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HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
by
Mota, Talia M.
, Jones, R. Brad
in
Adult T cell leukemia
/ Antigens
/ Asymptomatic
/ ATL (adult T-cell leukemia)
/ Cancer
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ Cell cycle
/ Cloning
/ DNA methylation
/ Epigenetics
/ Equilibrium
/ Genomes
/ HIV
/ HIV Infections - immunology
/ HIV Infections - virology
/ HIV-1 - immunology
/ HIV-1 - physiology
/ Host-Pathogen Interactions - immunology
/ HTLV-1
/ Human immunodeficiency virus
/ Human T-lymphotropic virus 1 - immunology
/ Human T-lymphotropic virus 1 - physiology
/ Humans
/ Immune response
/ Immune system
/ immunoediting
/ Immunology
/ Infections
/ Latency
/ Leukemia
/ Leukemia-Lymphoma, Adult T-Cell - immunology
/ Leukemia-Lymphoma, Adult T-Cell - virology
/ Lymphocytes
/ Lymphocytes T
/ Lymphoma
/ Malignancy
/ Models, Immunological
/ Mutation
/ Neoplasms - immunology
/ Neoplasms - virology
/ Peptides
/ Protein expression
/ Proteins
/ T-Lymphocytes, Cytotoxic - immunology
/ T-Lymphocytes, Cytotoxic - virology
/ Tumor cells
/ viral reservoir
/ Virus Replication - immunology
/ Virus Replication - physiology
/ Viruses
2019
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HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
by
Mota, Talia M.
, Jones, R. Brad
in
Adult T cell leukemia
/ Antigens
/ Asymptomatic
/ ATL (adult T-cell leukemia)
/ Cancer
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ Cell cycle
/ Cloning
/ DNA methylation
/ Epigenetics
/ Equilibrium
/ Genomes
/ HIV
/ HIV Infections - immunology
/ HIV Infections - virology
/ HIV-1 - immunology
/ HIV-1 - physiology
/ Host-Pathogen Interactions - immunology
/ HTLV-1
/ Human immunodeficiency virus
/ Human T-lymphotropic virus 1 - immunology
/ Human T-lymphotropic virus 1 - physiology
/ Humans
/ Immune response
/ Immune system
/ immunoediting
/ Immunology
/ Infections
/ Latency
/ Leukemia
/ Leukemia-Lymphoma, Adult T-Cell - immunology
/ Leukemia-Lymphoma, Adult T-Cell - virology
/ Lymphocytes
/ Lymphocytes T
/ Lymphoma
/ Malignancy
/ Models, Immunological
/ Mutation
/ Neoplasms - immunology
/ Neoplasms - virology
/ Peptides
/ Protein expression
/ Proteins
/ T-Lymphocytes, Cytotoxic - immunology
/ T-Lymphocytes, Cytotoxic - virology
/ Tumor cells
/ viral reservoir
/ Virus Replication - immunology
/ Virus Replication - physiology
/ Viruses
2019
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HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
by
Mota, Talia M.
, Jones, R. Brad
in
Adult T cell leukemia
/ Antigens
/ Asymptomatic
/ ATL (adult T-cell leukemia)
/ Cancer
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ Cell cycle
/ Cloning
/ DNA methylation
/ Epigenetics
/ Equilibrium
/ Genomes
/ HIV
/ HIV Infections - immunology
/ HIV Infections - virology
/ HIV-1 - immunology
/ HIV-1 - physiology
/ Host-Pathogen Interactions - immunology
/ HTLV-1
/ Human immunodeficiency virus
/ Human T-lymphotropic virus 1 - immunology
/ Human T-lymphotropic virus 1 - physiology
/ Humans
/ Immune response
/ Immune system
/ immunoediting
/ Immunology
/ Infections
/ Latency
/ Leukemia
/ Leukemia-Lymphoma, Adult T-Cell - immunology
/ Leukemia-Lymphoma, Adult T-Cell - virology
/ Lymphocytes
/ Lymphocytes T
/ Lymphoma
/ Malignancy
/ Models, Immunological
/ Mutation
/ Neoplasms - immunology
/ Neoplasms - virology
/ Peptides
/ Protein expression
/ Proteins
/ T-Lymphocytes, Cytotoxic - immunology
/ T-Lymphocytes, Cytotoxic - virology
/ Tumor cells
/ viral reservoir
/ Virus Replication - immunology
/ Virus Replication - physiology
/ Viruses
2019
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HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
Journal Article
HTLV-1 as a Model for Virus and Host Coordinated Immunoediting
2019
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Overview
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.
Publisher
Frontiers Media SA,Frontiers Media S.A
Subject
/ Antigens
/ Cancer
/ CD4-Positive T-Lymphocytes - immunology
/ CD4-Positive T-Lymphocytes - virology
/ Cloning
/ Genomes
/ HIV
/ Host-Pathogen Interactions - immunology
/ HTLV-1
/ Human immunodeficiency virus
/ Human T-lymphotropic virus 1 - immunology
/ Human T-lymphotropic virus 1 - physiology
/ Humans
/ Latency
/ Leukemia
/ Leukemia-Lymphoma, Adult T-Cell - immunology
/ Leukemia-Lymphoma, Adult T-Cell - virology
/ Lymphoma
/ Mutation
/ Peptides
/ Proteins
/ T-Lymphocytes, Cytotoxic - immunology
/ T-Lymphocytes, Cytotoxic - virology
/ Virus Replication - immunology
/ Virus Replication - physiology
/ Viruses
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