Identification of Interactions between Sindbis Virus Capsid Protein and Cytoplasmic vRNA as Novel Virulence Determinants
Fig 8
Proposed model of SINV C:R interaction site function.
After receptor mediated endocytosis the acidification of the endosome resulting in release of the nucleocapsid core into the host cytoplasm. Disassembly of the nucleocapsid core occurs shortly after endosomal release; and SINV capsid protein remains bound to the C:R interaction sites following disassembly. Retention of Capsid:RNA binding at the C:R interaction sites enables evasion of the host RNA decay machinery and rapid assembly of the host translational machinery. Collectively, these interactions lead to the efficient establishment of viral infection, including but not limited to the modulation of the host innate immune response resulting in viral disease and pathogenesis. Disruption of the C:R interaction sites (lower pathway), leading to the ablation of Capsid:RNA interactions, results in RNA instability and a reduction of genomic RNA function early during infection.