Congratulations to Luc and Joon as their manuscript was accepted in Brain (IF 10.848)! They equally contributed to this excellent paper.

Bertrand L*, Cho HJ*, Toborek M. Blood-brain barrier pericytes as a target for HIV-1 infection. Brain. 2019 Mar 1;142(3):502-511. doi: 10.1093/brain/awy339.
*equal contribution

Pericytes are multifunctional cells wrapped around endothelial cells via cytoplasmic processes that extend along the abluminal surface of the endothelium. The interactions between endothelial cells and pericytes of the blood-brain barrier (BBB) are necessary for proper formation, development, stabilization, and maintenance of the BBB. BBB pericytes regulate paracellular flow between cells, transendothelial fluid transport, maintain optimal chemical composition of the surrounding microenvironment, and protect endothelial cells from potential harmful substances. Thus, dysfunction or loss of BBB pericytes is an important factor in the pathogenesis of several diseases that are associated with microvascular instability. Importantly, recent research indicates that BBB pericytes can be a target of HIV-1 infection able to support productive HIV-1 replication. In addition, BBB pericytes are prone to establish a latent infection, which can be reactivated by a mixture of histone deacetylase inhibitors in combination with TNF. HIV-1 infection of BBB pericytes has been confirmed in a mouse model of HIV-1 infection and in human post-mortem samples of HIV-1-infected brains. Overall, recent evidence indicates that BBB pericytes can be a previously unrecognized HIV-1 target and reservoir in the brain.

November 2018


Figure for update

Structural and molecular BBB pericyte connections within the neurovascular unit. (A) BBB pericytes (yellow) and endothelial cells (red) share the basement membrane (sky blue) or are in direct contacts. In addition, BBB pericytes are surrounded by glial cells (astrocytes, green; microglia, dark blue) and neurons (purple). (B) BBB pericytes and endothelial cells communicate with each other by direct contact (gap and adherens junctions) or through signaling pathways, such as platelet-derived growth factor B (PDGF-B)/PDGFRβ and transforming growth factor-β (TGF-β)/type 2 TGF-β receptor (TGFβR2