ArticleNucleic acids research2026
PhoP-regulated VirK acts as an accessory factor to maintain virulence in polymyxin-resistant Klebsiella pneumoniae.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The genetic connection between virulence and antibiotic resistance remains poorly understood. Our previous RNA-Seq analysis of a polymyxin-resistant Klebsiella pneumoniae ATCC BAA2146 mutant identified a highly expressed VirK/YbjX family gene (kpn2146_RS17285), encoding a conserved membrane protein, designated virK (virulence required for Klebsiella pneumoniae). While PhoP-dependent antibiotic resistance is mediated through established pathways such as arn/pmr, we identify VirK as a PhoP-regulated factor specifically contributing to virulence. VirK localizes to the outer membrane and, although not involved in lipopolysaccharide modification, its deletion modestly reduced bacterial virulence in a mouse systemic infection model. Transcriptional and electrophoretic mobility shift assays demonstrated that virK is directly activated by the PhoP protein. A strong positive correlation between virK and phoP expression (r = 0.98) was also observed in multidrug-resistant clinical isolates. Since the PhoP/PhoQ two-component system mediates polymyxin resistance, its direct regulation of VirK uncovers an adaptive mechanism coupling enhanced virulence with antibiotic resistance. These findings reveal a previously unrecognized PhoP/VirK regulatory pathway that contributes to pathogenicity in polymyxin-resistant Klebsiella pneumoniae, offering new insights into bacterial evolution and suggesting that targeting PhoP/PhoQ could provide an effective strategy to combat multidrug-resistant K. pneumoniae infections.
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