Hantavirus Infection Suppresses Thrombospondin-1 Expression in Cultured Endothelial Cells in a Strain-Specific Manner

Hantavirus infection is associated with two frequently fatal diseases in humans: Hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The pathogenesis of hantavirus infection is complex and not fully understood; however, it is believed to involve virus-induced hyperi...

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Published inFrontiers in microbiology Vol. 7; p. 1077
Main Authors Khaiboullina, Svetlana F, Morzunov, Sergey P, St Jeor, Stephen C, Rizvanov, Albert A, Lombardi, Vincent C
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 19.07.2016
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Summary:Hantavirus infection is associated with two frequently fatal diseases in humans: Hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). The pathogenesis of hantavirus infection is complex and not fully understood; however, it is believed to involve virus-induced hyperinflammatory immune responses. Thrombospondin-1 (THBS1) is a large homotrimeric protein that plays a putative role in regulating blood homeostasis. Hyperresponsiveness to inflammatory stimuli has also been associated with defects in the THBS1 gene. Our data suggest that hantavirus infection of human umbilical cord vein endothelial cells (HUVEC) suppress the accumulation of THBS1 in the extracellular matrix. Additionally, this suppression is dependent on virus replication, implying a direct mechanism of action. Our data also imply that the pathogenic Andes and Hantaan strains inhibit THBS1 expression while the non-pathogenic Prospect Hill strain showed little inhibition. These observations suggest that a dysregulation of THBS1 may contribute to the pathogenesis of hantavirus infection.
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Edited by: Fabrice Merien, Auckland University of Technology, New Zealand
This article was submitted to Infectious Diseases, a section of the journal Frontiers in Microbiology
Reviewed by: Xiaodong Zhang, Jilin University, China; Bruno Pozzetto, Jean Monnet University, France
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2016.01077