EBV Infection and Human Primary Immune Deficiencies

Epstein-Barr virus (EBV) is a ubiquitous virus that infects 95% of adults worldwide; the vast majority of persons have asymptomatic or non-specific primary infection and no complications associated with EBV during their lifetime. Some persons, particularly those who are infected as adolescents or yo...

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description Epstein-Barr virus (EBV) is a ubiquitous virus that infects 95% of adults worldwide; the vast majority of persons have asymptomatic or non-specific primary infection and no complications associated with EBV during their lifetime. Some persons, particularly those who are infected as adolescents or young adults, develop infectious mononucleosis. EBV infects resting B cells and infection in vitro results in transformation and continuous proliferation of the cells, whereas infection in vivo results in a latent infection in which proliferation of the cells is controlled by virus-specific T cells and NK cells. Certain persons have mutations in genes that result in impaired cellular immunity involving the function of cytotoxic T cells or NK cells that result in impaired responses and failure to control EBV. These persons are at risk for fulminant infectious mononucleosis, EBV-associated hemophagocytosis, EBV B or T cell lymphoma, or other opportunistic infections. These genes encode proteins that are important for a variety of NK and T cell activities: T cell interactions with B cells, NK and T cell activation, NK and T cell cytotoxicity, priming and expansion of virus-specific T cells, and control of T cell apoptosis. For most of these diseases, hematopoietic stem cell transplantation has been the only curative therapy. However, identification of certain immune deficiencies has led to new approaches to therapy such as drugs to inhibit overactive signaling pathways or supplemental magnesium for patients with mutations in a magnesium transporter. The study of these EBV-associated immune deficiencies identifies the importance of these proteins for the function of T and NK cells and may lead to novel approaches to therapy for EBV diseases.
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spelling doab-20.500.12854ir-737232024-03-31T13:11:05Z EBV Infection and Human Primary Immune Deficiencies Meyts, Isabelle Cohen, Jeffrey I. Epstein-Barr virus immune deficiency lymphoproliferative disease hemophagocytic lymphohistiocytosis B-cell lymphoma thema EDItEUR::M Medicine and Nursing thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCM Immunology Epstein-Barr virus (EBV) is a ubiquitous virus that infects 95% of adults worldwide; the vast majority of persons have asymptomatic or non-specific primary infection and no complications associated with EBV during their lifetime. Some persons, particularly those who are infected as adolescents or young adults, develop infectious mononucleosis. EBV infects resting B cells and infection in vitro results in transformation and continuous proliferation of the cells, whereas infection in vivo results in a latent infection in which proliferation of the cells is controlled by virus-specific T cells and NK cells. Certain persons have mutations in genes that result in impaired cellular immunity involving the function of cytotoxic T cells or NK cells that result in impaired responses and failure to control EBV. These persons are at risk for fulminant infectious mononucleosis, EBV-associated hemophagocytosis, EBV B or T cell lymphoma, or other opportunistic infections. These genes encode proteins that are important for a variety of NK and T cell activities: T cell interactions with B cells, NK and T cell activation, NK and T cell cytotoxicity, priming and expansion of virus-specific T cells, and control of T cell apoptosis. For most of these diseases, hematopoietic stem cell transplantation has been the only curative therapy. However, identification of certain immune deficiencies has led to new approaches to therapy such as drugs to inhibit overactive signaling pathways or supplemental magnesium for patients with mutations in a magnesium transporter. The study of these EBV-associated immune deficiencies identifies the importance of these proteins for the function of T and NK cells and may lead to novel approaches to therapy for EBV diseases. 2021-11-18T16:23:23Z 2021-11-18T16:23:23Z 2020 book ONIX_20211118_9782889635719_855 9782889635719 https://directory.doabooks.org/handle/20.500.12854/73723 eng image/jpeg Attribution 4.0 International https://www.frontiersin.org/research-topics/5995/ebv-infection-and-human-primary-immune-deficiencies https://www.frontiersin.org/research-topics/5995/ebv-infection-and-human-primary-immune-deficiencies Frontiers Media SA 10.3389/978-2-88963-571-9 10.3389/978-2-88963-571-9 bf5ce210-e72e-4860-ba9b-c305640ff3ae 9782889635719 132 open access
spellingShingle Epstein-Barr virus
immune deficiency
lymphoproliferative disease
hemophagocytic lymphohistiocytosis
B-cell lymphoma
thema EDItEUR::M Medicine and Nursing
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCM Immunology
EBV Infection and Human Primary Immune Deficiencies
title EBV Infection and Human Primary Immune Deficiencies
title_full EBV Infection and Human Primary Immune Deficiencies
title_fullStr EBV Infection and Human Primary Immune Deficiencies
title_full_unstemmed EBV Infection and Human Primary Immune Deficiencies
title_short EBV Infection and Human Primary Immune Deficiencies
title_sort ebv infection and human primary immune deficiencies
topic Epstein-Barr virus
immune deficiency
lymphoproliferative disease
hemophagocytic lymphohistiocytosis
B-cell lymphoma
thema EDItEUR::M Medicine and Nursing
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCM Immunology
topic_facet Epstein-Barr virus
immune deficiency
lymphoproliferative disease
hemophagocytic lymphohistiocytosis
B-cell lymphoma
thema EDItEUR::M Medicine and Nursing
thema EDItEUR::M Medicine and Nursing::MJ Clinical and internal medicine::MJC Diseases and disorders::MJCM Immunology
url ONIX_20211118_9782889635719_855