Multiplicity of human immunodeficiency virus infections in lymphoid tissue
Multiplicity of human immunodeficiency virus infections in lymphoid tissue
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DOI：
10.1128/jvi.78.16.8942-8945.2004
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发表时间：
2004-08-01
影响因子：
5.4
通讯作者：
Perelson, AS
中科院分区：
文献类型：
--
作者：
Dixit, NM;Perelson, AS
人类免疫缺陷病毒1型（HIV-1）感染的人脾细胞最近显示平均每个细胞含有3至4个前病毒（A. Jung等人，Nature 418：144，2002）。然而，导致如此广泛的多重感染的机制尚不清楚。在这里，我们发现通过使用数学分析，两种机制定量捕获HIV-1感染的脾细胞中前病毒基因组的分布，一种是在靶细胞与游离病毒体和感染细胞的一系列连续感染接触中一次获得一个多个基因组，另一种是多个病毒体或基因组的细胞间传播是由靶细胞与受感染细胞的单次感染性接触引起的。这两种机制意味着感染细胞内前病毒的遗传多样性不同，因此通过重组产生耐药性的速率也不同。
Human immunodeficiency virus type 1 (HIV-1)-infected splenocytes in humans were recently shown to harbor three to four proviruses per cell on average (A. Jung et al., Nature 418:144, 2002). However, the mechanisms that lead to such extensive multiple infections are not understood. Here, we find by using mathematical analysis that two mechanisms quantitatively capture the distribution of proviral genomes in HIV-1-infected splenocytes, one where multiple genomes are acquired one at a time in a series of sequential infectious contacts of a target cell with free virions and infected cells, and the other where cell-to-cell transmission of multiple virions or genomes results from a single infectious contact of a target cell with an infected cell. The two mechanisms imply different genetic diversities of proviruses within an infected cell and therefore different rates of emergence of drug resistance via recombination.