Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/62585
Title: Coat protein complex I facilitates dengue virus production
Authors: Nopprarat Tongmuang
Umpa Yasamut
Pucharee Songprakhon
Thanyaporn Dechtawewat
Shilu Malakar
Sansanee Noisakran
Pa thai Yenchitsomanus
Thawornchai Limjindaporn
Authors: Nopprarat Tongmuang
Umpa Yasamut
Pucharee Songprakhon
Thanyaporn Dechtawewat
Shilu Malakar
Sansanee Noisakran
Pa thai Yenchitsomanus
Thawornchai Limjindaporn
Keywords: Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology;Medicine
Issue Date: 2-May-2018
Abstract: © 2018 Elsevier B.V. Dengue hemorrhagic fever is a life-threatening disease caused by the dengue virus (DENV). After DENV enters into host cells, it replicates to generate viral particles to infect other cells. DENV exploits components of the cellular trafficking pathway to achieve effective virion production. Understanding of the proteins required for this trafficking process is essential for revealing the pathogenesis of DENV infection. Coat protein complex and soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs), two host protein families in the cellular trafficking pathway, were investigated to elucidate their respective roles during DENV infection. Coat proteins (COPI and COPII) and SNAREs (STX 5 and NSF) were knocked down in a DENV-infected Huh7 cells by RNA interference. Depletion of COPI and COPII, but not of STX5 and NSF, decreased DENV production in DENV-infected Huh7 cells. DENV proteins, including DENV C, prM, E, and NS1, were significantly reduced in COPI-silenced DENV-infected Huh7 cells, when compared to those of control cells. COPI also facilitated DENV production in an endothelial cell line and in all DENV serotypes, indicating the importance of coat protein complex in facilitating DENV infection.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85053782064&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/62585
ISSN: 18727492
01681702
Appears in Collections:CMUL: Journal Articles

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