Ziegler R J, Pozos R S
Arch Virol. 1984;79(1-2):123-30. doi: 10.1007/BF01314310.
Various immune mechanisms were tested for their ability to alter a normally productive infection of herpes simplex virus in cultures of dissociated rat sensory neurons. These mechanisms included anti-HSV antibody with and without the aid of complement, HSV-sensitized "T" cells, natural killer cells, and "K" cells plus anti-HSV antibody (ADCC reactions). Although both anti-HSV antibody plus complement and the ADCC mechanism significantly limited infectious HSV production, no mechanism was capable of preventing the eventual infection of the majority of neurons. It appears, therefore, that none of these mechanisms by themselves can convert a normally productive infection of sensory neurons in culture to a non-productive or latent infection.
研究了多种免疫机制在离体大鼠感觉神经元培养物中改变单纯疱疹病毒正常增殖性感染的能力。这些机制包括有或无补体辅助的抗HSV抗体、HSV致敏的“T”细胞、自然杀伤细胞以及“K”细胞加抗HSV抗体(抗体依赖的细胞介导的细胞毒性反应)。虽然抗HSV抗体加补体以及抗体依赖的细胞介导的细胞毒性机制均显著限制了感染性HSV的产生,但没有一种机制能够阻止大多数神经元最终被感染。因此,似乎这些机制单独作用时,均无法将培养的感觉神经元中正常的增殖性感染转变为非增殖性或潜伏性感染。