A new mechanism of respiratory syncytial virus entry inhibition by small-molecule to overcome K394R-associated resistance.

ABSTRACT: Infection with respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract disease in young children and older people. Despite intensive efforts over the past few decades, no direct-acting small-molecule agents against RSV are available. Most small-molecule candidates targeting the RSV fusion (F) protein pose a considerable risk of inducing drug-resistant mutations. Here, we explored the in vitro and in vivo virological properties of the K394R variant, a cross-resistant mutant capable of evading multiple RSV fusion inhibitors. Our results demonstrated that the K394R variant is highly fusogenic in vitro and more pathogenic than the parental strain in vivo. The small molecule (2E,2'E)-N,N'-((1R,2S,3

SUBMITTER: Song Q 

PROVIDER: S-EPMC11389407 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature