Interference patterns of human immunodeficiency viruses HIV-1 and HIV-2.
Interference patterns of human immunodeficiency viruses HIV-1 and HIV-2.
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人类免疫缺陷病毒 HIV-1 和 HIV-2 的干扰模式。
DOI：
10.1016/0042-6822(90)90454-y
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发表时间：
1990
期刊：
影响因子：
3.7
通讯作者：
Cloyd,MW
中科院分区：
文献类型：
--
作者：
Hart,AR;Cloyd,MW
被一种逆转录病毒感染的细胞干扰另一种逆转录病毒的重复感染的能力通常涉及原代病毒对重复感染病毒受体的阻断。使用不同受体的逆转录病毒不会相互干扰，这一特性已被用于对不同类型的逆转录病毒进行分类。对不同的人类免疫缺陷病毒（HIV）分离株进行了这种类型的分析，发现所有HIV-1在T细胞和U937前单核细胞中相互交叉干扰，进一步证实所有分离株在这些细胞上使用相同的受体。发现HIV-2分离物能够干扰HIV-1 - s，但HIV-1 - s仅部分干扰HIV-2的重复感染，这表明HIV-1和HIV-2在受体相互作用上存在固有的差异。相比之下，d型灵长类逆转录病毒（srv）和小鼠两性性和异种性逆转录病毒的干扰模式显示，每种病毒都属于不同的干扰组，这表明人类T细胞至少具有四种不同的逆转录病毒受体。发现HIV干扰的机制是由于有效感染细胞中的受体阻断和潜伏感染T细胞中的受体消除。我们发现所有HIV-1完全相互干扰，并且这种干扰在急性感染后迅速发生，这表明HIV-1感染的细胞不允许后代或其他外源性hiv再次感染。反过来，这表明后代再感染可能不是HIV细胞病变感染后观察到的大量未整合病毒DNA的来源。
The ability of cells infected with a retrovirus to interfere with superinfection by another retrovirus usually involves blockage, by the primary virus, of the receptors for the superinfecting virus. Retroviruses using different receptors do not interfere with each other, and this property has been used to classify various types of retroviruses. Different isolates of human immunodeficiency virus (HIV) were subjected to this type of analysis, and it was found that all HIV-1 s cross-interfere with each other in T cells as well as in U937 promonocytic cells, substantiating further that all isolates use the same receptor on these cells. An HIV-2 isolate was found to interfere with HIV-1 s, but HIV-1 s only partially interfered with HIV-2 superinfection, indicating that inherent differences in receptor interactions exist between HIV-1s and HIV-2. For comparison, interference patterns of D-type primate retroviruses (SRVs) and murine amphotropic and xenotropic retroviruses revealed that each virus fell within distinct interference groups demonstrating that human T cells possess at least four distinct receptors for retroviruses. The mechanism of HIV interference was found to be due to receptor blockage in productively infected cells and to receptor elimination in latently infected T cells. Our findings that all HIV-1s completely interfere with each other and that interference occurs rapidly following acute infection suggests that a cell infected with HIV-1 will not permit reinfection by progeny or by other exogenous HIVs. This, in turn, suggests that progeny reinfection may not be the source of the large amount of unintegrated viral DNA observed following HIV cytopathic infection.