{Reference Type}: Journal Article
{Title}: Verapamil inhibits respiratory syncytial virus infection by regulating Ca2+ influx.
{Author}: Chen F;Shen H;Liu G;Zhang P;Zhang L;Lin S;Gao H;Peng H;Qi YF;Chen Y;Jiang Y;Huang J;Shen X;Luo YS;Zhang K;
{Journal}: Life Sci
{Volume}: 352
{Issue}: 0
{Year}: 2024 Sep 1
{Factor}: 6.78
{DOI}: 10.1016/j.lfs.2024.122877
{Abstract}: OBJECTIVE: The study evaluated the antiviral effect of Verapamil against respiratory syncytial virus (RSV) and investigated its underlying mechanism.
METHODS: RSV-infected BALB/c mice were treated with Verapamil. Body weight, survival rates, viral load, lung damage, inflammatory factors, and the expression of RSV fusion (F) protein were analyzed. In cellular studies, intracellular Ca2+ and viral titers were measured in the presence of Verapamil, Calcium Chloride, and EGTA. A time-of-addition assay assessed the antiviral effect of Verapamil.
RESULTS: Mice infected with RSV and treated with Verapamil exhibited a significant decrease in weight loss, an increase in survival rates, and reductions in viral titers, RSV F protein expression, inflammatory responses, and lung tissue injury. Verapamil reduced intracellular calcium levels, which correlated with reduced viral titers. The addition of calcium chloride reversed the anti-viral effects mediated by Verapamil, while EGTA potentiated them. The antiviral activity of Verapamil was observed during the early phase of RSV infection, likely by blocking Ca2+ channels and inhibiting virus replication.
CONCLUSIONS: Verapamil effectively inhibits RSV infection by blocking calcium channels and reducing intracellular calcium levels, thereby impeding viral replication. Thus, Verapamil shows promise as a treatment for RSV.