This indicates that OMT’s antiviral efficacy extends beyond the TLR3 signaling axis, potentially broadening its therapeutic utility against viruses that might evade or suppress TLR3-mediated responses because of mutations or other infection mechanisms [32]; additionally, it posits the existence of a polypharmacological landscape where OMT acts on various signaling pathways, possibly in parallel or synergistically, to mount a comprehensive defense against H9N2 AIV [33,34,35]. Here, TLR3 is linked to infection.