Abstract
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.
Highlights
Dengue virus (DENV) is a positive-stranded RNA virus in the Flaviviridae family, which is transmitted by mosquito vectors
dengue virus (DENV) viral protein synthesis was determined by western blotting and DENV production was measured by focus forming unit (FFU) assay
This hypothesis was supported by RNA interference (RNAi), which showed that DENV RNA was significantly reduced in DENV-infected Huh7 cells transfected with Adaptor protein complex (AP)-1A small interfering RNA (siRNA) compared with control siRNA
Summary
Dengue virus (DENV) is a positive-stranded RNA virus in the Flaviviridae family, which is transmitted by mosquito vectors. The genome of DENV has sequences encoding structural proteins including capsid (C), pre-membrane protein (prM), and envelope (E), and non-structural proteins (NS) including NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5 [1]. DENV consists of four serotypes, and secondary infection by different serotypes of DENV contributes to PLOS ONE | DOI:10.1371/journal.pone.0130065. AP-1A Faciliates DENV Replication severe dengue [2]. Patients with dengue hemorrhagic fever often present with plasma leakage, hemoconcentration, thrombocytopenia, and hemorrhagic tendencies. Serious complications of dengue hemorrhagic fever, such as organ failure, may lead to dengue shock syndrome [1,2,3]. There are no effective vaccines or antiviral drugs available; a better understanding of dengue pathogenesis is required
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