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Title: Adaptor protein 1A facilitates dengue virus replication
Authors: Umpa Yasamut
Nopprarat Tongmuang
Pa Thai Yenchitsomanus
Mutita Junking
Sansanee Noisakran
Chunya Puttikhunt
Justin Jang Hann Chu
Thawornchai Limjindaporn
Mahidol University
Thailand National Center for Genetic Engineering and Biotechnology
Yong Loo Lin School of Medicine
Keywords: Agricultural and Biological Sciences;Biochemistry, Genetics and Molecular Biology
Issue Date: 19-Jun-2015
Citation: PLoS ONE. Vol.10, No.6 (2015)
Abstract: © 2015 Yasamut et al. Rearrangement of membrane structure induced by dengue virus (DENV) is essential for replication, and requires host cellular machinery. Adaptor protein complex (AP)-1 is a host component, which can be recruited to components required for membrane rearrangement. Therefore, dysfunction of AP-1 may affect membrane organization, thereby decreasing replication of virus in infected cells. In the present study, AP-1-dependent traffic inhibitor inhibited DENV protein expression and virion production. We further clarified the role of AP-1A in the life cycle of DENV by RNA interference. AP-1A was not involved in DENV entry into cells. However, it facilitated DENV RNA replication. Viral RNA level was reduced significantly in Huh7 cells transfected with AP-1A small interfering RNA (siRNA) compared with control siRNA. Transfection of naked DENV viral RNA into Huh7 cells transfected with AP-1A siRNA resulted in less viral RNA and virion production than transfection into Huh7 cells transfected with control siRNA. Huh7 cells transfected with AP-1A siRNA showed greater modification of membrane structures and fewer vesicular packets compared with cells transfected with control siRNA. Therefore, AP-1A may partly control DENV-induced rearrangement of membrane structures required for viral replication.
ISSN: 19326203
Appears in Collections:Scopus 2011-2015

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