Longitudinal Assessment of Cytokine Expression and Plasminogen Activation in Hantavirus Cardiopulmonary Syndrome Reveals Immune Regulatory Dysfunction in End-Stage Disease
Posted by Adam Awdish on
Human PAI-1 ELISA Kit from Innovative Research (Molecular Innovations) was used in the following study:
Peter Simons, Yan Guo, Virginie Bondu, Susan L. Tigert, Michelle Harkins, Samuel Goodfellow, Cana Tompkins, Devon Chabot-Richards, Xuexian O. Yang, Laura Gonzalez Bosc, Steven Bradfute, Daniel A. Lawrence, and Tione Buranda
Viruses
August 12, 2021
Hantavirus cardiopulmonary syndrome (HCPS) cases are characterized by loss of pulmonary vascular endothelial integrity that has the potential to cause acute pulmonary edema. HCPS tends to present high levels of inflammatory mediators in the lungs and systemic circulation of its patients and progresses rapidly, with hospitalization usually occurring 3-6 days after onset and fatalities occurring 3 days after hospitalization.
One major cause of HCPS is the Sin Nombre virus (SNV), which is transmitted via airborne route to the lungs and has a fatality rate of 30-50%. SNV typically targets vascular endothelial cells, and severe cases require extracorporeal membrane oxygenation (ECMO) treatment. End-stage HCPS patients have been observed to express a rise in plasminogen activator inhibitor type 1 (PAI-1), which is linked to undesirable outcomes in diseases related to ischemic cardiovascular events, fibrosis, and cancer. PAI-1 is a potent inhibitor of plasminogen activators, tissue plasminogen activator (tPA), urokinase-type plasminogen activator (uPA), and plasmin.
Previous studies have looked to better understand the pathology of HCPS caused by SNV, however the correlations between innate and adaptive immune responses and disease outcomes are still not fully understood. In this study, researchers analyzed immune responses in 13 HCPS cases induced by SNV, 11 of which required ECMO treatment. It was observed robust proinflammatory responses appeared in many end-stage cases that resulted in mortality, giving insights into potential ways to identify and treat end-stage HCPS earlier in patients, as well as insights into the disease’s path of action in the body.
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