Dubuy H, Baron S, Uhlendorf C, Johnson M L
Infect Immun. 1973 Dec;8(6):977-84. doi: 10.1128/iai.8.6.977-984.1973.
The induction of interferon (IF) by lactic dehydrogenase virus (LDV) and the action of exogenous IF on LDV multiplication have been studied in vivo and in vitro. In vivo the induction of serum IF by LDV was shown to correspond with the virus challenge dose. In vitro LDV-infected macrophages did not produce detectable IF. As to the action of IF in vivo, the prophylactic or therapeutic administration of IF to mice reduced the LDV serum titers only temporarily. In vitro, (i) the sensitivity of LDV to IF in macrophage culture was 30 times less than that of vesicular stomatitis virus, and 5 times less than that of Sendai virus, and (ii) prolonged exposure of LDV-infected macrophages to high IF concentrations did not cure the chronic infection, but only decreased the virus titer. The probable role of IF in the establishment of the early phase of a persistent but reduced viremia in mice is discussed.
对乳酸脱氢酶病毒(LDV)诱导干扰素(IF)以及外源性IF对LDV增殖的作用进行了体内和体外研究。在体内,LDV诱导血清IF被证明与病毒攻击剂量相对应。在体外,受LDV感染的巨噬细胞未产生可检测到的IF。至于IF在体内的作用,给小鼠预防性或治疗性给予IF仅能暂时降低LDV血清滴度。在体外,(i)巨噬细胞培养中LDV对IF的敏感性比水疱性口炎病毒低30倍,比仙台病毒低5倍,并且(ii)将受LDV感染的巨噬细胞长时间暴露于高浓度IF并不能治愈慢性感染,而仅能降低病毒滴度。讨论了IF在小鼠建立持续但病毒血症降低的早期阶段可能发挥的作用。