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Published January 2, 2018 | Published + Supplemental Material
Journal Article Open

Dendritic cells efficiently transmit HIV to T Cells in a tenofovir and raltegravir insensitive manner


Dendritic cell (DC)-to-T cell transmission is an example of infection in trans, in which the cell transmitting the virus is itself uninfected. During this mode of DC-to-T cell transmission, uninfected DCs concentrate infectious virions, contact T cells and transmit these virions to target cells. Here, we investigated the efficiency of DC-to-T cell transmission on the number of cells infected and the sensitivity of this type of transmission to the antiretroviral drugs tenofovir (TFV) and raltegravir (RAL). We observed activated monocyte-derived and myeloid DCs amplified T cell infection, which resulted in drug insensitivity. This drug insensitivity was dependent on cell-to-cell contact and ratio of DCs to T cells in coculture. DC-mediated amplification of HIV-1 infection was efficient regardless of virus tropism or origin. The DC-to-T cell transmission of the T/F strain CH077.t/2627 was relatively insensitive to TFV compared to DC-free T cell infection. The input of virus modulated the drug sensitivity of DC-to-T cell infection, but not T cell infection by cell-free virus. At high viral inputs, DC-to-T cell transmission reduced the sensitivity of infection to TFV. Transmission of HIV by DCs in trans may have important implications for viral persistence in vivo in environments, where residual replication may persist in the face of antiretroviral therapy.

Additional Information

© 2018 Kim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Received: June 15, 2017; Accepted: December 5, 2017; Published: January 2, 2018. Data Availability Statement: All relevant data are within the paper and its Supporting Information files. This work was supported by the UCLA CTSI KL2 (KL2TR001882), National Institutes of Health (OPPGH5157), American Foundation for AIDS Research (108292-51-RGRL), UCLA/CFAR Virology Core Laboratory (5P30 AI028697), the UCLA Specialty Training and Advanced Research Program, and NIH AIDS Reagent Program. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors have declared that no competing interests exist.

Attached Files

Published - journal.pone.0189945.pdf

Supplemental Material - journal.pone.0189945.s001.pdf

Supplemental Material - journal.pone.0189945.s002.pdf

Supplemental Material - journal.pone.0189945.s003.pdf


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