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.
The International Committee on Taxonomy of Viruses (ICTV) has the decree to set the rules for the classification and naming of viruses. The species is the lowest level considered in the taxonomic hierarchy. In general, virus species are named according to the structure “ and the word ‘virus’”. A typical example is Tobacco mosaic virus [Genus: Tobamovirus]. With a few exceptions, this convention has been generally well accepted. As there is always room for improvement, virus nomenclature (King et al., 2011) can be managed more efficiently through several ways.
Infectious bursal disease virus (IBDV) causes infectious bursal disease, a highly contagious immunosuppressive disease that affects young chickens and causes economic losses in the poultry industry worldwide. IBDV replicates mainly in actively dividing B lymphocytes within the bursa of Fabricius (BF), leading to immunosuppression in affected flocks (Mahgoub et al., 2012). Viral protein 2 (VP2), the only structural component of the IBDV icosahedral capsid, is the major antigen responsible for inducing protective immunity in the host (Mahgoub et al., 2012).
In this study, multiplex PCR was used to amplify both the B2L gene partial coding region and a housekeeping gene. A substantial amount of research has been conducted on the B2L gene, and this presents opportunities for comparisons between different strains around the world. Field strains have been compared with human, sheep, and goat orf viruses and with other parapoxviruses such as PCPV and BPSV. Although the presence of the virus in Turkey was previously reported, its relationship with other orf viruses around the world has not yet been demonstrated, in contrast to parapoxvirus infections of cattle and humans in Turkey (Karakas et al., 2013; Oguzoglu et al., 2014). This study provides diagnostic and molecular characterization data for the economically damaging parapoxvirus infection that circulated among goat flocks in Turkey in the 2013–2014 lambing season.
Akabane virus (AKAV), an orthobunyavirus, is transmitted primarily by biting midges and is widely distributed throughout the world except the Europe. AKAV was first isolated from mosquitoes in Japan (Oya et al., 1961). Although pregnant cows, ewes, and goats infected with AKAV exhibit no clinical signs of disease, in utero infections result in abortion, premature birth, stillbirth, and congenital deformities such as arthrogryposis-hydranencephaly syndrome (Kurogi et al., 1976), causing economic losses in the livestock industry. The live, attenuated vaccine strain, TS-C2, was derived from the OBE-1 strain as a temperature sensitive mutant (Kurogi et al., 1979). Although vaccination has reduced the prevalence of the disease, antigenic and pathogenic variants of AKAV have been isolated (Lee et al., 2002; Ogawa et al., 2007a); for example, a variant Iriki strain was isolated from a calf with nonsuppurative encephalitis and neurological symptoms in Japan (Miyazato et al., 1989) and it shows low antigenic cross-reactivity with the reference strain in neutralization tests (Akashi and Inaba, 1997). Therefore, it is necessary to reconsider the vaccination strategy to effectively control the disease. Here we evaluated characters of a mutant virus with knockout of a nonstructural protein NSs, which acts as type I interferon antagonist and is involved in the regulation of host protein synthesis (Weber et al., 2002), by experimentally infecting pregnant goats. The pregnant goat model might be useful for AKAV studies, as suggested by previous reports of experimental transplacental infection of caprine fetuses (Kurogi et al., 1977).