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Related Concept Videos

Complement System01:27

Complement System

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 membrane...
Antimicrobial Proteins01:23

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
Smallpox01:24

Smallpox

Smallpox is a severe contagious disease caused by the Variola major virus, a double-stranded DNA member of the Poxviridae family.Variola major transmission occurs primarily via inhalation of virus-laden droplets or direct contact with infectious scabs. The incubation period averages approximately seven days, although it may range from 7 to 17 days depending on the inoculum and host factors.Clinically, the prodromal phase is marked by an abrupt onset of high fever, malaise, headache, and myalgia.
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

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
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview

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Isolation and Quantification of Zika Virus from Multiple Organs in a Mouse
10:31

Isolation and Quantification of Zika Virus from Multiple Organs in a Mouse

Published on: August 15, 2019

Surviving mousepox infection requires the complement system.

Elizabeth A Moulton1, John P Atkinson, R Mark L Buller

  • 1Rheumatology Division, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Plos Pathogens
|December 30, 2008
PubMed
Summary
This summary is machine-generated.

The complement system is crucial for controlling poxvirus infections. Loss of complement component C3 in mice led to increased mortality and viral spread, highlighting complement

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Published on: November 1, 2015

Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Poxviruses employ immunomodulatory proteins to evade host immunity.
  • The ectromelia virus in mice serves as a model for studying poxvirus-host immune co-evolution.
  • The complement system is a key component of innate immunity with known antiviral functions.

Purpose of the Study:

  • To investigate the role of the complement system in poxvirus infection using the ectromelia virus mouse model.
  • To determine the impact of complement deficiency on viral dissemination, pathogenesis, and mortality.
  • To elucidate the specific complement pathways involved in antiviral defense against poxviruses.

Main Methods:

  • Utilized C57BL/6 mice with targeted deficiencies in complement components (C3, C4, Factor B).
  • Administered ectromelia virus via multiple inoculation routes to assess mortality and viral load.
  • Performed in vitro neutralization assays using mouse sera with varying complement pathway activities.
  • Analyzed viral dissemination, organ titers, hepatic inflammation, and necrosis.

Main Results:

  • Mice lacking C3 exhibited significantly increased mortality (7-10 days post-infection) and earlier viral dissemination.
  • Higher viral titers in target organs of C3-deficient mice correlated with increased hepatic inflammation and necrosis.
  • In vitro studies demonstrated that complement activation via classical and alternative pathways, along with natural antibodies, neutralizes ectromelia virus.
  • Deficiencies in C4 or Factor B also led to increased mortality, underscoring the importance of both pathways.

Conclusions:

  • The complement system provides essential early control of poxviral infections, bridging the gap until adaptive immunity develops.
  • Complement component C3 is critical for limiting viral replication and dissemination, thereby preventing lethal outcomes.
  • Both the classical and alternative complement pathways are required for effective host survival during ectromelia virus infection.