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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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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.
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Immune Surveillance by NK Cells and Phagocytes01:25

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Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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Intralumenal Vesicles and Multivesicular Bodies01:38

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Intraluminal vesicles (ILVs) are small vesicles 50-80 nm in diameter formed during the maturation of early endosomes. A specialized endosome containing numerous ILVs is called a multivesicular body (MVB). ILVs contain internalized molecules such as antigens, nucleic acids, proteins, and metabolites. Some of these molecules are released from the MVBs inside exosomes and are transported to other cells. Other MVBs contain molecules that are retained in the ILVs and are later degraded within the...
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Antigen Processing Pathways

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MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
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Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
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Related Experiment Video

Updated: Feb 16, 2026

Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV
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Identifying Dysregulated Genes Induced by Kaposi's Sarcoma-associated Herpesvirus KSHV

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Extracellular vesicles from KSHV-infected endothelial cells activate the complement system.

Hyungtaek Jeon1, Seung-Min Yoo1, Hyo Sun Choi2

  • 1Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon, South Korea.

Oncotarget
|December 17, 2017
PubMed
Summary

Extracellular vesicles (EVs) from Kaposi's sarcoma-associated herpesvirus (KSHV)-infected cells activate the complement system. This activation promotes KSHV latent infection by enhancing cell survival.

Keywords:
KSHValternative complement pathwaycomplement systemendothelial cellsextracellular vesicles

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Establishment and Quantification of De Novo Lytic Infection by Cell-free Kaposi's Sarcoma-Associated Herpesvirus

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Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Extracellular vesicles (EVs) mediate cell-to-cell communication and share similarities with viruses.
  • Virus-infected cells release EVs, but separating them from viruses is challenging.
  • Understanding virus-induced EVs is crucial for viral infection and pathogenesis research.

Purpose of the Study:

  • To isolate and characterize EVs from *de novo* Kaposi's sarcoma-associated herpesvirus (KSHV)-infected human endothelial cells.
  • To investigate the role of these EVs in complement system activation.
  • To elucidate the mechanism by which EVs influence KSHV infection.

Main Methods:

  • Isolation of EVs from KSHV-infected endothelial cells.
  • Proteomic analysis of isolated EVs.
  • Functional assays to assess complement activation and pathway involvement.
  • Investigation of downstream signaling pathways (e.g., NF-κB).

Main Results:

  • Successful isolation of EVs from *de novo* KSHV-infected endothelial cells.
  • Proteomics revealed alterations in the complement system within these EVs.
  • EVs potently activated the alternative complement pathway using C3 and properdin.
  • Complement activation promoted KSHV latent infection via NF-κB signaling, enhancing cell survival and inhibiting viral lytic replication.

Conclusions:

  • EVs induced during *de novo* KSHV infection play a novel role in viral pathogenesis.
  • These EVs activate the complement system, contributing to persistent KSHV infection.
  • The findings reveal a new mechanism linking EVs, complement activation, and viral persistence.