Viral immune evasion: a masterpiece of evolution

Vossen, Mireille T. M.; Westerhout, Ellen M.; Söderberg‐Nauclér, Cecilia; Wiertz, Emmanuel J. H. J.

doi:10.1007/s00251-002-0493-1

Cited by 224 publications

(183 citation statements)

References 191 publications

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“…Immune evasion mechanisms are frequently found in virus-infected cells and tumor cells and allow them to escape from CTLmediated immune control (8,9,14,15). One of the most frequently observed mechanisms is impairment at the bottleneck: the peptide transporter TAP that delivers peptides into the ER for loading onto MHC class I molecules (45).…”

Section: Discussionmentioning

confidence: 99%

“…An important complication in this respect is the finding that viruses and tumors display diverse mechanisms by which they can evade CTL responses. Viruses that cause lifelong persistence in the host, such as the herpesviruses EBV, CMV, varicella-zoster virus, and HSV, especially have developed sophisticated immune evasion strategies (8,9). Reactivation of these viruses is a clinical problem in immune-compromised patients, illustrating the delicate balance between viral persistence and elimination by the CTL immune system.…”

Section: Regulates the Presentation Of Ctl Epitopes By Qa-1 B1mentioning

confidence: 99%

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The Varicellovirus-Encoded TAP Inhibitor UL49.5 Regulates the Presentation of CTL Epitopes by Qa-1b1

Hall

Laban

Koppers-Lalić

et al. 2007

The Journal of Immunology

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Impairment of MHC class I Ag processing is a commonly observed mechanism that allows viruses and tumors to escape immune destruction by CTL. The peptide transporter TAP that is responsible for the delivery of MHC class I-binding peptides into the endoplasmic reticulum is a pivotal target of viral-immune evasion molecules, and expression of this transporter is frequently lost in advanced cancers. We recently described a novel population of CTL that intriguingly exhibits reactivity against such tumor-immune escape variants and that recognizes self-peptides emerging at the cell surface due to defects in the processing machinery. Investigations of this new type of CTL epitopes are hampered by the lack of an efficient inhibitor for peptide transport in mouse cells. In this article, we demonstrate that the varicellovirus protein UL49.5, in contrast to ICP47 and US6, strongly impairs the activity of the mouse transporter and mediates degradation of mouse TAP1 and TAP2. Inhibition of TAP was witnessed by a strong reduction of surface MHC class I display and a decrease in recognition of conventional tumor-specific CTL. Analysis of CTL reactivity through the nonclassical molecule Qa-1b revealed that the presentation of the predominant leader peptide was inhibited. Interestingly, expression of UL49.5 in processing competent tumor cells induced the presentation of the new category of peptides. Our data show that the varicellovirus UL49.5 protein is a universal TAP inhibitor that can be exploited for preclinical studies on CTL-based immune intervention.

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Section: Discussionmentioning

confidence: 99%

Section: Regulates the Presentation Of Ctl Epitopes By Qa-1 B1mentioning

confidence: 99%

The Varicellovirus-Encoded TAP Inhibitor UL49.5 Regulates the Presentation of CTL Epitopes by Qa-1b1

Hall

Laban

Koppers-Lalić

et al. 2007

The Journal of Immunology

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“…Alphaherpesviruses, like other herpesviruses, are able to interfere with the host's innate and adaptative immune responses. A growing list of immune evasion mechanisms is described [139], such as, for example, inhibition of TAP proteins [66] or Fc receptor activity of viral glycoproteins [43].…”

Section: Pathogenesis and Clinical Signsmentioning

confidence: 99%

Ruminant alphaherpesviruses related to bovine herpesvirus 1

et al. 2006

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-Herpesviruses have mainly co-evolved with their hosts for millions of years. Consequently, different related host species may have been infected by various genetically related herpesviruses. Illustrating this concept, several ruminant alphaherpesviruses have been shown to form a cluster of viruses closely related to bovine herpesvirus 1 (BoHV-1): namely bovine herpesvirus 5, bubaline herpesvirus 1, caprine herpesvirus 1, cervid herpesviruses 1 and 2 and elk herpesvirus 1. These viruses share common antigenic properties and the serological relationships between them can be considered as a threat to BoHV-1 eradication programmes. BoHV-1 is a herpesvirus responsible for infectious bovine rhinotracheitis, which is a disease of major economic concern. In this article, the genetic properties of these ruminant alphaherpesviruses are reviewed on a comparative basis and the issue of interspecific recombination is assessed. The pathogenesis of these infections is described with emphasis on the host range and crossing of the host species barrier. Indeed, the non bovine ruminant species susceptible to these ruminant alphaherpesviruses may be potential BoHV-1 reservoirs. The differential diagnosis of these related infections is also discussed. In addition, available epidemiological data are used to assess the potential of cross-infection in ruminant populations. A better knowledge of these ruminant alphaherpesvirus infections is essential to successfully control infectious bovine rhinotracheitis.

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“…Similar rapid, dynamic, tightly coupled co-evolution of pathogen surface properties with the immunoglobulin repertoire of the host has since been found in viruses (e.g. HIV and herpesvirus) [124,125], other protists (e.g. Plasmodium) and parasitic worms (e.g.…”

Section: The Range Of Issues (A) Medically Significant Genetic Variationmentioning

confidence: 99%

Evolutionary medicine: its scope, interest and potential

2012

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This review is aimed at readers seeking an introductory overview, teaching courses and interested in visionary ideas. It first describes the range of topics covered by evolutionary medicine, which include human genetic variation, mismatches to modernity, reproductive medicine, degenerative disease, hostpathogen interactions and insights from comparisons with other species. It then discusses priorities for translational research, basic research and health management. Its conclusions are that evolutionary thinking should not displace other approaches to medical science, such as molecular medicine and cell and developmental biology, but that evolutionary insights can combine with and complement established approaches to reduce suffering and save lives. Because we are on the cusp of so much new research and innovative insights, it is hard to estimate how much impact evolutionary thinking will have on medicine, but it is already clear that its potential is enormous.

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Viral immune evasion: a masterpiece of evolution

Cited by 224 publications

References 191 publications

The Varicellovirus-Encoded TAP Inhibitor UL49.5 Regulates the Presentation of CTL Epitopes by Qa-1b1

The Varicellovirus-Encoded TAP Inhibitor UL49.5 Regulates the Presentation of CTL Epitopes by Qa-1b1

Ruminant alphaherpesviruses related to bovine herpesvirus 1

Evolutionary medicine: its scope, interest and potential

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