Abstract
Background Transmission of HIV-1 between CD4+ T cells is by cellfree infection or direct cell-to-cell spread at intercellular junctions called virological synapses (VS). Transmission at VS has been shown to be orders of magnitude more efficient than cell-free infection. Increasing evidence suggests a key role for cell-cell spread in HIV-1 dissemination, replication and pathogenesis. Our previous work showed that HIV-1 VS formation is associated with striking organelle polarization to intercellular junctions and that a large volume of the synaptic cytoplasm in the infected cell is occupied by mitochondria. However, whether this occurs in response to contact and the functional consequences imparted by this are unclear. Therefore, we set out to investigate the potential role of mitochondria in the formation of the HIV-1 VS and in HIV-1 cell-cell spread.
Highlights
Transmission of HIV-1 between CD4+ T cells is by cellfree infection or direct cell-to-cell spread at intercellular junctions called virological synapses (VS)
Using immunofluorescence staining we found a strong association between Gag enrichment at the VS and copolarization of mitochondria within the infected cell
Live cell imaging showed that mitochondria polarization in the infected cell occurred within minutes of establishment of contact with the target cell and was concomitant with that of Gag
Summary
Transmission of HIV-1 between CD4+ T cells is by cellfree infection or direct cell-to-cell spread at intercellular junctions called virological synapses (VS). Contact-induced polarization shapes HIV-1 infected T cells for efficient HIV-1 dissemination at the virological synapse Background Transmission of HIV-1 between CD4+ T cells is by cellfree infection or direct cell-to-cell spread at intercellular junctions called virological synapses (VS).
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