Replication of lactate dehydrogenase-elevating virus in macrophages. 2. Mechanism of persistent infection in mice and cell culture.
Replication of lactate dehydrogenase-elevating virus in macrophages. 2. Mechanism of persistent infection in mice and cell culture.
复制标题
乳酸脱氢酶升高病毒在巨噬细胞中的复制。
DOI：
10.1099/0022-1317-59-2-263
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Plagemann,PG
中科院分区：
文献类型：
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作者：
Stueckemann,JA;Holth,M;Swart,WJ;Kowalchyk,K;Smith,MS;Wolstenholme,AJ;Cafruny,WA;Plagemann,PG
用乳酸脱氢酶升高病毒（LDV）对腹膜巨噬细胞培养物的初次感染导致3%至20%的细胞的生产性感染。当培养物中孵育的巨噬细胞生长因子（MGF）的情况下，LDV生产停止后，一个单一的周期，但在培养物中，其中巨噬细胞复制刺激的存在下的MGF LDV生产持续数周，在低水平，不超过1%的急性期观察到的。显著量的干扰素不存在于急性或持续感染的培养物中，并且用抗干扰素球蛋白或用LDV重复感染治疗持续感染的培养物并不显著刺激LDV复制。巨噬细胞培养建立与腹腔巨噬细胞LDV感染的小鼠也表现出只有低水平的LDV复制和抵抗LDV的重复感染。另一方面，小鼠肝炎病毒、塞姆利基森林病毒和水泡性口炎病毒在LDV持续感染的巨噬细胞培养物中正常复制。LDV复制是相对抵抗干扰素是否添加到文化或内源性产生的感染与纽卡斯尔病病毒或缺陷干扰（DI）颗粒水泡性口炎病毒。在LDV持续感染的培养物或慢性感染的小鼠中未检测到LDV的温度敏感突变体或DI颗粒。结果支持我们的假设，即在小鼠或巨噬细胞培养物中，在急性期结束时LDV产生的减少是由于允许LDV的巨噬细胞亚群的破坏，并且低水平的持续感染涉及病毒向新的允许细胞的传递，所述新的允许细胞从非允许前体细胞连续产生，尽管速率较低。
A primary infection of peritoneal macrophage cultures with the lactate dehydrogenase-elevating virus (LDV) results in productive infection of 3 to 20% of the cells. When cultures were incubated in the absence of macrophage growth factor (MGF), LDV production ceased after a single cycle, but in cultures in which macrophage replication was stimulated by the presence of MGF LDV production continued for several weeks at a low level, representing not more than 1% of that observed during the acute phase. Significant amounts of interferon were not present in either acutely or persistently infected cultures, and treatment of persistently infected cultures with anti-interferon globulin or superinfection with LDV did not significantly stimulate LDV replication. Macrophage cultures established with peritoneal macrophages from LDV-infected mice also showed only a low level of LDV replication and were resistant to superinfection by LDV. Mouse hepatitis virus, Semliki Forest virus and vesicular stomatitis virus, on the other hand, replicated normally in LDV-persistently infected macrophage cultures. LDV replication was relatively resistant to interferon whether added to the cultures or generated endogenously by infection with Newcastle disease virus or defective-interfering (DI) particles of vesicular stomatitis virus. Temperature-sensitive mutants or DI particles of LDV were not detected in LDV-persistently infected cultures or chronically infected mice. The results support our hypothesis that the decrease in LDV production in mice or macrophage cultures at the end of the acute phase results from the destruction of the subpopulation of macrophages that is permissive for LDV, and that the low level persistent infection involves the passage of the virus to new permissive cells that are generated continuously, although at a low rate, from non-permissive precursor cells.