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© Therese Couderc, Marc Lecuit
Publication : Infection and immunity

Spontaneous Loss of Virulence in Natural Populations of Listeria monocytogenes

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Infection and immunity - 18 Oct 2017

Maury MM, Chenal-Francisque V, Bracq-Dieye H, Han L, Leclercq A, Vales G, Moura A, Gouin E, Scortti M, Disson O, Vázquez-Boland JA, Lecuit M

Link to Pubmed [PMID] – 28827366

Infect. Immun. 2017 11;85(11)

The pathogenesis of depends on the ability of this bacterium to escape from the phagosome of the host cells via the action of the pore-forming toxin listeriolysin O (LLO). Expression of the LLO-encoding gene () requires the transcriptional activator PrfA, and both and genes are essential for virulence. Here, we used the hemolytic activity of LLO as a phenotypic marker to screen for spontaneous virulence-attenuating mutations in Sixty nonhemolytic isolates were identified among a collection of 57,820 confirmed strains isolated from a variety of sources (0.1%). In most cases (56/60; 93.3%), the nonhemolytic phenotype resulted from nonsense, missense, or frameshift mutations in Five strains carried mutations leading to a single amino acid substitution (G299V) or a premature stop codon causing strong virulence attenuation in mice. In one strain, both and (encoding a glutathione synthase required for full PrfA activity) were missing due to genomic rearrangements likely caused by a transposable element. The PrfA/LLO loss-of-function (PrfA/LLO) mutants belonged to phylogenetically diverse clades of , and most were identified among nonclinical strains (57/60). Consistent with the rare occurrence of loss-of-virulence mutations, we show that and are under purifying selection. Although occurring at a low frequency, PrfA/LLO mutational events in lead to niche restriction and open an evolutionary path for obligate saprophytism in this facultative intracellular pathogen.

https://www.ncbi.nlm.nih.gov/pubmed/28827366