DesGroseillers L, Barrette M, Jolicoeur P
J Virol. 1984 Nov;52(2):356-63. doi: 10.1128/JVI.52.2.356-363.1984.
We have recently shown that a molecularly cloned ecotropic retrovirus, initially isolated from the brain of a paralyzed wild mouse, retained the ability to induce hind limb paralysis when inoculated into susceptible mice (Jolicoeur et al., J. Virol. 45:1159-1163, 1983). To map the viral DNA sequences encoding the determinant of paralysis, we constructed chimeric viral DNA genomes in vitro between parental cloned infectious viral DNA genomes from this neurotropic murine leukemia virus (MuLV) and from nonneurotropic amphotropic 4070-A MuLV. Infectious chimeric MuLVs, recovered after microinjection of NIH 3T3 cells with these recombinant DNAs, were inoculated into newborn SIM.S and SWR/J mice to test the paralysis-inducing potential. We found that the 3.9-kilobase-pair SalI-ClaI fragment of the neurotropic MuLV comprising the 3' end of pol and all env sequences was sufficient to confer the paralysis-inducing potential to chimeric viruses. Therefore, this region of the neurotropic MuLV genome most likely harbors the primary determinant of paralysis.
我们最近发现，一种分子克隆的亲嗜性逆转录病毒，最初从一只瘫痪的野生小鼠大脑中分离出来，接种到易感小鼠体内时仍保留诱导后肢麻痹的能力（乔利厄尔等人，《病毒学杂志》45:1159 - 1163，1983年）。为了定位编码麻痹决定簇的病毒DNA序列，我们在体外构建了嵌合病毒DNA基因组，其亲本克隆的感染性病毒DNA基因组分别来自这种嗜神经性小鼠白血病病毒（MuLV）和非嗜神经性双嗜性4070 - A MuLV。用这些重组DNA显微注射NIH 3T3细胞后回收的感染性嵌合MuLV，接种到新生的SIM.S和SWR/J小鼠体内，以测试其诱导麻痹的潜力。我们发现，嗜神经性MuLV的3.9千碱基对的SalI - ClaI片段，包含pol的3'端和所有env序列，足以赋予嵌合病毒诱导麻痹的潜力。因此，嗜神经性MuLV基因组的这一区域很可能包含麻痹的主要决定簇。
