Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.

Diseases caused by dengue virus (DV) infection vary in severity, with symptoms ranging from mild fever to life threatening dengue hemorrhage fever (DHF) and dengue shock syndrome (DSS). Clinical studies have shown that significant decrease in the level of lipoproteins is correlated with severe illne...

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Main Authors: Yujia Li, Cherie Kakinami, Qi Li, Baojun Yang, Hongwei Li
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3722190?pdf=render
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spelling doaj-f7abc9280d8b40c8a5c681cbe587ada22020-11-24T20:52:37ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0187e7039010.1371/journal.pone.0070390Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.Yujia LiCherie KakinamiQi LiBaojun YangHongwei LiDiseases caused by dengue virus (DV) infection vary in severity, with symptoms ranging from mild fever to life threatening dengue hemorrhage fever (DHF) and dengue shock syndrome (DSS). Clinical studies have shown that significant decrease in the level of lipoproteins is correlated with severe illness in DHF/DSS patients. Available evidence also indicates that lipoproteins including high-density lipoprotein (HDL) and low-density lipoprotein (LDL) are able to facilitate cell entry of HCV or other flaviviruses via corresponding lipoprotein receptors. In this study, we found that pre-incubation of DV with human serum leads to an enhanced DV infectivity in various types of cells. Such enhancement could be due to interactions between serum components and DV particles. Through co-immunoprecipitation we revealed that apolipoprotein A-I (ApoA-I), the major protein component in HDL, is associated with DV particles and is able to promote DV infection. Based on that observation, we further found that siRNA knockdown of the scavenger receptor class B type I (SR-BI), the cell receptor of ApoA-I, abolished the activity of ApoA-I in enhancement of DV infection. This suggests that ApoA-I bridges DV particles and cell receptor SR-BI and facilitates entry of DV into cells. FACS analysis of cell surface dengue antigen after virus absorption further confirmed that ApoA-I enhances DV infection via promoting initial attachment of the virus to cells. These findings illustrate a novel entry route of DV into cells, which may provide insights into the functional importance of lipoproteins in dengue pathogenesis.http://europepmc.org/articles/PMC3722190?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Yujia Li
Cherie Kakinami
Qi Li
Baojun Yang
Hongwei Li
spellingShingle Yujia Li
Cherie Kakinami
Qi Li
Baojun Yang
Hongwei Li
Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
PLoS ONE
author_facet Yujia Li
Cherie Kakinami
Qi Li
Baojun Yang
Hongwei Li
author_sort Yujia Li
title Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
title_short Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
title_full Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
title_fullStr Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
title_full_unstemmed Human apolipoprotein A-I is associated with dengue virus and enhances virus infection through SR-BI.
title_sort human apolipoprotein a-i is associated with dengue virus and enhances virus infection through sr-bi.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description Diseases caused by dengue virus (DV) infection vary in severity, with symptoms ranging from mild fever to life threatening dengue hemorrhage fever (DHF) and dengue shock syndrome (DSS). Clinical studies have shown that significant decrease in the level of lipoproteins is correlated with severe illness in DHF/DSS patients. Available evidence also indicates that lipoproteins including high-density lipoprotein (HDL) and low-density lipoprotein (LDL) are able to facilitate cell entry of HCV or other flaviviruses via corresponding lipoprotein receptors. In this study, we found that pre-incubation of DV with human serum leads to an enhanced DV infectivity in various types of cells. Such enhancement could be due to interactions between serum components and DV particles. Through co-immunoprecipitation we revealed that apolipoprotein A-I (ApoA-I), the major protein component in HDL, is associated with DV particles and is able to promote DV infection. Based on that observation, we further found that siRNA knockdown of the scavenger receptor class B type I (SR-BI), the cell receptor of ApoA-I, abolished the activity of ApoA-I in enhancement of DV infection. This suggests that ApoA-I bridges DV particles and cell receptor SR-BI and facilitates entry of DV into cells. FACS analysis of cell surface dengue antigen after virus absorption further confirmed that ApoA-I enhances DV infection via promoting initial attachment of the virus to cells. These findings illustrate a novel entry route of DV into cells, which may provide insights into the functional importance of lipoproteins in dengue pathogenesis.
url http://europepmc.org/articles/PMC3722190?pdf=render
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AT cheriekakinami humanapolipoproteinaiisassociatedwithdenguevirusandenhancesvirusinfectionthroughsrbi
AT qili humanapolipoproteinaiisassociatedwithdenguevirusandenhancesvirusinfectionthroughsrbi
AT baojunyang humanapolipoproteinaiisassociatedwithdenguevirusandenhancesvirusinfectionthroughsrbi
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