TLR3 and Herpesviridae infectious disease: This is consistent with the findings of TLR3-deficient mice infected with HSV-1 [37], HSV-2 [38], and EMCV [39] in the early stages, which showed consistently higher tissue inflammation, suggesting that TLR3 modulation may be a common immune escape mechanism for multiple herpesviruses, and TLR3 plays a key role in the antiviral response to herpesvirus infection.