Umpa YasamutNopprarat TongmuangPa Thai YenchitsomanusMutita JunkingSansanee NoisakranChunya PuttikhuntJustin Jang Hann ChuThawornchai LimjindapornMahidol UniversityThailand National Center for Genetic Engineering and BiotechnologyYong Loo Lin School of Medicine2018-11-232018-11-232015-06-19PLoS ONE. Vol.10, No.6 (2015)193262032-s2.0-84939143087https://repository.li.mahidol.ac.th/handle/20.500.14594/35141© 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.Mahidol UniversityAgricultural and Biological SciencesBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1371/journal.pone.0130065