Background: Immature dendritic cells are among the first cells infected by retroviruses after mucosal exposure, and pathogen-host interactions during early stages of infection can have a profound influence on later stages of infection.

Methods: We explored the effects of HIV-1 and its Tat transactivator on these primary antigen-presenting cells using a combination of DNA microarray analysis and functional assays.

Results: We found that HIV-1 infection or Tat production can induce expression of IFN-responsive genes in immature human dendritic cells without inducing dendritic cell maturation. Several of the genes induced by HIV-1 and its Tat transactivator encode chemokines that recruit activated T-cells and macrophages, the ultimate target cells for the virus. These results are relevant to retroviral infection in vivo, because SIV-infected dendritic cells present in the lymph nodes of macaques have elevated levels of the chemokine MCP-2.

Conclusions: These results reveal a novel function for HIV-1 Tat, namely the reprogramming of host dendritic cell gene expression to facilitate expansion of the infection.