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. 2009 Jan 15;113(3):671-4.
doi: 10.1182/blood-2008-09-175000. Epub 2008 Nov 17.

Cellular microRNA expression correlates with susceptibility of monocytes/macrophages to HIV-1 infection

Xu Wang  1 , Li Ye, Wei Hou, Yu Zhou, Yan-Jian Wang, David S Metzger, Wen-Zhe Ho
Affiliations

Cellular microRNA expression correlates with susceptibility of monocytes/macrophages to HIV-1 infection

Xu Wang et al. Blood. .

Abstract

Although both monocytes and macrophages possess essential requirements for HIV-1 entry, peripheral blood monocytes are infrequently infected with HIV-1 in vivo and in vitro. In contrast, tissue macrophages and monocyte-derived macrophages in vitro are highly susceptible to infection with HIV-1 R5 tropic strains. We investigated intracellular anti-HIV-1 factors that contribute to differential susceptibility of monocytes/macrophages to HIV-1 infection. Freshly isolated monocytes from peripheral blood had significantly higher levels of the anti-HIV-1 microRNAs (miRNA, miRNA-28, miRNA-150, miRNA-223, and miRNA-382) than monocyte-derived macrophages. The suppression of these anti-HIV-1 miRNAs in monocytes facilitates HIV-1 infectivity, whereas increase of the anti-HIV-1 miRNA expression in macrophages inhibited HIV-1 replication. These findings provide compelling and direct evidence at the molecular level to support the notion that intracellular anti-HIV-1 miRNA-mediated innate immunity may have a key role in protecting monocytes/macrophages from HIV-1 infection.

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Figures

Figure 1
Figure 1
Differential HIV-1 infectivity and anti–HIV-1 miRNAs expression in monocytes and macrophages. (A) HIV-1 infection of monocytes and macrophages. Cells were infected with HIV-1 Bal strain either immediately after isolation (D0 monocytes) or after having been cultured for 7 days (D7 macrophages). Replication kinetics of HIV-1 Bal in cell culture was measured by RT activity in culture supernatants. Culture supernatants were collected at the indicated time points postinfection. The data shown are the mean (± SD) of triplicate cultures, representative of three experiments using cells from three different donors. The inserts shown in A are the morphologies of freshly isolated monocytes (D0 monocytes) and 7-day cultured monocytes (D7 macrophages). (B) Anti-HIV-1 miRNAs expression during monocyte differentiation. Cells collected at the indicated time points were subjected RNA extraction for miRNA expression by real-time RT PCR. The data shown are the mean (± SD) of triplicate cultures representative of 3 experiments using cells from 3 different donors.
Figure 2
Figure 2
Effect of modulation of the anti-HIV-1 miRNA expression on HIV-1 infection of monocytes and macrophages. (A) D0 monocytes were transfected with the combined microRNA (miRNA-28, 150, 223, and 382) inhibitors or the negative control inhibitor (Anti-miRNA Ctl) for 48 hours, and then infected with the HIV-1 Bal or Yu2 strain. Culture supernatants were collected for HIV-1 RT activity at day 12 postinfection. (B) D7 macrophages were transfected with the combined miRNAs (miRNA-28, 150, 223, and 382) or negative control miRNAs (miRNA Ctl) for 48 hours, and then infected with HIV-1 Bal or Yu2 strain. Culture supernatants were collected for HIV-1 RT activity at day 12 postinfection. The data shown are the mean (± SD) of triplicate culture, representative of 3 experiments using cells from 3 different donors (*P < 0.05, **P < 0.01; combined miRNAs or combined anti-miRNAs vs miRNAs Ctl or anti-miRNA Ctl).
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