The 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.

中文翻译：

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衣壳寡聚化增加对登革热病毒颗粒的产生有害

登革热病毒的衣壳蛋白 (C) 是病毒传染性所必需的，因为它将病毒 RNA 基因组包装成传染性颗粒。C 作为同型二聚体存在，通过单体的 α2 和 α4 螺旋之间的疏水相互作用形成。为了识别对病毒颗粒产生重要的 C 区，采用了一种互补系统，其中通过反式产生单轮感染性颗粒。-通过在蚊子细胞中表达的重组 C 对病毒 C 缺失的基因组进行衣壳化。在 α3 螺旋中含有完全 α3 缺失或双重 Ile65-/Trp69-to-Ala 取代的突变体表现出感染性病毒的产生减少。出乎意料的是，与野生型对应物相比，在表达两种突变形式的细胞中检测到更高比例的寡聚 C，表明 α3 螺旋通过其内部疏水残基可能在颗粒形成过程中下调 C 的寡聚化。与野生型 C 相比，Ile65-/Trp69 到 Ala 的双重突变似乎阻碍了病毒感染性，但不会阻碍 C 和基因组 RNA 掺入假感染病毒颗粒，这表明增加的 C 寡聚化可能会损害细胞进入步骤的 DENV 复制.