Responses of mice to murine coronavirus immunization.
Responses of mice to murine coronavirus immunization.
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小鼠对鼠冠状病毒免疫的反应。
DOI：
10.1007/bf01309627
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发表时间：
1992
影响因子：
2.7
通讯作者：
Barthold,SW
中科院分区：
文献类型：
--
作者：
Smith,AL;deSouza,MS;Finzi,D;Barthold,SW
口服和/或鼻内接种易感基因型小鼠JHM株小鼠肝炎病毒（MHV-JHM）一致导致T细胞功能障碍，这反映在对有丝分裂原或同种异体细胞的体外增殖反应中。检查观察到的功能性T细胞抑制机制的一种方法是确定其诱导是否需要病毒复制。为此，小鼠经口鼻接种经短波紫外线、倍他丙内酯或补骨脂素灭活的MHV-JHM。小鼠从同种型或异型的MHV感染恢复后也接种活的MHV- jhm。经口鼻接种灭活MHV-JHM的BALB小鼠脾细胞在connaavin A刺激后产生了非常不同的体外增殖反应。mhv易感小鼠经口鼻或腹腔接触经任何最低限度有效治疗灭活的病毒，均不能进行血清转化。经补骨脂素处理过的病毒在弗氏完全佐剂中腹腔注射或经口鼻注射均不能预防活病毒的攻击，但在攻击后两周，与模拟免疫对照组相比，幸存者的病毒特异性血清IgG抗体滴度升高。从同型活病毒感染中恢复后，小鼠的脾细胞受到攻击，并没有表现出通常在原发性感染急性阶段观察到的深刻的体外T细胞抑制。相比之下，异型活MHV-S免疫小鼠的MHV-JHM攻击导致体外T细胞功能明显下降。综合数据表明，病毒复制或暴露于更浓缩的抗原可能是诱导MHV-JHM感染引起的戏剧性T细胞功能障碍以及可检测的mhv特异性体液反应所必需的。
Oral and/or intranasal inoculation of susceptible mouse genotypes with the JHM strain of mouse hepatitis virus (MHV-JHM) consistently results in T cell dysfunction as reflected by in vitro proliferative responses to mitogens or allogeneic cells. One approach to examining the mechanism responsible for the observed functional T cell suppression is to determine whether virus replication is required for its induction. To this end, mice were inoculated oronasally with MHV-JHM that was inactivated with short-wave ultraviolet light, betapropiolactone or psoralen. Mice were also inoculated with live MHV-JHM after recovery from homotypic or heterotypic MHV infection. Spleen cells from BALB mice inoculated oronasally with inactivated MHV-JHM yielded extremely variable in vitro proliferative responses after concanavalin A stimulation. MHV-susceptible mice exposed oronasally or intraperitoneally to virus inactivated by any of the minimum effective treatments failed to seroconvert. Immunization with psoralen-treated virus intraperitoneally in Freund's complete adjuvant or oronasally failed to protect from live virus challenge, but survivors had elevated virus-specific serum IgG antibody titers compared to mock-immunized controls at two weeks post-challenge. Spleen cells from mice that were challenged after recovery from homotypic live virus infection did not exhibit the profound in vitro T cell suppression normally observed during the acute stage of primary infection. In contrast, MHV-JHM challenge of mice vaccinated with heterotypic live MHV-S resulted in significantly depressed in vitro T cell function. The combined data suggest that either virus replication or exposure to more concentrated antigen may be required for induction of the dramatic T cell dysfunction that occurs as a consequence of MHV-JHM infection as well as for a detectable MHV-specific humoral response.