| Genestier et al. (2005) |
PVL may inactivate mitochondria, leading to apoptosis |
| Voyich et al. (2006) |
In mouse model of SSTI and sepsis, PVL in an MRSA strain did not affect strain virulence |
| Bubeck Wardenburg et al. (2007) |
In mouse model of pneumonia, PVL in S. aureus did not affect mortality; use of isogenic PVL knockouts of USA300 and USA400 did not alter cytopathic effect in vitro in alveolar epithelial cells |
| Labandeira-Rey et al. (2007) |
In mouse model both purified PVL protein alone and an S. aureus strain overexpressing PVL caused necrotizing pneumonia |
| Wolter et al. (2007) |
Allelic variation exists in PVL genes from various S. aureus isolates; 7 nt substitutions were identified in 28 isolates collected over a long period of time at different geographical sites around the world |
| Bubeck Wardenburg et al. (2008) |
In rodent models of SSTI and pneumonia, no differences noted in USA300 and an isogenic PVL knockout |
| Montgomery et al. (2008) |
In rat model of pneumonia, wild-type and isogenic PVL knockout strains of USA300 and USA400 caused similar disease |
| Diep et al. (2008) |
(1) USA300 and isogenic PVL knockout did not differ in their proteomes or in their global gene expression profiles; (2) in rabbit sepsis model, competition assay showed that at 24 and 48 h, wild-type USA300 was present in a higher concentration in the kidney tissue than was its isogenic PVL knockout; PVL may provide survival benefit to USA300 early in infection |
| O’Hara et al. (2008) |
Two major allelic variants of PVL were identified in a large international collection of clinical S. aureus isolates; the R variant was found in USA300 and USA400 while the H variant was in other genetic backgrounds |
| Dumitrescu et al. (2008) |
In a large collection of clinical isolates, the R variant of PVL was identified in USA300, USA400 and in a CC93 isolate from Australia; the H variant was in many other lineages and dominated in MSSA and MRSA strain backgrounds from outside of North America |
| Tristan et al. (2009) |
PVL may be a factor in the adhesion of S. aureus to mucous membranes |
| Bae et al. (2009) |
Human SSTIs caused by a PVL+ MRSA strain were not associated with a worse outcome than those caused by PVL-negative MRSA strains |
| Tseng et al. (2009) |
In mouse model of myositis, wild-type USA300 caused greater tissue damage in young (and not older) mice than its isogenic PVL knockout |
| Hongo et al. (2009) |
PVL did not lyse neutrophils from mice but did lyse human neutrophils; this lysis was prevented in the presence of monoclonal anti-PVL antibodies |
| Montgomery et al. (2009) |
In a rat pneumonia model, USA300 and its isogenic PVL knockout did not differ in the initial, rapid massive inflammatory cytokine response as measured by RT-PCR |
| Hermos et al. (2010) |
Children with PVL+ MRSA infections have high serum titres of anti-PVL antibodies that strongly inhibit PVL-mediated lysis of human neutrophils; even in children with a high titre of these protective antibodies PVL+ MRSA strains can cause skin infections |
| Löffler et al. (2010) |
PVL lysed human and rabbit neutrophils, but did not lyse neutrophils from mice or monkeys |
| Varshney et al. (2010) |
PVL production by S. aureus strains varies; in a mouse SSTI model, MSSA and MRSA strains with greater PVL production caused larger lesions with a greater number of bacteria recovered from them than a strain with lower PVL production |
| Dumitrescu et al. (2011) |
In CA-MRSA isolates in vitro and in a mouse pneumonia model, PVL transcription was increased in the presence of imipenem and oxacillin (but not β-lactams that are PBP2, -3 or -4 selective); this was likely mediated by PBP1 binding and induction of the global virulence regulator sarA and reduction in the transcription of rot
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| Malachowa et al. (2011) |
PVL gene expression by microarray analysis increased in a USA300 strain in human blood compared with the strain in TSB, along with several other virulence factors |
| Zivkovic et al. (2011) |
In a mouse model, lung inflammatory response to PVL is mediated via NF-κB in alveolar macrophages by direct binding of PVL to CD14/TLR2 |
| Kobayashi et al. (2011) |
In a rabbit SSTI model, the virulence of USA300 and its isogenic PVL knockout strain did not differ until >11 days into the infection, when the PVL knockout lesions were larger than those caused by wild-type USA300 |
| Ma et al. (2012) |
In a rabbit pneumonia model, PVL protein led to NF-κB-mediated release of inflammatory cytokines derived from neutrophils; the injury resulting from this cytokine release was mild in neutropenic rabbits, suggesting the central role of neutrophils mediation in the pathogenic effect of PVL in the lung |
