α/β干扰素可增强宿主对鼠类艾滋病的抵抗力。
Alpha/beta interferons increase host resistance to murine AIDS.
作者信息
Heng J K, Price P, Lai C M, Beilharz M W
机构信息
Department of Microbiology, Queen Elizabeth II Medical Centre, University of Western Australia, Australia.
出版信息
J Virol. 1996 Jul;70(7):4517-22. doi: 10.1128/JVI.70.7.4517-4522.1996.
Murine AIDS (MAIDS) is caused by a defective retrovirus present in the LP-BM5 murine leukemia virus mixture. Strains of inbred mice differ in resistance to MAIDS development; some are susceptible (e.g., C57BL/6), while others are resistant (e.g., CBA and B10.BR). As an early block to viral replication in resistant mice has been demonstrated previously by PCR studies, we postulated that alpha/beta interferons (IFN-alpha/beta) may be involved in resistance to MAIDS. Susceptible C57BL/6 mice infected with LP-BM5 were treated with IFN-alpha/beta or Newcastle disease virus. Newcastle disease virus induces high endogenous IFN-alpha/beta production in mice. Both treatments delayed the development of MAIDS, as assessed by splenomegaly and T- and B-cell proliferation. In addition, an IFN-alpha/beta response was detected by reverse transcription-PCR and dot blotting 3, 6, and 9 h after LP-BM5 infection in resistant mice but not in susceptible mice. These results suggest that the ability to produce IFN-alpha/beta in response to LP-BM5 infection may contribute to host resistance to MAIDS.
鼠类获得性免疫缺陷综合征（MAIDS）由存在于LP - BM5鼠白血病病毒混合物中的一种缺陷逆转录病毒引起。近交系小鼠品系对MAIDS发展的抵抗力存在差异；一些品系易感（如C57BL/6），而其他品系具有抗性（如CBA和B10.BR）。由于先前通过PCR研究已证明抗性小鼠中存在对病毒复制的早期阻断，我们推测α/β干扰素（IFN - α/β）可能参与对MAIDS的抗性。用IFN - α/β或新城疫病毒处理感染LP - BM5的易感C57BL/6小鼠。新城疫病毒可诱导小鼠产生高水平的内源性IFN - α/β。通过脾肿大以及T细胞和B细胞增殖评估，两种处理均延迟了MAIDS的发展。此外，在抗性小鼠中，LP - BM5感染后3、6和9小时通过逆转录PCR和斑点印迹检测到IFN - α/β反应，而在易感小鼠中未检测到。这些结果表明，对LP - BM5感染产生IFN - α/β的能力可能有助于宿主对MAIDS的抗性。
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