Pfau C J, Gresser I, Hunt K D
J Gen Virol. 1983 Aug;64 (Pt 8):1827-30. doi: 10.1099/0022-1317-64-8-1827.
After intracerebral inoculation of adult C3H mice, the 'docile' strain of lymphocytic choriomeningitis (LCM) virus multiplied to high titre in several visceral organs. Although the virus content of lung, liver, spleen and brain was high, these mice did not die but became long-term carriers of the virus. Injection of mice with the same dose of the 'aggressive' strain of LCM virus resulted in much lower virus titres in these organs; nevertheless, 100% of the mice died within 7 to 9 days. The results presented here show that mice infected with the 'aggressive' virus do not die if treated with anti-interferon globulin. Under these conditions the titres of 'aggressive' virus were as high in the different organs as in mice injected with the 'docile' virus. These results are consistent with the hypothesis that inhibition of LCM virus multiplication in various organs by interferon results in a lethal disease. The possible mechanisms underlying this seemingly paradoxical phenomenon are discussed.
成年C3H小鼠经脑内接种淋巴细胞性脉络丛脑膜炎（LCM）病毒的“温顺”株后，该病毒在多个内脏器官中大量繁殖至高滴度。尽管肺、肝、脾和脑中的病毒含量很高，但这些小鼠并未死亡，而是成为了该病毒的长期携带者。给小鼠注射相同剂量的LCM病毒“侵袭性”株后，这些器官中的病毒滴度要低得多；然而，100%的小鼠在7至9天内死亡。此处呈现的结果表明，感染“侵袭性”病毒的小鼠若用抗干扰素球蛋白治疗则不会死亡。在这些条件下，“侵袭性”病毒在不同器官中的滴度与注射“温顺”病毒的小鼠中的滴度一样高。这些结果与以下假设一致，即干扰素对LCM病毒在各种器官中的繁殖的抑制导致了致命疾病。文中讨论了这一看似矛盾的现象背后的可能机制。
