Pathogenesis of Sendasi virus infection in mice. On the possible role of interferon on the development of disease.

M Degré, H Rollag
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Abstract

Intraperitoneally (i.p.) injected interferon prolonged the survival time of mice inoculated intranasally (i.n.) with Sendai virus and reduced the mortality in mice inoculated i.n. with Haemophilus influenzae. Moderate concentrations of interferon were demonstrated in homogenized lungs of Sendai virus infected mice as long as the virus was present. Similar concentrations could be produced by i.p. injection of Sendai virus or interferon. Alveolar macrophages from mice treated i.p. with interferon or Sendai virus phagocytized more actively than control macropages. From the present and earlier data it is concluded that interferon may have a direct effect on the Sendai virus infection. The total effect of virus pneumonia is a reduction of the lung macrophage antimicrobial activity, and therefore the phagocytosis-modifying effect of interferon produced in the lungs is probably of minor importance for the outcome of the disease.

森达西病毒感染小鼠的发病机制。关于干扰素在疾病发展中的可能作用。
腹腔注射干扰素可延长鼻内接种仙台病毒小鼠的存活时间,降低流感嗜血杆菌接种小鼠的死亡率。只要仙台病毒存在,均质化的仙台病毒感染小鼠肺中就存在中等浓度的干扰素。通过注射仙台病毒或干扰素也能产生类似的浓度。干扰素或仙台病毒对小鼠肺泡巨噬细胞的吞噬活性高于对照组。从目前和早期的数据可以得出结论,干扰素可能对仙台病毒感染有直接影响。病毒性肺炎的总效应是肺巨噬细胞抗微生物活性的降低,因此肺中产生的干扰素的吞噬调节作用可能对疾病的结局不太重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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