Dengue virus (DENV) poses a considerable threat to public health on a global scale, since about two-thirds of the world's population is currently at risk of contracting this arbovirus. Being transmitted by mosquitoes, this virus is associated with a range of illnesses and a small percentage of infected individuals might suffer from severe vascular leakage. This leakage leads to hypovolemic shock syndrome, generally known as dengue shock syndrome, organ failure, and bleeding complications. The severe form of this disease is believed to be, at least partially, associated with inflammatory and thrombotic states. These issues are significantly affected by the activation of platelets and leukocytes, as well as their interactions, which may influence its prognosis. The platelets present in a thrombus are able to attract leukocytes to the site of injury. The intricate process leads to the significant accumulation, activation, and migration of leukocytes, thereby promoting thrombotic events and triggering inflammatory responses. The occurrence of these events, combined with the direct viral infection of endothelial cells, leads to vascular endothelialitis, the disruption of cellular membranes, and the subsequent release of DAMPs. As a result, considerable damage occurs in the endothelium, which activates neutrophils and platelets; thisleads to their interaction and initiates the process of Netosis. Collectively, these processes exacerbate inflammatory and thrombotic conditions. In this respect, current research has focused on understanding whether effective anti-inflammatory protocols can prevent thrombotic events or, conversely, if efficient anticoagulant regimens may lead to a reduction in cytokine storms and tissue damage. This review article aims to illuminate the platelet leukocyte crosstalk, detailing the mechanisms through which platelets may play a role in the pathogenesis of DENV. The research outputs are particularly important in severe cases, in which case their interactions with leukocytes can exacerbate both inflammation and thrombosis in a mutually reinforcing manner.