Doll S C, Johnson T C
Section of Virology and Oncology, Kansas State University, Manhattan 66506.
J Neuroimmunol. 1989 Sep;24(1-2):47-53. doi: 10.1016/0165-5728(89)90097-0.
A single intracerebroventricular injection of 100 ng of beta-endorphin altered the course of the central nervous system (CNS) infection of a temperature-sensitive mutant of vesicular stomatitis virus (VSV), tsG31-KS5. When mice were administered beta-endorphin and then 24 h later infected intracerebrally with tsG31-KS5 VSV, 70% of the animals died within 8 days of infection. In comparison, less than 10% of the animals had died after 21 days when infected with tsG31-KS5 VSV alone. When mice were injected with beta-endorphin and tsG31-KS5 VSV simultaneously, or with beta-endorphin 21 days after infection, the more aggressive clinical disease was not observed. Superficially, the more lethal disease induced by beta-endorphin appeared to be a result of a mild hypothermia caused by the neuropeptide. beta-Endorphin, however, did not influence the disease in nude (nu/nu) mice even though their core temperatures were reduced to an extent similar to that of BALB/c (+/+) mice, implicating the involvement of T lymphocytes in the alteration of the course of infection in normal mice.
脑室内单次注射100纳克β-内啡肽改变了水疱性口炎病毒(VSV)温度敏感突变体tsG31-KS5的中枢神经系统(CNS)感染进程。当给小鼠注射β-内啡肽,然后在24小时后经脑内接种tsG31-KS5 VSV时,70%的动物在感染后8天内死亡。相比之下,仅感染tsG31-KS5 VSV时,21天后死亡的动物不到10%。当小鼠同时注射β-内啡肽和tsG31-KS5 VSV,或在感染后21天注射β-内啡肽时,未观察到更严重的临床疾病。表面上看,β-内啡肽诱导的更致命疾病似乎是该神经肽引起的轻度体温过低的结果。然而,β-内啡肽对裸鼠(nu/nu)的疾病没有影响,尽管它们的核心体温降低程度与BALB/c(+/+)小鼠相似,这表明T淋巴细胞参与了正常小鼠感染进程的改变。