Anandan Vysakh, Bao Liang, Zhu Zan, Bradley Jennifer, Assi Valery-Francine, Chavda Henna, Kitten Todd, Xu Ping
The Philips Institute for Oral Health Research, School of Dentistry, Virginia Commonwealth University, Richmond, VA.
Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA, USA.
bioRxiv. 2024 Jul 3:2024.07.03.601854. doi: 10.1101/2024.07.03.601854.
We identified the role of a conserved hypothetical protein (SSA_0451) in that is involved in the virulence of infective endocarditis. An whole blood killing assay and rabbit endocarditis model studies revealed that the SSA_0451 mutant (ΔSSA_0451) was significantly less virulent than the wild-type (SK36) and its complementation mutant (ΔSSA_0451C). The mechanism underlying the SSA_0451 mutant's reduced virulence in infective endocarditis was evidentially linked to oxidative stress and environmental stress. The genes related to the survival of in an oxidative stress environment were downregulated in ΔSSA_0451, which affected its survival in blood. Our findings suggest that SSA_0451 is a novel IE virulence factor and a new target for drug discovery against IE.
我们确定了一种保守的假设蛋白(SSA_0451)在感染性心内膜炎毒力中所起的作用。全血杀伤试验和兔心内膜炎模型研究表明,SSA_0451突变体(ΔSSA_0451)的毒力明显低于野生型(SK36)及其互补突变体(ΔSSA_0451C)。SSA_0451突变体在感染性心内膜炎中毒力降低的潜在机制显然与氧化应激和环境应激有关。在ΔSSA_0451中,与在氧化应激环境中生存相关的基因表达下调,这影响了其在血液中的生存。我们的研究结果表明,SSA_0451是一种新型的感染性心内膜炎毒力因子,也是针对感染性心内膜炎药物研发的新靶点。