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.
Subject(s)
Interferon Type I/immunology , Leukocytes, Mononuclear/immunology , Leukocytes, Mononuclear/virology , Mimiviridae/immunology , Mimiviridae/pathogenicity , Cells, Cultured , Humans , Interferon Regulatory Factors/metabolism , Interferon Type I/pharmacology , Mimiviridae/drug effects , STAT Transcription Factors/metabolism , Virus Replication/drug effectsABSTRACT
BACKGROUND: Acanthamoeba polyphaga mimivirus (APMV), the largest known virus, has been studied as a putative pneumonia agent, especially in hospital environments. Despite the repercussions of the discovery of APMV, there has been no study related to the control of APMV and the susceptibility of this virus to disinfectants. OBJECTIVES: This work investigated the virucidal activity against mimivirus of chemical biocides commonly used in clinical practice for the disinfection of hospital equipment and rooms. STUDY DESIGN: APMV was dried on sterilized steel coupons, exposed to different concentrations of alcohols (ethanol, 1-propanol and 2-propanol) and commercial disinfectants (active chlorine, glutaraldehyde and benzalkonium chloride) and titrated in amoebas using the TCID50 value. The stability of APMV on an inanimate surface was also tested in the presence and absence of organic matter for 30 days. RESULTS: APMV showed a high level of resistance to chemical biocides, especially alcohols. Only active chlorine and glutaraldehyde were able to decrease the APMV titers to undetectable levels. Dried APMV showed long-lasting stability on an inanimate surface (30 days), even in the absence of organic matter. CONCLUSIONS: The data presented herein may help health and laboratory workers plan the best strategy to control this putative pneumonia agent from surfaces and devices.
