Multiple virulence determinants likely affect S. aureus induction of SSTIs [39], and the host response to infection is currently under investigation by several laboratories.
The results of this study provide evidence for the cooperative role of multiple virulence determinants in C. neoformans pathogenesis and suggest new avenues for the development of anti-infective agents in the prevention of fungal tissue invasion.
Theoretically, a pathogenic strain could be generated that no longer expresses any virulence proteins, but this is not a practical strategy, as most pathogens encode multiple virulence determinants, some of which are likely not currently known.
RopB mutation in this particular strain does not result in the kind of global phenotypic change found with covR/S mutation where differential expression was observed of multiple genes encoding virulence determinants, including sic, ska, slo, speA, speJ, scpC and the hyaluronic acid synthesis operon [37] which were all unaffected in the ropB mutant examined in this work.
Although, notably, it has been previously demonstrated that K12 E. coli strains that carry the entire 220 kb Shigella virulence plasmid are completely avirulent in animal models of disease, likely due to the absence of multiple chromosomally encoded Shigella virulence determinants.
Given the presence of homologous sequences in known and putative virulence determinants from multiple species, we hypothesized that the N-terminal 130 aa segment of BteA may perform a conserved cellular function, possibly by directing localization.
The pSLBT plasmid also harbored multiple virulence genes and integron-borne resistance determinants as previously described (6).
Almost all of the known virulence determinants are virulent Bvg+ phase-specific genes.
The Pfam database encompasses altogether 13,672 protein families also including toxic protein families and virulence determinants, which are all represented by multiple sequence alignments and hidden Markov models [ 49].
B. cenocepacia strains possess multiple quorum sensing systems, which regulate the expression of versatile virulence determinants, such as biofilm formation and motility.
Loss of the third replicon, pC3 (a non-essential megaplasmid associated with several virulence determinants), results in highly attenuated infection in multiple hosts, including zebrafish embryos (Agnoli et al., 2012; Agnoli et al., 2014).
