Figure 1
Figure 1. hBD2 inhibits the accumulation of early reverse transcription products of HIV. PBMCs were infected with DNase I–treated X4 HIVIIIB (A) or R5 HIVBaL (B). After virus removal and washing, hBD2 (0.8-20 μg/mL) was added to the tissue culture media. Cells were pretreated with AZT (2.67 μg/mL) or T20 (11.25 μg/mL) as controls. Total cellular DNA was isolated at the indicated time points, and the presence of early reverse transcription products was determined by real-time PCR. Triplicate readings were averaged, and inhibition was determined as a percentage of the number of copies of early reverse transcription products in infected treated cells in reference to copies measured in untreated control infections. Shown here are mean percentage of inhibition (± SEM) of 4 independent experiments that used cells from different donors.

hBD2 inhibits the accumulation of early reverse transcription products of HIV. PBMCs were infected with DNase I–treated X4 HIVIIIB (A) or R5 HIVBaL (B). After virus removal and washing, hBD2 (0.8-20 μg/mL) was added to the tissue culture media. Cells were pretreated with AZT (2.67 μg/mL) or T20 (11.25 μg/mL) as controls. Total cellular DNA was isolated at the indicated time points, and the presence of early reverse transcription products was determined by real-time PCR. Triplicate readings were averaged, and inhibition was determined as a percentage of the number of copies of early reverse transcription products in infected treated cells in reference to copies measured in untreated control infections. Shown here are mean percentage of inhibition (± SEM) of 4 independent experiments that used cells from different donors.

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