Reducing the ability for NADPH synthesis impacts the in vivo virulence of Streptococcus pneumoniae

Nicotinamide adenine dinucleotide phosphate (NADPH) plays an important role as an electron donor and has been suggested as an antibacterial drug target. In Streptococcus. pneumoniae, a side branch of the Embden-Meyerhof-Parnas pathway, catalyzed by GapN, forms an important source of NADPH. In this study, we investigated the consequences of non-functional GapN on S. pneumoniae virulence.