Virus replication begins in dendritic cells during the transmission of HIV-1 from mature dendritic cells to T cells.

Background: To initiate immunity, dendritic cells (DCs) capture antigens or viruses at body surfaces, undergo maturation to express T-cell costimulatory molecules, and then migrate to lymphoid organs. DCs at body surfaces can capture human immunodeficiency virus 1 (HIV-1), but mature DCs do not support replication of the virus unless T cells are added. The initial site for HIV-1 replication remains unknown and it is unclear whether replication can take place in DCs or whether the virus must first be transmitted from DCs to T cells.

Mature dendritic cells respond to SDF-1, but not to several beta-chemokines.

Immature dendritic cells (DCs) are highly motile, but after differentiation they stop migration. Chemokines are chemotactic cytokines that direct leukocyte trafficking, therefore we looked for the expression and function of chemokine receptors in immature and mature DCs. As a model, we used the human DCs that develop from CD14+ peripheral blood monocytes cultured with GM-CSF and IL-4.

Immature dendritic cells selectively replicate macrophagetropic (M-tropic) human immunodeficiency virus type 1, while mature cells efficiently transmit both M- and T-tropic virus to T cells.

Dendritic cells (DCs) can develop from CD14+ peripheral blood monocytes cultured in granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4). By 6 days in culture, the cells have the characteristics of immature DCs and can be further induced to mature by inflammatory stimuli or by monocyte-conditioned medium. After infection with macrophagetropic (M-tropic) human immunodeficiency virus type 1 (HIV-1), monocytes and mature DCs show a block in reverse transcription and only form early transcripts that can be amplified with primers for the R/U5 region.