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Related Concept Videos

Immunodeficiency Diseases01:25

Immunodeficiency Diseases

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Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
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Cytomegalovirus Disease01:27

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Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
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Development of Immunocompetence01:22

Development of Immunocompetence

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The initiation of cell-mediated immunity can be observed as early as the third month of fetal growth, with active antibody-mediated immunity following approximately one month later.
The initial cells that migrate from the fetal thymus settle within the skin and epithelial tissues lining the mouth, digestive tract, and in females, the uterus and vagina. These cells, including skin-based dendritic cells, serve as antigen-presenting cells, playing a key role in T cell activation.
Subsequent T...
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Pulmonary Tuberculosis I01:29

Pulmonary Tuberculosis I

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Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
Causative Organism
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Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
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Separation of Immune Cell Subpopulations in Peripheral Blood Samples from Children with Infectious Mononucleosis
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Primary Immunodeficiencies Associated with EBV Disease.

Jeffrey I Cohen1

  • 1Medical Virology Section, Laboratory of Infectious Diseases, National Institutes of Health, 50 South Drive, MSC 8007, Bethesda, MD, 20892, USA. jcohen@niaid.nih.gov.

Current Topics in Microbiology and Immunology
|October 2, 2015
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Summary
This summary is machine-generated.

Understanding Epstein-Barr virus (EBV) control involves studying genetic disorders affecting T and NK cell functions. Identifying key proteins in EBV-infected B cell interactions may reveal new immunosuppressive therapy targets.

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Epstein-Barr virus (EBV) infects most humans, typically asymptomatically or causing infectious mononucleosis in young adults.
  • EBV-infected B cells are primarily controlled by Natural Killer (NK) cells, invariant Natural Killer T (iNKT) cells, CD4 T cells, and CD8 T cells.
  • While B cell mutations don't cause severe EBV, certain genetic disorders impacting T and NK cell function lead to uncontrolled EBV without increased susceptibility to other viruses.

Purpose of the Study:

  • To investigate the genetic basis of EBV control and severe EBV-associated diseases.
  • To identify critical proteins involved in T and NK cell interactions with EBV-infected B cells.
  • To explore potential therapeutic targets for EBV-related conditions.

Main Methods:

  • Analysis of genetic disorders affecting T and NK cell function.
  • Review of mutations associated with hemophagocytic lymphohistiocytosis (HLH) and severe chronic active EBV disease.
  • Examination of immunodeficiencies predisposing to severe EBV and other infections.

Main Results:

  • Mutations in genes like SH2D1A, BIRC4, ITK, CD27, MAGT1, CORO1A, and LRBA impair EBV control but not general viral immunity.
  • Mutations in HLH-associated genes (PRF1, STXBP2, UNC13D) can lead to severe chronic active EBV disease.
  • Other immunodeficiencies (e.g., due to PIK3CD, CTPS1, GATA2 mutations) and severe combined immunodeficiency (SCID) increase susceptibility to severe EBV, other infections, and EBV-associated lymphomas.

Conclusions:

  • EBV is unique in inducing B cell proliferation, making its study crucial for understanding T/NK-B cell interactions.
  • Identifying proteins critical for EBV control can inform the development of novel immunosuppressive therapies.
  • Understanding these genetic underpinnings is vital for managing EBV-related complications and immunodeficiencies.