Herrmann J E, West K, Bruns M, Ennis F A
Division of Infectious Diseases, University of Massachusetts Medical School, Worcester 01655.
J Infect Dis. 1990 Feb;161(2):180-4. doi: 10.1093/infdis/161.2.180.
Administration of rimantadine to mice via drinking water, following a prophylactic dose, reduced lung virus titers by greater than 3 log10 plague-forming units (pfu)/ml but caused only marginal reductions in lung virus titers when therapy was started 8 h after exposure to virus. Mice given rimantadine prophylactically plus therapeutically were resistant to rechallenge with virus at a dose equivalent to that used for the primary infection (50 pfu/mouse) but not to a high dose (1 x 10(5) pfu/mouse). Virus-neutralizing-antibody titers were reduced only by rimantadine treatment, which included prophylaxis, whereas the cytotoxic T lymphocyte (CTL) response was depressed by treatment given with or without prophylaxis. Mice infected with rimantadine-resistant virus had no decrease in CTL or antibody responses when treated with rimantadine. Therefore, the depression in CTL and antibody responses associated with rimantadine treatment appears to be due to a decrease in the amount of viral antigen available or interference with viral antigen processing and not to nonspecific immunosuppressive effects.
在预防性给药后，通过饮水给小鼠施用金刚乙胺，可使肺病毒滴度降低超过3个对数10蚀斑形成单位（pfu）/毫升，但在接触病毒8小时后开始治疗时，仅使肺病毒滴度略有降低。预防性和治疗性给予金刚乙胺的小鼠对相当于用于初次感染的剂量（50 pfu/小鼠）的病毒再攻击具有抗性，但对高剂量（1×10⁵ pfu/小鼠）则无抗性。仅通过包括预防在内的金刚乙胺治疗可降低病毒中和抗体滴度，而无论有无预防措施，细胞毒性T淋巴细胞（CTL）反应均会因治疗而受到抑制。用金刚乙胺治疗感染了金刚乙胺抗性病毒的小鼠时，CTL或抗体反应均未降低。因此，与金刚乙胺治疗相关的CTL和抗体反应的抑制似乎是由于可用病毒抗原量的减少或对病毒抗原加工的干扰，而不是由于非特异性免疫抑制作用。
