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Citation: Jean-Michel Claverie, Chantal Abergel. CRISPR-Cas-like system in giant viruses: why MIMIVIRE is not likely to be an adaptive immune system [J].VIROLOGICA SINICA, 2016, 31(3) : 193-196.  http://dx.doi.org/10.1007/s12250-016-3801-x

CRISPR-Cas-like system in giant viruses: why MIMIVIRE is not likely to be an adaptive immune system

  • Giant viruses from the Mimiviridae family (Mimivirus, Megavirus, etc.) replicate inside their Acanthamoeba host by the mean of a large intracytoplasmic virion factory within which DNA transcription and replication take place using the virus encoded machineries. Members of the Mimiviridae have been isolated in association with much smaller dsDNA viruses called "virophages" that replicate within the virion factory, behaving as parasites of the giant virus. In a recent work Levasseur et al. (2016) used a silencing approach to identify candidate genes possibly involved in the inhibition of the Zamilon virophage in a specific clade of Mimiviridae. Based on the presence of four copies of a short Zamilon sequence in one of the Mimivirus candidate gene, the authors proposed that resistance to virophages was conferred by a CRISPR-Cas-like system (called MIMIVIRE). Here we dispute this interpretation on the ground that 1) the simultaneous and co-localized replication of the virophage and Mimivirus genomes makes the acquisition of a nucleic acid-based immunity unlikely, 2) the Zamilonlike sequence allegedly acquired by Mimivirus are neither regularly spaced nor flanked by recognizable repeats, 3) the corresponding Zamilon sequence is devoid of distinct flanking sequences that may serve as Protospacer Adjacent Motifs (PAM) discriminating between the virophage and its host. We propose a simpler protein-based interaction model that explains the observed phenomena without having to extend the realm of adaptive immunity to the world of eukaryotic viruses, a revolutionary step that would require stronger experimental evidences.

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    CRISPR-Cas-like system in giant viruses: why MIMIVIRE is not likely to be an adaptive immune system

    Abstract: Giant viruses from the Mimiviridae family (Mimivirus, Megavirus, etc.) replicate inside their Acanthamoeba host by the mean of a large intracytoplasmic virion factory within which DNA transcription and replication take place using the virus encoded machineries. Members of the Mimiviridae have been isolated in association with much smaller dsDNA viruses called "virophages" that replicate within the virion factory, behaving as parasites of the giant virus. In a recent work Levasseur et al. (2016) used a silencing approach to identify candidate genes possibly involved in the inhibition of the Zamilon virophage in a specific clade of Mimiviridae. Based on the presence of four copies of a short Zamilon sequence in one of the Mimivirus candidate gene, the authors proposed that resistance to virophages was conferred by a CRISPR-Cas-like system (called MIMIVIRE). Here we dispute this interpretation on the ground that 1) the simultaneous and co-localized replication of the virophage and Mimivirus genomes makes the acquisition of a nucleic acid-based immunity unlikely, 2) the Zamilonlike sequence allegedly acquired by Mimivirus are neither regularly spaced nor flanked by recognizable repeats, 3) the corresponding Zamilon sequence is devoid of distinct flanking sequences that may serve as Protospacer Adjacent Motifs (PAM) discriminating between the virophage and its host. We propose a simpler protein-based interaction model that explains the observed phenomena without having to extend the realm of adaptive immunity to the world of eukaryotic viruses, a revolutionary step that would require stronger experimental evidences.