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HTLV-1 as a Model for Virus and Host Coordinated Immunoediting

Immunoediting is a process that occurs in cancer, whereby the immune system acts to initially repress, and subsequently promote the outgrowth of tumor cells through the stages of elimination, equilibrium, and escape. Here we present a model for a virus that causes cancer where immunoediting is coord...

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Detalles Bibliográficos
Autores principales: Mota, Talia M., Jones, R. Brad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768981/
https://www.ncbi.nlm.nih.gov/pubmed/31616431
http://dx.doi.org/10.3389/fimmu.2019.02259
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author Mota, Talia M.
Jones, R. Brad
author_facet Mota, Talia M.
Jones, R. Brad
author_sort Mota, Talia M.
collection PubMed
description Immunoediting is a process that occurs in cancer, whereby the immune system acts to initially repress, and subsequently promote the outgrowth of tumor cells through the stages of elimination, equilibrium, and escape. Here we present a model for a virus that causes cancer where immunoediting is coordinated through synergistic viral- and host-mediated events. We argue that the initial viral replication process of the Human T cell leukemia virus type I (HTLV-1), which causes adult T cell leukemia/lymphoma (ATL) in ~5% of individuals after decades of latency, harmonizes with the host immune system to create a population of cells destined for malignancy. Furthermore, we explore the possibility for HIV to fit into this model of immunoediting, and propose a non-malignant escape phase for HIV-infected cells that persist beyond equilibrium.
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spelling pubmed-67689812019-10-15 HTLV-1 as a Model for Virus and Host Coordinated Immunoediting Mota, Talia M. Jones, R. Brad Front Immunol Immunology Immunoediting is a process that occurs in cancer, whereby the immune system acts to initially repress, and subsequently promote the outgrowth of tumor cells through the stages of elimination, equilibrium, and escape. Here we present a model for a virus that causes cancer where immunoediting is coordinated through synergistic viral- and host-mediated events. We argue that the initial viral replication process of the Human T cell leukemia virus type I (HTLV-1), which causes adult T cell leukemia/lymphoma (ATL) in ~5% of individuals after decades of latency, harmonizes with the host immune system to create a population of cells destined for malignancy. Furthermore, we explore the possibility for HIV to fit into this model of immunoediting, and propose a non-malignant escape phase for HIV-infected cells that persist beyond equilibrium. Frontiers Media S.A. 2019-09-24 /pmc/articles/PMC6768981/ /pubmed/31616431 http://dx.doi.org/10.3389/fimmu.2019.02259 Text en Copyright © 2019 Mota and Jones. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Mota, Talia M.
Jones, R. Brad
HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title_full HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title_fullStr HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title_full_unstemmed HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title_short HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
title_sort htlv-1 as a model for virus and host coordinated immunoediting
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6768981/
https://www.ncbi.nlm.nih.gov/pubmed/31616431
http://dx.doi.org/10.3389/fimmu.2019.02259
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