Loïc Talignani

TL;DR: It is shown that human dermal fibroblasts, epidermal keratinocytes, and immature dendritic cells are permissive to the most recent ZikV isolate, responsible for the epidemic in French Polynesia, and a major role is shown for the phosphatidylserine receptor AXL as a ZIKV entry receptor and for cellular autophagy in enhancing ZIKv replication in permissive cells.

TL;DR: Information is reviewed on the epidemiology and clinical features of Zika disease with a particular emphasis on the host-virus interactions that contribute to the pathogenicity of ZIKV in humans.

TL;DR: It is reported that Chikungunya virus (CHIKV) and West Nile virus (WNV) elicit a common antiviral signature in primary human dermal fibroblasts, attesting for the up regulation of interferon signaling pathways and leading to an increased expression of IFN-β, interleukins and chemokines.

TL;DR: It is shown that compounds interfering with intracellular cholesterol transport have the capacity to inhibit CHIKV replication in human skin fibroblasts, a major viral entry site in the human host.

TL;DR: The permissiveness of primary human astrocytes for two clinically relevant, Asian and African ZIKV strains are reported and it is shown that both isolates strongly induce antiviral immune responses in these cells albeit with markedly different kinetics.