Lnc-DARVR/miR-365-1-5p/LAMB1 axis regulates rotavirus replication via the complement C3 pathway

• DOI: 10.1128/jvi.02114-24
• Publication Date: 2025-04-16T13:03:06Z
• Authors: Xiaopeng Song; Lida Yao; Yan Li; Jinlan Wang; Chenxing Lu; Jinmei Li; Qingmei Leng; Xianqiong Tang; Xiaoqing Hu; Jinyuan Wu; Rong Chen; Xiaochen Lin; Jun Ye; Xiangjun Kuang; Guangming Zhang; Maosheng Sun; Yan Zhou; Hongjun Li
• Keywords: Competing Endogenous RNA

ABSTRACT Antiviral effectors and cytokines are critical components of host innate immunity. However, the regulatory mechanisms governing roles these molecules in host–virus interactions still unclear. Although long non-coding RNAs (lncRNAs) have been recognized as key players various biological processes, their involvement complement system antiviral defenses remains to be explored. In this study, we discovered a novel, unannotated lncRNA, called DARVR. DARVR was found an intergenic lncRNA inhibited rotavirus (RV) replication MA104 cells. Mechanistically, that 3 (C3) upregulated following RV infection LAMB1-dependent manner. LAMB1 expression downregulated by miR-365-1-5p, resulting inhibition C3-mediated reaction. functioned competing endogenous RNA against promoting thereby enhancing C3 activity inhibiting replication. These results not only provide evidence demonstrating lncRNAs regulation but also highlight role factors IMPORTANCE Long play versatile interactions, offering significant potential for developing targeted therapies prevent or treat viral infections. Despite importance, underexplored. This study identifies novel enhances factor through (ceRNA) mechanism, effectively across different subtypes. findings underscore complex molecular interplay regulating during valuable insights into host's mechanisms. research paves way innovative therapeutic strategies targeting combat infections more effectively.