Sarzotti M, Dean T A, Remington M, Hoffman P M
Retrovirus Research Center, Veterans Affairs Medical Center, Baltimore, Maryland 21201.
AIDS Res Hum Retroviruses. 1994 Dec;10(12):1695-702. doi: 10.1089/aid.1994.10.1695.
Newborn NFS/N mice are susceptible to the neurological disease induced by infection with Cas-Br-M murine leukemia virus (Cas), and do not develop a protective cytotoxic T cell (CTL)-mediated response to Cas infection. Here we demonstrate that whole UV light-inactivated Cas (UV-Cas), inoculated in newborn NFS/N mice, induced a strong, Cas-specific CTL response detectable 2 weeks postinoculation and persisting in vivo for > or = 36 weeks. The magnitude of the UV-Cas-induced splenic CTL response, mediated by CD8+ T cells, inversely correlated with the level of proviral cas env sequences detectable in the spleen of the UV-Cas-inoculated mice, as revealed by PCR amplification of tissue DNA. The transfer of UV-Cas-primed splenocytes, with Cas-specific CTL activity, protected 100% of recipient newborn mice from the development of neurological disease induced by infection with live Cas, for more than 28 weeks, and reduced the level of viral replication in the recipients.
新生的NFS/N小鼠易患由感染Cas-Br-M小鼠白血病病毒（Cas）诱发的神经疾病，且对Cas感染不会产生保护性细胞毒性T细胞（CTL）介导的反应。在此我们证明，接种于新生NFS/N小鼠体内的经紫外线完全灭活的Cas（UV-Cas），在接种后2周可诱导出强烈的、Cas特异性CTL反应，且该反应在体内持续存在≥36周。如通过组织DNA的PCR扩增所显示，由CD8 + T细胞介导的UV-Cas诱导的脾CTL反应强度，与在接种UV-Cas小鼠脾脏中可检测到的原病毒cas env序列水平呈负相关。具有Cas特异性CTL活性的经UV-Cas致敏的脾细胞转移，可使100%的受体新生小鼠在超过28周的时间里免受感染活Cas诱发的神经疾病，并降低受体中的病毒复制水平。
