In addition, the expression of duck LECT2 was significantly increased in liver and spleen by duck hepatitis virus type I infection [16], or the treatment of polyinosinic-polycytidylic acid (poly [I:C]), implying the LECT2 may play a role in the defense mechanism against viral infections in duck and be regulated by innate immune receptor signaling pathways, i.e., toll-like receptors 3 (TLR3). The gene discussed is TLR3; the disease is viral infectious disease.