“…The same authors also provided the first insights into the genetic variability of PBCVd through the identification of different sequence variants (using conventional Sanger sequencing) that revealed the quasiespecies nature of this viroid, as previously proposed for RNA viruses (Holland et al, 1982). A high number of point mutations affecting the PBCVd CCR have been reported (Ambros et al, 1995a;Yesilcollou et al, 2010), and many complete viroid variants from different isolates, hosts and geographic origin have been characterized Ambrós et al, 1995a;Joyce et al, 2006;Lolic et al, 2007;Kaponi et al, 2010;Yesilcollou et al, 2010;Nome et al, 2011;Elleuch et al, 2013), allowing the identification of 115 polymorphic positions distributed along the viroid genome and showing that the viroid size may range from 312 to 317 nt. Interestingly, most polymorphic positions map at loops and/or are compensatory mutations preserving the secondary structure foreseen for PBCVd (Fig.…”