A resourceful giant: APMV is able to interfere with the human type I interferon system
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Updated: May 5, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Lorena C F Silva1, Gabriel M F Almeida1, Danilo B Oliveira1
1Universidade Federal de Minas Gerais, Instituto de Ciências Biológicas, Laboratório de Vírus, Belo Horizonte, Minas Gerais, Brazil.
Abstract:
Acanthamoeba polyphaga mimivirus (APMV) is a giant, double-stranded virus of the Mimiviridae family that was discovered in 2003. Recent studies have shown that this virus is able to replicate in murine and human phagocytes and might be considered a putative human pathogen that causes pneumonia. However, there is little data regarding APMV and its host defense relationship. In the present study, we investigated how some components of the interferon (IFN) system are stimulated by APMV in human peripheral blood mononuclear cells (PBMCs) and how APMV replication is affected by IFN treatment. Our results demonstrated that APMV is able to replicate in human PBMCs, inducing type I Interferons (IFNs) but inhibiting interferon stimulated genes (ISG) induction by viroceptor and STAT-1 and STAT-2 dephosphorylation independent mechanisms. We also showed that APMV is resistant to the antiviral action of interferon-alpha2 (IFNA2) but is sensitive to the antiviral action of interferon-beta (IFNB1). Our results demonstrated the productive infection of professional phagocytes with APMV and showed that this virus is recognized by the immune system of vertebrates and inhibits it. It provides the first data regarding APMV and the IFN system interaction and raise new and relevant evolutional questions about the relationship between APMV and vertebrate hosts.
Insights
Acanthamoeba polyphaga mimivirus (APMV) infects human cells and triggers type I interferons (IFNs). However, APMV inhibits interferon-stimulated genes, showing resistance to IFNA2 but sensitivity to IFNB1.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Acanthamoeba polyphaga mimivirus (APMV), a giant virus, replicates in human phagocytes and may cause pneumonia.
- Limited data exists on APMV's interaction with host defense mechanisms, particularly the interferon (IFN) system.
Purpose of the Study:
- To investigate how APMV stimulates the IFN system in human peripheral blood mononuclear cells (PBMCs).
- To determine the effect of IFN treatment on APMV replication.
- To elucidate APMV's host-pathogen interaction within the vertebrate immune system.
Main Methods:
- Culturing human PBMCs and infecting them with APMV.
- Measuring type I IFN induction and interferon-stimulated genes (ISGs) expression.
- Assessing APMV replication under different IFN treatments (IFN-alpha2 and IFN-beta1).
Main Results:
- APMV replicates productively in human PBMCs, inducing type I IFNs.
- APMV inhibits ISG induction via mechanisms independent of STAT-1/STAT-2 dephosphorylation.
- APMV is resistant to IFN-alpha2 but sensitive to IFN-beta1's antiviral effects.
Conclusions:
- APMV is recognized by and actively inhibits the vertebrate immune system, specifically the IFN response.
- This study provides the first insights into APMV-IFN system interactions.
- Findings raise evolutionary questions regarding APMV and vertebrate host relationships.
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