Ameobal pathogen mimivirus infects macrophages through phagocytosis

Mimivirus, or Acanthamoeba polyphaga mimivirus (APMV), a giant double-stranded DNA virus that grows in amoeba, was identified for the first time in 2003. Entry by phagocytosis within amoeba has been suggested but not demonstrated. We demonstrate here that APMV was internalized by macrophages but not...

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Bibliographic Details
Published in:PLoS pathogens 2008-06, Vol.4 (6), p.e1000087-e1000087
Main Authors: Ghigo, Eric, Kartenbeck, Jürgen, Lien, Pham, Pelkmans, Lucas, Capo, Christian, Mege, Jean-Louis, Raoult, Didier
Format: Article
Language:English
Subjects:
Acanthamoeba polyphaga
Amoeba
Amoeba - virology
Animals
Atoms & subatomic particles
Bacteria
Deoxyribonucleic acid
DNA
DNA viruses
DNA Viruses - pathogenicity
Dynamin II - physiology
Endocytosis
Experiments
Health aspects
Macrophages
Macrophages - virology
Microbiology
Microbiology/Microbial Evolution and Genomics
Phagocytosis
Physiological aspects
Pinocytosis
Proteins
Risk factors
Software
Virus diseases
Virus Internalization
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Summary:Mimivirus, or Acanthamoeba polyphaga mimivirus (APMV), a giant double-stranded DNA virus that grows in amoeba, was identified for the first time in 2003. Entry by phagocytosis within amoeba has been suggested but not demonstrated. We demonstrate here that APMV was internalized by macrophages but not by non-phagocytic cells, leading to productive APMV replication. Clathrin- and caveolin-mediated endocytosis pathways, as well as degradative endosome-mediated endocytosis, were not used by APMV to invade macrophages. Ultrastructural analysis showed that protrusions were formed around the entering virus, suggesting that macropinocytosis or phagocytosis was involved in APMV entry. Reorganization of the actin cytoskeleton and activation of phosphatidylinositol 3-kinases were required for APMV entry. Blocking macropinocytosis and the lack of APMV colocalization with rabankyrin-5 showed that macropinocytosis was not involved in viral entry. Overexpression of a dominant-negative form of dynamin-II, a regulator of phagocytosis, inhibited APMV entry. Altogether, our data demonstrated that APMV enters macrophages through phagocytosis, a new pathway for virus entry in cells. This reinforces the paradigm that intra-amoebal pathogens have the potential to infect macrophages.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1000087