Because DV-EVs can activate CLEC5A and TLR2 to induce NET formation and proinflammatory cytokine release, simultaneous blockade of CLEC5A and TLR2 by a bi-specific mAb may be able to protect host from DV-EVs-induced NETosis and inflammatory reactions during viral infections. The gene discussed is TLR2; the disease is viral infectious disease.