Novel humanized anti-PcrV monoclonal antibody COT-143 protects mice from lethal infection via inhibition of toxin translocation by the type III secretion system.

Treatment of infection is challenging due to its intrinsic and acquired antibiotic resistance. As the number of current therapeutic options for infections is limited, developing novel treatments against the pathogen is an urgent clinical priority. The suppression of virulence of could be a new therapeutic option, and the type III secretion system (T3SS), which enables the bacteria to translocate various kinds of toxins into host cells and inhibits cellular functions, is considered as one possible target.

CvfA protein and polynucleotide phosphorylase act in an opposing manner to regulate Staphylococcus aureus virulence.

We previously identified CvfA (SA1129) as a Staphylococcus aureus virulence factor using a silkworm infection model. S. aureus cvfA-deleted mutants exhibit decreased expression of the agr locus encoding a positive regulator of hemolysin genes and decreased hemolysin production.

Mobile genetic element SCCmec-encoded psm-mec RNA suppresses translation of agrA and attenuates MRSA virulence.

Community acquired-methicillin resistant Staphylococcus aureus (CA-MRSA) is a socially problematic pathogen that infects healthy individuals, causing severe disease. CA-MRSA is more virulent than hospital associated-MRSA (HA-MRSA). The underlying mechanism for the high virulence of CA-MRSA is not known.