Abstract
Vancomycin-resistant enterococci (VRE) are a serious threat to human health, with few treatment options being available. New therapeutics are urgently needed to relieve the health and economic burdens presented by VRE. A potential target for new therapeutics is the VanRS two-component system, which regulates the expression of vancomycin resistance in VRE. VanS is a sensor histidine kinase that detects vancomycin and in turn activates VanR; VanR is a response regulator that, when activated, directs expression of vancomycin-resistance genes. This review of VanRS examines how the expression of vancomycin resistance is regulated, and provides an update on one of the field’s most pressing questions: How does VanS sense vancomycin?
Highlights
In the early 1950s, the glycopeptide vancomycin was isolated from Amycolatopsis orientalis and soon emerged as a promising new treatment for infections caused by penicillinresistant staphylococci and other Gram-positive bacteria [1,2]
C-type and -subtype proteins were not annotated as such, so they were subtyped based on nucleotide identity of vanC genes to type C1 E. gallinarum strain BM4174, type C2/3 E. casseliflavus strain nonredundant protein sequence entries being listed to the right of each branch
VanRS was established as the regulatory two-component system (TCS) of vancomycin resistance expression in
Summary
In the early 1950s, the glycopeptide vancomycin was isolated from Amycolatopsis orientalis and soon emerged as a promising new treatment for infections caused by penicillinresistant staphylococci and other Gram-positive bacteria [1,2]. Alternatives became available (e.g., methicillin), and as a result vancomycin was used only sparingly until the early 1980s, when the increasing prevalence of methicillin-resistant S. aureus prompted its use as an antibiotic of last resort [8,9,10,11,12]. Vancomycin became a popular treatment option for enterococcal infections, which are tolerant of or resistant to some other antibiotic classes [13,14]. This increased use of vancomycin encouraged the development and spread of vancomycin-resistant enterococci (VRE).
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