Buller R M, Yetter R A, Fredrickson T N, Morse H C
J Virol. 1987 Feb;61(2):383-7. doi: 10.1128/JVI.61.2.383-387.1987.
Strain C57BL/6 (B6) mice infected with LP-BM5 murine leukemia virus (MuLV) develop a disease which combines abnormal lymphoproliferation with profound immunosuppression and has many features in common with human acquired immunodeficiency syndrome induced by HTLV-III/LAV retroviruses. To determine whether this LP-BM5 MuLV infection would affect the innate resistance of B6 mice to a naturally occurring, highly virulent murine pathogen, mice were exposed to ectromelia virus at various times after treatment with LP-BM5 viruses. At week 4 after infection with LP-BM5, mice challenged with ectromelia virus were unable to generate a humoral immune response to this virus, and between weeks 8 and 10 after infection, challenged mice lost the ability to generate an ectromelia virus-specific cytotoxic-T-cell response. Loss of the cellular immune responses to ectromelia virus was associated with an increased susceptibility to the lethal effects of the virus.
感染LP - BM5鼠白血病病毒（MuLV）的C57BL/6（B6）品系小鼠会患上一种疾病，该疾病兼具异常淋巴细胞增殖和严重免疫抑制的特征，并且与由HTLV - III/LAV逆转录病毒引起的人类获得性免疫缺陷综合征有许多共同之处。为了确定这种LP - BM5 MuLV感染是否会影响B6小鼠对一种自然存在的、高致病性鼠病原体的天然抵抗力，在用LP - BM5病毒治疗后的不同时间，将小鼠暴露于痘苗病毒。在感染LP - BM5后第4周，用痘苗病毒攻击的小鼠无法对该病毒产生体液免疫反应，并且在感染后第8至10周之间，受攻击的小鼠失去了产生痘苗病毒特异性细胞毒性T细胞反应的能力。对痘苗病毒的细胞免疫反应丧失与对该病毒致死效应的易感性增加有关。
