This study adds evidence to the notion that novel PVL phages would be generated through illegitimate recombination events by acquiring the region at which hol, ami, see more luk, and int genes would line up upon lytic growth, and suggests that the PVL-positive MRSA clones that have emerged worldwide may carry distinct phages. Panton–Valentine leukocidin (PVL) is a two-component and hetero-oligomeric pore-forming cytolytic toxin identified in 1932 by Panton and Valentine (Panton & Valentine, 1932). Most of the community-associated methicillin-resistant Staphylococcus
aureus (CA-MRSA) strains that have emerged in recent years carry the genes encoding PVL, lukS-PV and lukF-PV, and cause a spectrum of infections (CDC, 1999; Baba et al., 2002; Diep et al., 2006). The role of PVL in the pathogenicity was re-evaluated, and PVL has been shown to play a key role in the pathogenesis of necrotizing pneumonia (Labandeira-Rey et al., 2007; Cremieux et al., 2009). PVL-positive S. aureus strains are lysogens of PVL phages, which belonged to Siphoviridae, a family of double-stranded DNA AZD9291 solubility dmso viruses that share a long noncontractile tail and capsid with an isometric or an elongated
shape (Kaneko et al., 1998; Narita et al., 2001; Baba et al., 2002; Kaneko & Kamio, 2004; Diep et al., 2006; Ma et al., 2008). Canchaya et al. (2003) classified S. aureus prophages into five groups based on differences in structural module, for example tail and capsid: groups 1–3 Sfi21-like cos-site Siphoviridae, and groups 1 and 2 sfi11-like pac-site Siphoviridae. PVL phages reported to date belong to either group 1 (isometric head type) or group 2 (elongated head type) of Sfi21-like cos-site Siphoviridae (Canchaya et al., 2003; Kaneko & Kamio, 2004). However, considerable differences exist
in the DNA replication/transcriptional regulation region of PVL phages. We developed a PCR system to classify PVL phages based on differences in this region (Ma et al., selleck kinase inhibitor 2008). To date, many PVL-positive MRSA and methicillin-susceptible S. aureus (MSSA) clones have been reported (Vandenesch et al., 2003; Rasigade et al., 2010) but there are few reports describing the correlations between the structure of prophage and genetic background of host cells. The representative CA-MRSA strains in the United States belong to CC1 [USA400 in pulsed-field type (PFT)] and CC8 (USA300 in PFT) (McDougal et al., 2003). These strains are presumed to carry prophages similar to φSa2mw carried by MW2 (a CC1 clone) or φSa2USA carried by FPR3757 (a CC8 clone) (Baba et al., 2002; Diep et al., 2006). Boakes et al. (2011) reported that the majority of CC22 strains disseminated in England carry PVL phages belonging to group 1 Siphoviridae (Boakes et al., 2011). However, the structure of PVL phages carried by other CA-MRSA clones, for example CC80 MRSA strains, the major CA-MRSA clone in Europe (Faria et al., 2005; Holmes et al.