IFNAR1 and infection: Mice lacking the interferon-alpha receptor (IFNAR-/-), which serves as a critical early mediator of the innate immune response, supported statistically higher LDV viral loads during the acute phase of infection (1 and 15 dpi) compared to the wild-type mice; however, the magnitude of this effect was small (3.5-fold at 1 dpi and 4.5-fold at 15 dpi) and became non-significant in the chronic phase (30 and 100 dpi).