Abstract
Hantavirus pulmonary syndrome (HPS) is an acute zoonotic disease transmitted primarily through inhalation of virus-contaminated aerosols. Hantavirus infection of endothelial cells leads to increased vascular permeability without a visible cytopathic effect. For this reason, it has been suggested that the pathogenesis of HPS is indirect with immune responses, such as cytokine production, playing a dominant role. In order to investigate their potential contribution to HPS pathogenesis, we analyzed the serum of hantavirus-infected subjects and healthy controls for 68 different cytokines, chemokines, angiogenic, and growth factors. Our analysis identified differential expression of cytokines that promote tissue migration of mononuclear cells including T lymphocytes, natural killer cells, and dendritic cells. Additionally, we observed a significant upregulation of cytokines known to regulate leukocyte migration and subsequent repair of lung tissue, as well as cytokines known to increase endothelial monolayer permeability and facilitate leukocyte transendothelial migration. Conversely, we observed a downregulation of cytokines associated with platelet numbers and function, consistent with the thrombocytopenia observed in subjects with HPS. This study corroborates clinical findings and extends our current knowledge regarding immunological and laboratory findings in subjects with HPS.
Highlights
Hantavirus pulmonary syndrome (HPS) is a severe life threatening disease caused by members of the genus Hantavirus
Anti-Hantavirus Titer in HPS Serum Twelve serum samples from subjects suspected of having hantavirus infection were tested for the presence of anti-hantavirus IgG and IgM antibodies
Infection of endothelial cells leads to increased vascular permeability without an observable cytopathic effect; the pathogenesis of HPS is likely indirect with immune responses, such as cytokine production, playing an important role
Summary
Hantavirus pulmonary syndrome (HPS) is a severe life threatening disease caused by members of the genus Hantavirus. HPS was first diagnosed as a clinical entity in 1993 in response to the four corners outbreak [6], retrospective studies have identified hantavirus-associated fatalities as early as 1978 [7]. HPS cases have been reported in 34 states with the majority occurring in the Southwestern states; several have been reported in the Northwestern and Midwestern states. Through April 2014, the Center for Disease Control and Prevention has confirmed 639 total cases of HPS in the U.S, with the majority occurring in New Mexico (94 cases), Colorado (81 cases), and Arizona (72 cases) [8]. The prevalence of HPS is low in the U.S, 36% of all reported HPS cases have resulted in death, underscoring the potential impact to public health
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