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. 2006 Feb;80(3):1290–1301. doi: 10.1128/JVI.80.3.1290-1301.2006

FIG. 3.

FIG. 3.

DC-SIGN(R)-mediated enhancement of infection in primary cell cultures. (A) Titration of 293T-derived (open triangles) and C6/36-derived (closed triangles) WNV strain NY2000 on immature MDDCs. Percentages of infection were assessed after 20 h by intracellular FACS. Similar results were obtained using MDDCs from two other donors. (B) Blockade of MDDC infection by inhibitors of DC-SIGN. MDDCs were preincubated with the indicated inhibitors and infected with 293T- or C6/36-derived NY2000. Percentages of infection were assessed after 20 h by intracellular FACS. MAbs were used at 10 μg/ml, and mannan was used at 500 μg/ml. Infections were performed at an MOI of 0.09 for NY2000 grown in 293T cells and at an MOI of 0.04 for C6/36-derived virus. One representative experiment out of two performed is shown. (C) HUVECs were infected with lentiviruses encoding a control gene (lacZ), DC-SIGN, or DC-SIGNR at an MOI of 0.1. Seventy-two h posttransduction, cells were infected with 293T-derived NY2000 at an MOI of 0.05. After 20 h, intracellular staining for WNV E protein and DC-SIGN(R) expression was performed. For HUVECs transduced with DC-SIGN or DC-SIGNR lentiviruses, percentages of infection were assessed in both DC-SIGN(R)-expressing (DC11-PE-positive) and nonexpressing (DC11-PE-negative) cell populations.