Sutha SangiambutNatcha PromphetSuwipa ChaiyaloomChunya PuttikhuntPanisadee AvirutnanWatchara KasinrerkNopporn SittisombutPrida MalasitSiriraj HospitalThailand National Center for Genetic Engineering and BiotechnologyThailand National Science and Technology Development AgencyChiang Mai University2022-08-042022-08-042021-01-01Journal of General Virology. Vol.102, No.8 (2021)14652099002213172-s2.0-85114100271https://repository.li.mahidol.ac.th/handle/20.500.14594/77346The capsid protein (C) of dengue virus is required for viral infectivity as it packages viral RNA genome into infectious particles. C exists as a homodimer that forms via hydrophobic interactions between the α2 and α4 helices of monomers. To identify C region(s) important for virus particle production, a complementation system was employed in which single-round infectious particles are generated by trans-encapsidation of a viral C-deleted genome by recombinant C expressed in mosquito cells. Mutants harbouring a complete α3 deletion, or a dual Ile65-/Trp69-to-Ala substitution in the α3 helix, exhibited reduced production of infectious virus. Unexpectedly, higher proportions of oligomeric C were detected in cells expressing both mutated forms as compared with the wild-type counterpart, indicating that the α3 helix, through its internal hydrophobic residues, may down-modulate oligomerization of C during particle formation. Compared with wild-type C, the double Ile65-/Trp69 to Ala mutations appeared to hamper viral infectivity but not C and genomic RNA incorporation into the pseudo-infectious virus particles, suggesting that increased C oligomerization may impair DENV replication at the cell entry step.Mahidol UniversityImmunology and MicrobiologyArticleSCOPUS10.1099/JGV.0.001635