Kenyon A J
Am J Vet Res. 1983 Apr;44(4):652-6.
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.
急性和慢性感染仙台病毒的小鼠，其切口伤口的愈合受到损害。通过将巨噬细胞刺激剂酵母聚糖和葡聚糖注入全层切开的伤口，可以克服这种损害，而免疫调节剂左旋咪唑对这些伤口的抗张强度（断裂强度）没有影响。另一种常见的鼠类病毒，即鼠肝炎病毒，也会降低感染小鼠伤口的抗张强度。然而，致病性更强的1型单纯疱疹病毒鼠株，并未降低抗张强度。尽管伤口长度和伤口断裂强度的测量清楚地显示了病毒感染的不利影响，但对感染仙台病毒和鼠肝炎病毒的小鼠伤口进行组织学评估，并未始终如一地揭示伤口“细胞聚集中心”组成的类似变化。
