB) | HTML Full-text | XML Full-text
Abstract
Lifelong persistent infection by herpesviruses depends on the balance between host immune responses and viral immune evasion. CD4 T cells responding to antigens presented on major histocompatibility complex class II (MHC-II) molecules are known to play an important role in controlling herpesvirus infections.
[...] Read more.
Lifelong persistent infection by herpesviruses depends on the balance between host immune responses and viral immune evasion. CD4 T cells responding to antigens presented on major histocompatibility complex class II (MHC-II) molecules are known to play an important role in controlling herpesvirus infections. Here we review, with emphasis on human herpesvirus infections, the strategies evolved to evade CD4 T cell immunity. These viruses target multiple points on the MHC class II antigen presentation pathway. The mechanisms include: suppression of CIITA to inhibit the synthesis of MHC class II molecules, diversion or degradation of HLA-DR molecules during membrane transport, and direct targeting of the invariant chain chaperone of HLA-DR. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Herpesvirus Exploitation of Host Immune Inhibitory Pathways
Viruses 2012, 4(8), 1182-1201; doi:10.3390/v4081182
Received: 29 June 2012 / Revised: 21 July 2012 / Accepted: 23 July 2012 / Published: 3 August 2012
Cited by 7 | PDF Full-text (311 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Herpesviruses employ a plethora of mechanisms to circumvent clearance by host immune responses. A key feature of mammalian immune systems is the employment of regulatory pathways that limit immune responsiveness. The primary functions of these mechanisms are to control autoimmunity and limit exuberant
[...] Read more.
Herpesviruses employ a plethora of mechanisms to circumvent clearance by host immune responses. A key feature of mammalian immune systems is the employment of regulatory pathways that limit immune responsiveness. The primary functions of these mechanisms are to control autoimmunity and limit exuberant responses to harmless antigen in mucosal surfaces. However, such pathways can be exploited by viral pathogens to enable acute infection, persistence and dissemination. Herein, we outline the current understanding of inhibitory pathways in modulating antiviral immunity during herpesvirus infections in vivo and discuss strategies employed by herpesviruses to exploit these pathways to limit host antiviral immunity. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview T Cell Memory in the Context of Persistent Herpes Viral Infections
Viruses 2012, 4(7), 1116-1143; doi:10.3390/v4071116
Received: 4 July 2012 / Revised: 18 July 2012 / Accepted: 19 July 2012 / Published: 20 July 2012
Cited by 14 | PDF Full-text (738 KB) | HTML Full-text | XML Full-text
Abstract
The generation of a functional memory T cell pool upon primary encounter with an infectious pathogen is, in combination with humoral immunity, an essential process to confer protective immunity against reencounters with the same pathogen. A prerequisite for the generation and maintenance of
[...] Read more.
The generation of a functional memory T cell pool upon primary encounter with an infectious pathogen is, in combination with humoral immunity, an essential process to confer protective immunity against reencounters with the same pathogen. A prerequisite for the generation and maintenance of long-lived memory T cells is the clearance of antigen after infection, which is fulfilled upon resolution of acute viral infections. Memory T cells play also a fundamental role during persistent viral infections by contributing to relative control and immuosurveillance of active replication or viral reactivation, respectively. However, the dynamics, the phenotype, the mechanisms of maintenance and the functionality of memory T cells which develop upon acute/resolved infection as opposed to chronic/latent infection differ substantially. In this review we summarize current knowledge about memory CD8 T cell responses elicited during α-, β-, and γ-herpes viral infections with major emphasis on the induction, maintenance and function of virus-specific memory CD8 T cells during viral latency and we discuss how the peculiar features of these memory CD8 T cell responses are related to the biology of these persistently infecting viruses. Full article
(This article belongs to the Special Issue Immune Evasion)
Open AccessReview Immune Evasion Strategies of Ranaviruses and Innate Immune Responses to These Emerging Pathogens
Viruses 2012, 4(7), 1075-1092; doi:10.3390/v4071075
Received: 22 May 2012 / Revised: 19 June 2012 / Accepted: 20 June 2012 / Published: 28 June 2012
Cited by 22 | PDF Full-text (1314 KB) | HTML Full-text | XML Full-text
Abstract
Ranaviruses (RV, Iridoviridae) are large double-stranded DNA viruses that infect fish, amphibians and reptiles. For ecological and commercial reasons, considerable attention has been drawn to the increasing prevalence of ranaviral infections of wild populations and in aquacultural settings. Importantly, RVs appear to
[...] Read more.
Ranaviruses (RV, Iridoviridae) are large double-stranded DNA viruses that infect fish, amphibians and reptiles. For ecological and commercial reasons, considerable attention has been drawn to the increasing prevalence of ranaviral infections of wild populations and in aquacultural settings. Importantly, RVs appear to be capable of crossing species barriers of numerous poikilotherms, suggesting that these pathogens possess a broad host range and potent immune evasion mechanisms. Indeed, while some of the 95–100 predicted ranavirus genes encode putative evasion proteins (e.g., vIFα, vCARD), roughly two-thirds of them do not share significant sequence identity with known viral or eukaryotic genes. Accordingly, the investigation of ranaviral virulence and immune evasion strategies is promising for elucidating potential antiviral targets. In this regard, recombination-based technologies are being employed to knock out gene candidates in the best-characterized RV member, Frog Virus (FV3). Concurrently, by using animal infection models with extensively characterized immune systems, such as the African clawed frog, Xenopus laevis, it is becoming evident that components of innate immunity are at the forefront of virus-host interactions. For example, cells of the macrophage lineage represent important combatants of RV infections while themselves serving as targets for viral infection, maintenance and possibly dissemination. This review focuses on the recent advances in the understanding of the RV immune evasion strategies with emphasis on the roles of the innate immune system in ranaviral infections. Full article
(This article belongs to the Special Issue Immune Evasion)

Other

Jump to: Research, Review

Open AccessCorrection Brockman, M.A., et al., Human Leukocyte Antigen (HLA) Class I Down-Regulation by Human Immunodeficiency Virus Type 1 Negative Factor (HIV-1 Nef): What Might We Learn From Natural Sequence Variants? Viruses 2012, 4, 1711-1730
Viruses 2012, 4(10), 2014-2015; doi:10.3390/v4102014
Received: 4 October 2012 / Revised: 5 October 2012 / Accepted: 5 October 2012 / Published: 5 October 2012
Cited by 1 | PDF Full-text (386 KB) | HTML Full-text | XML Full-text
Abstract In the original manuscript, the text in figure 1 is illegible. Furthermore, there is an unnecessary carriage return (page 1716, ~line 18) "crystallographic ... methods". [...] Full article
(This article belongs to the Special Issue Immune Evasion)
Figures

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