GENETICALLY-DETERMINED DIFFERENCE IN THE ANTIVIRAL ACTION OF ALPHA-BETA INTERFERON IN CELLS FROM MICE RESISTANT OR SUSCEPTIBLE TO HERPES-SIMPLEX VIRUS TYPE-2
GENETICALLY-DETERMINED DIFFERENCE IN THE ANTIVIRAL ACTION OF ALPHA-BETA INTERFERON IN CELLS FROM MICE RESISTANT OR SUSCEPTIBLE TO HERPES-SIMPLEX VIRUS TYPE-2
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DOI：
10.1099/0022-1317-67-9-1859
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发表时间：
1986-09-01
影响因子：
3.8
通讯作者：
MOGENSEN, SC
中科院分区：
文献类型：
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作者：
ELLERMANNERIKSEN, S;JUSTESEN, J;MOGENSEN, SC
小鼠对单纯疱疹病毒2型（HSV-2）感染的抵抗力由遗传决定。根据空斑面积、空斑效率、终点滴定和病毒产量判断，来自易感BALB/c和抗性C57 BL/6小鼠的胚胎细胞对HSV-2感染同样敏感。来自C57 BL/6小鼠的细胞显示出比来自BALB/c小鼠的细胞对α/β的两种制剂的保护作用更高的敏感性。β的干扰素抗HSV-2攻击。这一点从c.p.e.抑制和产率降低实验。敏感性的差异取决于病毒剂量，并且在低病毒剂量下最大（高达50倍）。α/的遗传学分析β的来自亲代小鼠胚胎和来自HSV-2抗性和HSV-2易感小鼠之间相互交配的胚胎的细胞中的干扰素敏感性表明干扰素敏感性作为共显性常染色体性状遗传。干扰素诱导的酶2“-5”-寡腺苷酸合成的诱导在来自两种小鼠品系的细胞中也不同，因为仅在来自C57 BL/6小鼠的细胞中检测到显著水平。提示HSV-2耐药和敏感小鼠细胞对干扰素敏感性的差异可能是感染过程中的一个重要因素。
Resistance of mice to infection with herpes simplex virus type 2 (HSV-2) is genetically determined. Embryonic cells from susceptible BALB/c and resistant C57BL/6 mice were equally sensitive to infection with HSV-2 as judged by plaque area, plaquing efficiency, endpoint tiration and virus yield. Cells from C57BL/6 mice showed a higher sensitivity than cells from BALB/c mice to the protective action of two preparations of .alpha./.beta. interferon against challenge with HSV-2. This was evident both from c.p.e. inhibition and yield reduction experiments. The difference in sensitivity was dependent on virus dose and was greatest (up to 50-fold) with low virus doses. An analysis of the genetics of the .alpha./.beta. interferon sensitivity in cells from embryos of parental mice and embryos derived from reciprocal matings between HSV-2-resistant and -susceptible mice suggested that interferon sensitivity is inherited as a co-dominant autosomal trait. The induction of the interferon-induced enzyme 2''-5''-oligoadenylate synthetaste was also different in cells from the two mouse strains, since significant levels were only detected in cells from C57BL/6 mice. It is suggested that differential interferon sensitivity of cells from HSV-2-resistant and -susceptible mice might be a factor of importance for the course of the infection.