TLR2 and endocarditis: In views of the fact that many SCV isolates lose their TLR2 activatory potential (Fig. 2 and 5) and that other isolates with only low to absent induction of host TLR2-activity were cultured from chronic infections such as endocarditis (INV30), osteomyelitis (INV20) or deep wound infections after implant of cardiac devices (INV32) (Fig. 2), it is well conceivable that loss of TLR2 activation capacity accompanies host adaptation and reduces the need for capsule expression.