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Year : 2023, Volume : 25, Issue : 2
First page : ( 84) Last page : ( 92)
Print ISSN : 0972-0561. Online ISSN : 0973-9149. Published online : 2023  02.
Article DOI : 10.5958/0973-9149.2023.00012.6

A Review on the Endotheliotropic Nature of Bluetongue Virus: Implications for Pathogenesis

Singh Deepti, Saminathan M.*, Chatla Arun, Deva R., Singh K.P.

Centre for Animal Disease Research and Diagnosis (CADRAD), ICAR-Indian Veterinary Research Institute (ICAR-IVRI), Izatnagar-243122, Bareilly, Uttar Pradesh, India

*Corresponding author email id: drswamyvet@gmail.com

Online Published on 02 March, 2024.

Received:  05  November,  2023; :  17  November,  2023; Accepted:  18  November,  2023.


Bluetongue (BT) is a non-contagious, infectious viral disease transmitted by insect vectors of Culicoides species, affecting both domestic and wild ruminants. It is caused by the genus Orbivirus of the Reoviridae family. The lesions of BTV primarily result from direct injury to the endothelial cells of the blood vessels or indirect injury via cytokines, leading to increased cell permeability, causing hemorrhages, exudation of fluid, and thrombosis. The vasodilatory substances secreted by the endothelium of vessels include prostacyclin, hyperpolarizing factors, natriuretic peptide of C-type, and nitric oxide (NO). Vasoconstrictors are also secreted by the endothelium. Angiotensin II, reactive oxygen species (ROS), thromboxane A2, and endothelin-1 are vasoactive mediators. Inflammatory agents produced by the endothelium include NF-κB, intercellular adhesion molecule-1 (ICAM-1), Eselectin, nitric oxide (NO), and VCAM-1. Bluetongue virus can damage endothelial cells, resulting in vascular thrombosis, tissue infarction, hemorrhage, and consumptive coagulopathy (disseminated intravascular coagulation). Host-derived vasoactive mediators during bluetongue virus infection play a role in endothelial dysfunction and an increase in vascular permeability. Vascular permeability is influenced by vasoactive mediators and cytokines upregulated during bluetongue virus infection. These include cyclooxygenase-2, inducible nitric oxide synthase (iNOS), interleukin 1 (IL-1), IL-8, IL-6, thromboxane and prostacyclin ratio, and TNF-α. These agents increase vascular permeability, induce vasodilation, and stimulate the secretion of acute phase reactants, leading to fever, hyperemia, and fluid exudation into soft tissues and body cavities. These are common clinical characteristics of Bluetongue (BT). Additionally, the endothelium ultimately undergoes damage, resulting in cell death and sloughing off, causing hemorrhage and thrombosis.



Endothelium, Bluetongue virus, Pathogenesis, Injury, Vasoactive mediators, Cytokines.


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