Center for Infectious Medicine, F59, Karolinska Institutet, Dept. of Medicine Karolinska Huddinge, S-141 86 Stockholm, Sweden.
Abstracts of the papers presented at the International Conference of Indian Virological Society on “Emerging and Re-emerging viral Diseases of the Tropics and Subtropics” at Indian Agricultural Research Institute, New Delhi, India, December 11–14, 2007.
Dendritic cells (DCs) are antigen presenting cells with capacity to initiate primary T cell responses against pathogens such as HIV-1. In addition, DCs express receptors required for HIV-1 infection and are probably one of the first target cells during mucosal transmission of HIV-1. Their localization in mucosal epithelial and in the T cell areas of lymphoid organs as well as their role in capturing antigen and initiating T cell responses, highlights their importance during HIV-1 pathogenesis. We have studied the effects of HIV-1 infection on DC function. We found that monocyte-derived DCs were productively infected by HIV-1 after in vitro exposure. HIV1 infected monocyte-derived DCs upregulated co-stimulatory molecules in response to CD40L stimulation comparable to uninfected DCs. However, intracellular cytokine staining revealed that HIV-1 infected DCs failed to produce IL12p70, although they could respond with TNF-alpha production. This may impact the ability of DCs to induce optimal HIV-1 specific immune responses. In addition, we found a differential susceptibility to HIV-1 infection of primary isolated myeloid and plasmacytoid dendritic cells. Productively infected myeloid and plasmacytoid DCs efficiently transferred HIV-1 to autolgous CD4+ T cells and antigen-reactivated T cells were more frequently infected than resting T cells. Altogether, these findings suggest that DCs are under certain conditions impaired by HIV-1 infection but can still transfer HIV-1 to CD4+ T cells.
