Kyasanur Forest disease virus infection activates human vascular endothelial cells and monocyte-derived dendritic cells

0498830 - BC 2019 RIV GB eng J - Článek v odborném periodiku
Širmarová, J. - Salát, J. - Palus, Martin - Hönig, Václav - Langhansová, Helena - Holbrook, M.R. - Růžek, Daniel
Kyasanur Forest disease virus infection activates human vascular endothelial cells and monocyte-derived dendritic cells.
Emerging Microbes & Infections. Roč. 7, č. 1 (2018), č. článku 175. E-ISSN 2222-1751
Grant CEP: GA MZd(CZ) NV16-34238A
Institucionální podpora: RVO:60077344
Klíčová slova: CONGO HEMORRHAGIC-FEVER * INTERCELLULAR-ADHESION MOLECULE-1 * NECROSIS-FACTOR-ALPHA * GENE-EXPRESSION * ELEVATED LEVELS * RENAL SYNDROME * EBOLA-VIRUS * CYTOKINE * MONOCYTES/MACROPHAGES
Obor OECD: Microbiology
Impakt faktor: 6.212, rok: 2018
https://www.nature.com/articles/s41426-018-0177-z

Kyasanur Forest disease virus (KFDV) is a highly pathogenic tick-borne flavivirus enzootic to India. In humans, KFDV causes a severe febrile disease. In some infected individuals, hemorrhagic manifestations, such as bleeding from the nose and gums and gastrointestinal bleeding with hematemesis and/or blood in the stool, have been reported. However, the mechanisms underlying these hemorrhagic complications remain unknown, and there is no information about the specific target cells for KFDV. We investigated the interaction of KFDV with vascular endothelial cells (ECs) and monocyte-derived dendritic cells (moDCs), which are key targets for several other hemorrhagic viruses. Here, we report that ECs are permissive to KFDV infection, which leads to their activation, as demonstrated by the upregulation of E-selectin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 at the mRNA and protein levels. Increased expression of these adhesive molecules correlated with increased leukocyte adhesion. Infected ECs upregulated the expression of interleukin (IL)-6 but not IL-8. Additionally, moDCs were permissive to KFDV infection, leading to increased release of IL-6 and tumor necrosis factor-α. Supernatants from KFDV-infected moDCs caused EC activation, as measured by leukocyte adhesion. The results indicate that ECs and moDCs can be targets for KFDV and that both direct and indirect mechanisms can contribute to EC activation.
Trvalý link: http://hdl.handle.net/11104/0291103