In the spring of 1993, an unknown group of hantaviruses emerged in the United States as the cause of an acute respiratory disease currently termed as Hantavirus pulmonary symdrome (HPS), also referred to as hantavirus cardiopulmonary syndrome (HCPS). HPS, a pan-American viral zoonosis, is a deadly viral hemorrhagic disease caused by sin nombre virus (SNV) and the extreme manifestations include increased capillary permeability (causing vascular leakage), circulatory instability, diffuse hemorrhage and thrombocytopenia. Virus infects the endothelial cells but does not disrupt the endothelium but leads to dramatic changes in both the function of infected endothelial cells and barrier function of endothelium. It has also been observed that capillary leakage is triggered by cytotoxic CD8+T cells (CTLs) and that cytokines contribute to the increased capillary permeability. Vascular permeability can also be increased by terminal soluble complement complex and this complement activation is linked to severity of hantavirus infection. But still to cure this deadly disease there is no effective treatment. A better understanding of viral biology and pathophysiology could lead to more specific and effective therapeutic modalities in the future.
Key words: Hantavirus pulmonary syndrome (HPS); Rodents; Epidemiology; Pathophysiology
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