Delayed wound healing in mice associated with viral alteration of macrophages.

Mice acutely and chronically infected with Sendai virus had impaired healing of incisional wounds. This impairment could be overcome by instilling the macrophage-stimulators zymosan and glucan into full-thickness incised wounds, whereas levamisole, an immunomodulator, had no effect on tensile strength of these wounds (breaking strengths). Another commonly occurring murine virus, murine hepatitis virus, also reduced wound tensile strength in infected mice. However, the murine strain of herpes simplex virus, type 1, which caused greater morbidity, did not reduce tensile strength. Although measurements of wound length and wound breaking strength clearly showed the adverse effect of viral infection, histologic evaluation of wounds did not consistently reveal a similar change in composition of wound "cell aggregation centers" for mice infected with the Sendai and murine hepatitis viruses.