Search for SARS-CoV-2 RNA in platelets from COVID-19 patients.

The frequent finding of thrombocytopenia in patients with severe SARS-CoV-2 infection (COVID-19) and previous evidence that several viruses enter platelets suggest that SARS-CoV-2 might be internalized by platelets of COVID-19. Aim of our study was to assess the presence of SARS-CoV-2 RNA in platelets from hospitalized patients with aconfirmed diagnosis of COVID-19. RNA was extracted from platelets, leukocytes and serum from 24 COVID-19 patients and 3 healthy controls, real-time PCR and ddPCR for viral genes were carried out.

Association of Neutrophil Activation, More Than Platelet Activation, With Thrombotic Complications in Coronavirus Disease 2019.

Background: Severe acute respiratory syndrome coronavirus 2 infection is associated with hypercoagulability, which predisposes to venous thromboembolism (VTE). We analyzed platelet and neutrophil activation in patients with coronavirus disease 2019 (COVID-19) and their association with VTE.

Methods: Hospitalized patients with COVID-19 and age- and sex-matched healthy controls were studied.

Anti-platelet treatments in cancer: Basic and clinical research.

Over the past few decades the central role that platelets play in cancer development and progression, and especially in metastasis, has been elucidated. The molecular mechanisms responsible for initiating and mediating tumor cell-induced platelet aggregation and secretion have been largely unravelled. Considerable mechanistic insight into how platelets contribute to tumor angiogenesis, immunoevasion and cancer cell invasion have been clarified and, consequently, platelets have been identified as potential new drug targets for cancer therapy.

Modeling CD40-based molecular communications in blood vessels.

This paper presents a mathematical characterization of the main features of the molecular communication between platelets and endothelial cells via CD40 signaling during the initial phases of atherosclerosis, known also as atherogenesis. We demonstrate through laboratory experimentation that the release of soluble CD40L molecules from platelets in a fluid medium is enough to trigger expression of adhesion molecules on endothelial cell's surface; that is, physical contact between the platelets and the endothelial cells is not necessary. We also propose the mathematical model of this communication, and we quantify the model parameters by matching the experiment results to the model.