According to published data, our hypothesis in developing these protocols was that the primary fibroblast cell line DHF, considered to be healthy fibroblasts, should be able to respond efficiently to HSV-1 infection due to the stimulation of the TLR3 receptor and therefore be less infected than the SV40 immortalized TLR3-/- fibroblast cell line which are deficient in their TLR3 pathway, leading to increased sensitivity to infection. Here, TLR3 is linked to infection.