Stohlman S A, Hinton D R, Cua D, Dimacali E, Sensintaffar J, Hofman F M, Tahara S M, Yao Q
Department of Neurology, University of Southern California School of Medicine, Los Angeles 90033, USA.
J Virol. 1995 Sep;69(9):5898-903. doi: 10.1128/JVI.69.9.5898-5903.1995.
Neutralizing anti-tumor necrosis factor alpha (TNF-alpha) antibody treatment of mice infected with the neurotropic JHMV strain of mouse hepatitis virus showed no reduction of either virus-induced encephalomyelitis or central nervous system demyelination. TNF-alpha-positive cells were present in the central nervous system during infection; however, TNF-alpha could not be colocalized with JHMV-infected cells. In vitro, TNF-alpha mRNA rapidly accumulated following JHMV infection; however, no TNF-alpha was secreted because of inhibition of translation. Both live and UV-inactivated virus inhibited TNF-alpha secretion induced by lipopolysaccharide. These data show that TNF-alpha is not secreted from infected cells and indicate that if contributes to either JHMV-induced acute encephalomyelitis nor primary demyelination.
用中和性抗肿瘤坏死因子α（TNF-α）抗体治疗感染嗜神经小鼠肝炎病毒JHMV株的小鼠，结果显示病毒诱导的脑脊髓炎或中枢神经系统脱髓鞘均未减轻。感染期间中枢神经系统存在TNF-α阳性细胞；然而，TNF-α无法与感染JHMV的细胞共定位。在体外，JHMV感染后TNF-α mRNA迅速积累；然而，由于翻译受到抑制，没有分泌出TNF-α。活病毒和紫外线灭活病毒均抑制脂多糖诱导的TNF-α分泌。这些数据表明，感染细胞不会分泌TNF-α，并且提示其对JHMV诱导的急性脑脊髓炎和原发性脱髓鞘均无作用。
